---
_id: '12157'
abstract:
- lang: eng
  text: 'Polygenic adaptation is thought to be ubiquitous, yet remains poorly understood.
    Here, we model this process analytically, in the plausible setting of a highly
    polygenic, quantitative trait that experiences a sudden shift in the fitness optimum.
    We show how the mean phenotype changes over time, depending on the effect sizes
    of loci that contribute to variance in the trait, and characterize the allele
    dynamics at these loci. Notably, we describe the two phases of the allele dynamics:
    The first is a rapid phase, in which directional selection introduces small frequency
    differences between alleles whose effects are aligned with or opposed to the shift,
    ultimately leading to small differences in their probability of fixation during
    a second, longer phase, governed by stabilizing selection. As we discuss, key
    results should hold in more general settings and have important implications for
    efforts to identify the genetic basis of adaptation in humans and other species.'
acknowledgement: "We thank Guy Amster, Jeremy Berg, Nick Barton, Yuval Simons and
  Molly Przeworski for many helpful discussions, and Jeremy Berg, Graham Coop, Joachim
  Hermisson, Guillaume Martin, Will Milligan, Peter Ralph, Yuval Simons, Leo Speidel
  and Molly Przeworski for comments on the manuscript.\r\nNational Institutes of Health
  GM115889 Laura Katharine Hayward Guy Sella \r\nNational Institutes of Health GM121372
  Laura Katharine Hayward"
article_number: '66697'
article_processing_charge: No
article_type: original
author:
- first_name: Laura
  full_name: Hayward, Laura
  id: fc885ee5-24bf-11eb-ad7b-bcc5104c0c1b
  last_name: Hayward
- first_name: Guy
  full_name: Sella, Guy
  last_name: Sella
citation:
  ama: Hayward L, Sella G. Polygenic adaptation after a sudden change in environment.
    <i>eLife</i>. 2022;11. doi:<a href="https://doi.org/10.7554/elife.66697">10.7554/elife.66697</a>
  apa: Hayward, L., &#38; Sella, G. (2022). Polygenic adaptation after a sudden change
    in environment. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.66697">https://doi.org/10.7554/elife.66697</a>
  chicago: Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change
    in Environment.” <i>ELife</i>. eLife Sciences Publications, 2022. <a href="https://doi.org/10.7554/elife.66697">https://doi.org/10.7554/elife.66697</a>.
  ieee: L. Hayward and G. Sella, “Polygenic adaptation after a sudden change in environment,”
    <i>eLife</i>, vol. 11. eLife Sciences Publications, 2022.
  ista: Hayward L, Sella G. 2022. Polygenic adaptation after a sudden change in environment.
    eLife. 11, 66697.
  mla: Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change
    in Environment.” <i>ELife</i>, vol. 11, 66697, eLife Sciences Publications, 2022,
    doi:<a href="https://doi.org/10.7554/elife.66697">10.7554/elife.66697</a>.
  short: L. Hayward, G. Sella, ELife 11 (2022).
date_created: 2023-01-12T12:09:00Z
date_published: 2022-09-26T00:00:00Z
date_updated: 2023-08-04T09:04:58Z
day: '26'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.7554/elife.66697
external_id:
  isi:
  - '000890735600001'
file:
- access_level: open_access
  checksum: 28de155b231ac1c8d4501c98b2fb359a
  content_type: application/pdf
  creator: dernst
  date_created: 2023-01-24T12:21:32Z
  date_updated: 2023-01-24T12:21:32Z
  file_id: '12363'
  file_name: 2022_eLife_Hayward.pdf
  file_size: 18935612
  relation: main_file
  success: 1
file_date_updated: 2023-01-24T12:21:32Z
has_accepted_license: '1'
intvolume: '        11'
isi: 1
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
  eissn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Polygenic adaptation after a sudden change in environment
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '12208'
abstract:
- lang: eng
  text: The inadequate understanding of the mechanisms that reversibly convert molecular
    sulfur (S) into lithium sulfide (Li<jats:sub>2</jats:sub>S) via soluble polysulfides
    (PSs) formation impedes the development of high-performance lithium-sulfur (Li-S)
    batteries with non-aqueous electrolyte solutions. Here, we use operando small
    and wide angle X-ray scattering and operando small angle neutron scattering (SANS)
    measurements to track the nucleation, growth and dissolution of solid deposits
    from atomic to sub-micron scales during real-time Li-S cell operation. In particular,
    stochastic modelling based on the SANS data allows quantifying the nanoscale phase
    evolution during battery cycling. We show that next to nano-crystalline Li<jats:sub>2</jats:sub>S
    the deposit comprises solid short-chain PSs particles. The analysis of the experimental
    data suggests that initially, Li<jats:sub>2</jats:sub>S<jats:sub>2</jats:sub>
    precipitates from the solution and then is partially converted via solid-state
    electroreduction to Li<jats:sub>2</jats:sub>S. We further demonstrate that mass
    transport, rather than electron transport through a thin passivating film, limits
    the discharge capacity and rate performance in Li-S cells.
acknowledgement: "This project has received funding from the European Union’s Horizon
  2020 research and innovation program under the Marie Skłodowska-Curie grant NanoEvolution,
  grant agreement No 894042. The authors acknowledge the CERIC-ERIC Consortium for
  the access to the Austrian SAXS beamline and TU Graz for support through the Lead
  Project LP-03.\r\nLikewise, the use of SOMAPP Lab, a core facility supported by
  the Austrian Federal Ministry of Education, Science and Research, the Graz University
  of Technology, the University of Graz, and Anton Paar GmbH is acknowledged. In addition,
  the authors acknowledge access to the D-22SANS beamline at the ILL neutron source.
  Electron microscopy measurements were performed at the Scientific Scenter for Optical
  and Electron Microscopy (ScopeM) of the Swiss Federal Institute of Technology. C.P.
  and J.M.M. thank A. Senol for her support with the SANS\r\nbeamtime preparation.
  S.D.T, A.V. and R.D. acknowledge the financial support by the Slovenian Research
  Agency (ARRS) research core funding P2-0393 and P2-0423. Furthermore, A.V. acknowledge
  the funding from the Slovenian Research Agency, research project Z2−1863.\r\nS.A.F.
  is indebted to IST Austria for support. "
article_number: '6326'
article_processing_charge: No
article_type: original
author:
- first_name: Christian
  full_name: Prehal, Christian
  last_name: Prehal
- first_name: Jean-Marc
  full_name: von Mentlen, Jean-Marc
  last_name: von Mentlen
- first_name: Sara
  full_name: Drvarič Talian, Sara
  last_name: Drvarič Talian
- first_name: Alen
  full_name: Vizintin, Alen
  last_name: Vizintin
- first_name: Robert
  full_name: Dominko, Robert
  last_name: Dominko
- first_name: Heinz
  full_name: Amenitsch, Heinz
  last_name: Amenitsch
- first_name: Lionel
  full_name: Porcar, Lionel
  last_name: Porcar
- first_name: Stefan Alexander
  full_name: Freunberger, Stefan Alexander
  id: A8CA28E6-CE23-11E9-AD2D-EC27E6697425
  last_name: Freunberger
  orcid: 0000-0003-2902-5319
- first_name: Vanessa
  full_name: Wood, Vanessa
  last_name: Wood
citation:
  ama: Prehal C, von Mentlen J-M, Drvarič Talian S, et al. On the nanoscale structural
    evolution of solid discharge products in lithium-sulfur batteries using operando
    scattering. <i>Nature Communications</i>. 2022;13. doi:<a href="https://doi.org/10.1038/s41467-022-33931-4">10.1038/s41467-022-33931-4</a>
  apa: Prehal, C., von Mentlen, J.-M., Drvarič Talian, S., Vizintin, A., Dominko,
    R., Amenitsch, H., … Wood, V. (2022). On the nanoscale structural evolution of
    solid discharge products in lithium-sulfur batteries using operando scattering.
    <i>Nature Communications</i>. Springer Nature. <a href="https://doi.org/10.1038/s41467-022-33931-4">https://doi.org/10.1038/s41467-022-33931-4</a>
  chicago: Prehal, Christian, Jean-Marc von Mentlen, Sara Drvarič Talian, Alen Vizintin,
    Robert Dominko, Heinz Amenitsch, Lionel Porcar, Stefan Alexander Freunberger,
    and Vanessa Wood. “On the Nanoscale Structural Evolution of Solid Discharge Products
    in Lithium-Sulfur Batteries Using Operando Scattering.” <i>Nature Communications</i>.
    Springer Nature, 2022. <a href="https://doi.org/10.1038/s41467-022-33931-4">https://doi.org/10.1038/s41467-022-33931-4</a>.
  ieee: C. Prehal <i>et al.</i>, “On the nanoscale structural evolution of solid discharge
    products in lithium-sulfur batteries using operando scattering,” <i>Nature Communications</i>,
    vol. 13. Springer Nature, 2022.
  ista: Prehal C, von Mentlen J-M, Drvarič Talian S, Vizintin A, Dominko R, Amenitsch
    H, Porcar L, Freunberger SA, Wood V. 2022. On the nanoscale structural evolution
    of solid discharge products in lithium-sulfur batteries using operando scattering.
    Nature Communications. 13, 6326.
  mla: Prehal, Christian, et al. “On the Nanoscale Structural Evolution of Solid Discharge
    Products in Lithium-Sulfur Batteries Using Operando Scattering.” <i>Nature Communications</i>,
    vol. 13, 6326, Springer Nature, 2022, doi:<a href="https://doi.org/10.1038/s41467-022-33931-4">10.1038/s41467-022-33931-4</a>.
  short: C. Prehal, J.-M. von Mentlen, S. Drvarič Talian, A. Vizintin, R. Dominko,
    H. Amenitsch, L. Porcar, S.A. Freunberger, V. Wood, Nature Communications 13 (2022).
date_created: 2023-01-16T09:45:09Z
date_published: 2022-10-24T00:00:00Z
date_updated: 2023-08-04T09:15:31Z
day: '24'
ddc:
- '540'
department:
- _id: StFr
doi: 10.1038/s41467-022-33931-4
external_id:
  isi:
  - '000871563700006'
  pmid:
  - '36280671'
file:
- access_level: open_access
  checksum: 5034336dbf0f860030ef745c08df9e0e
  content_type: application/pdf
  creator: dernst
  date_created: 2023-01-27T07:19:11Z
  date_updated: 2023-01-27T07:19:11Z
  file_id: '12411'
  file_name: 2022_NatureCommunications_Prehal.pdf
  file_size: 4216931
  relation: main_file
  success: 1
file_date_updated: 2023-01-27T07:19:11Z
has_accepted_license: '1'
intvolume: '        13'
isi: 1
keyword:
- General Physics and Astronomy
- General Biochemistry
- Genetics and Molecular Biology
- General Chemistry
- Multidisciplinary
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: On the nanoscale structural evolution of solid discharge products in lithium-sulfur
  batteries using operando scattering
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 13
year: '2022'
...
---
_id: '12217'
abstract:
- lang: eng
  text: The development dynamics and self-organization of glandular branched epithelia
    is of utmost importance for our understanding of diverse processes ranging from
    normal tissue growth to the growth of cancerous tissues. Using single primary
    murine pancreatic ductal adenocarcinoma (PDAC) cells embedded in a collagen matrix
    and adapted media supplementation, we generate organoids that self-organize into
    highly branched structures displaying a seamless lumen connecting terminal end
    buds, replicating in vivo PDAC architecture. We identify distinct morphogenesis
    phases, each characterized by a unique pattern of cell invasion, matrix deformation,
    protein expression, and respective molecular dependencies. We propose a minimal
    theoretical model of a branching and proliferating tissue, capturing the dynamics
    of the first phases. Observing the interaction of morphogenesis, mechanical environment
    and gene expression in vitro sets a benchmark for the understanding of self-organization
    processes governing complex organoid structure formation processes and branching
    morphogenesis.
acknowledgement: "A.R.B. acknowledges the financial support of the European Research
  Council (ERC) through the funding of the grant Principles of Integrin Mechanics
  and Adhesion (PoINT) and the German Research Foundation (DFG, SFB 1032, project
  ID 201269156). E.H. was supported by the European Union (European Research Council
  Starting Grant 851288). D.S., M.R., and R.R. acknowledge the support by the German
  Research Foundation (DFG, SFB1321 Modeling and Targeting Pancreatic Cancer, Project
  S01, project ID 329628492). C.S. and M.R. acknowledge the support by the German
  Research Foundation (DFG, SFB1321 Modeling and Targeting Pancreatic Cancer, Project
  12, project ID 329628492). M.R. was supported by the German Research Foundation
  (DFG RE 3723/4-1). A.P. and M.R. were supported by the German Cancer Aid (Max-Eder
  Program 111273 and 70114328).\r\nOpen Access funding enabled and organized by Projekt
  DEAL."
article_number: '5219'
article_processing_charge: No
article_type: original
author:
- first_name: S.
  full_name: Randriamanantsoa, S.
  last_name: Randriamanantsoa
- first_name: A.
  full_name: Papargyriou, A.
  last_name: Papargyriou
- first_name: H. C.
  full_name: Maurer, H. C.
  last_name: Maurer
- first_name: K.
  full_name: Peschke, K.
  last_name: Peschke
- first_name: M.
  full_name: Schuster, M.
  last_name: Schuster
- first_name: G.
  full_name: Zecchin, G.
  last_name: Zecchin
- first_name: K.
  full_name: Steiger, K.
  last_name: Steiger
- first_name: R.
  full_name: Öllinger, R.
  last_name: Öllinger
- first_name: D.
  full_name: Saur, D.
  last_name: Saur
- first_name: C.
  full_name: Scheel, C.
  last_name: Scheel
- first_name: R.
  full_name: Rad, R.
  last_name: Rad
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: M.
  full_name: Reichert, M.
  last_name: Reichert
- first_name: A. R.
  full_name: Bausch, A. R.
  last_name: Bausch
citation:
  ama: Randriamanantsoa S, Papargyriou A, Maurer HC, et al. Spatiotemporal dynamics
    of self-organized branching in pancreas-derived organoids. <i>Nature Communications</i>.
    2022;13. doi:<a href="https://doi.org/10.1038/s41467-022-32806-y">10.1038/s41467-022-32806-y</a>
  apa: Randriamanantsoa, S., Papargyriou, A., Maurer, H. C., Peschke, K., Schuster,
    M., Zecchin, G., … Bausch, A. R. (2022). Spatiotemporal dynamics of self-organized
    branching in pancreas-derived organoids. <i>Nature Communications</i>. Springer
    Nature. <a href="https://doi.org/10.1038/s41467-022-32806-y">https://doi.org/10.1038/s41467-022-32806-y</a>
  chicago: Randriamanantsoa, S., A. Papargyriou, H. C. Maurer, K. Peschke, M. Schuster,
    G. Zecchin, K. Steiger, et al. “Spatiotemporal Dynamics of Self-Organized Branching
    in Pancreas-Derived Organoids.” <i>Nature Communications</i>. Springer Nature,
    2022. <a href="https://doi.org/10.1038/s41467-022-32806-y">https://doi.org/10.1038/s41467-022-32806-y</a>.
  ieee: S. Randriamanantsoa <i>et al.</i>, “Spatiotemporal dynamics of self-organized
    branching in pancreas-derived organoids,” <i>Nature Communications</i>, vol. 13.
    Springer Nature, 2022.
  ista: Randriamanantsoa S, Papargyriou A, Maurer HC, Peschke K, Schuster M, Zecchin
    G, Steiger K, Öllinger R, Saur D, Scheel C, Rad R, Hannezo EB, Reichert M, Bausch
    AR. 2022. Spatiotemporal dynamics of self-organized branching in pancreas-derived
    organoids. Nature Communications. 13, 5219.
  mla: Randriamanantsoa, S., et al. “Spatiotemporal Dynamics of Self-Organized Branching
    in Pancreas-Derived Organoids.” <i>Nature Communications</i>, vol. 13, 5219, Springer
    Nature, 2022, doi:<a href="https://doi.org/10.1038/s41467-022-32806-y">10.1038/s41467-022-32806-y</a>.
  short: S. Randriamanantsoa, A. Papargyriou, H.C. Maurer, K. Peschke, M. Schuster,
    G. Zecchin, K. Steiger, R. Öllinger, D. Saur, C. Scheel, R. Rad, E.B. Hannezo,
    M. Reichert, A.R. Bausch, Nature Communications 13 (2022).
date_created: 2023-01-16T09:46:53Z
date_published: 2022-09-05T00:00:00Z
date_updated: 2023-08-04T09:25:23Z
day: '05'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1038/s41467-022-32806-y
ec_funded: 1
external_id:
  isi:
  - '000850348400025'
file:
- access_level: open_access
  checksum: 295261b5172274fd5b8f85a6a6058828
  content_type: application/pdf
  creator: dernst
  date_created: 2023-01-27T08:14:48Z
  date_updated: 2023-01-27T08:14:48Z
  file_id: '12416'
  file_name: 2022_NatureCommunications_Randriamanantsoa.pdf
  file_size: 22645149
  relation: main_file
  success: 1
file_date_updated: 2023-01-27T08:14:48Z
has_accepted_license: '1'
intvolume: '        13'
isi: 1
keyword:
- General Physics and Astronomy
- General Biochemistry
- Genetics and Molecular Biology
- General Chemistry
- Multidisciplinary
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
project:
- _id: 05943252-7A3F-11EA-A408-12923DDC885E
  call_identifier: H2020
  grant_number: '851288'
  name: Design Principles of Branching Morphogenesis
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
  record:
  - id: '13068'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: Spatiotemporal dynamics of self-organized branching in pancreas-derived organoids
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 13
year: '2022'
...
---
_id: '12224'
abstract:
- lang: eng
  text: Muskelin (Mkln1) is implicated in neuronal function, regulating plasma membrane
    receptor trafficking. However, its influence on intrinsic brain activity and corresponding
    behavioral processes remains unclear. Here we show that murine <jats:italic>Mkln1</jats:italic>
    knockout causes non-habituating locomotor activity, increased exploratory drive,
    and decreased locomotor response to amphetamine. Muskelin deficiency impairs social
    novelty detection while promoting the retention of spatial reference memory and
    fear extinction recall. This is strongly mirrored in either weaker or stronger
    resting-state functional connectivity between critical circuits mediating locomotor
    exploration and cognition. We show that <jats:italic>Mkln1</jats:italic> deletion
    alters dendrite branching and spine structure, coinciding with enhanced AMPAR-mediated
    synaptic transmission but selective impairment in synaptic potentiation maintenance.
    We identify muskelin at excitatory synapses and highlight its role in regulating
    dendritic spine actin stability. Our findings point to aberrant spine actin modulation
    and changes in glutamatergic synaptic function as critical mechanisms that contribute
    to the neurobehavioral phenotype arising from <jats:italic>Mkln1</jats:italic>
    ablation.
acknowledgement: "The authors are grateful to the UKE Animal Facilities (Hamburg)
  for animal husbandry and Dr. Bastian Tiemann for his veterinary expertise and supervision
  of animal care. We thank Dr. Franco Lombino for critically reading the manuscript
  and for helpful discussion. This work was supported by grants from the Deutsche
  Forschungsgemeinschaft (DFG) (FOR2419-KN556/11-1, FOR2419-KN556/11-2, KN556/12-1)
  and the Landesforschungsförderung Hamburg (LFF-FV76) to M.K.\r\nOpen Access funding
  enabled and organized by Projekt DEAL."
article_number: '589'
article_processing_charge: No
article_type: original
author:
- first_name: Mary W
  full_name: Muhia, Mary W
  id: ab7ed20f-09f7-11eb-909c-d5d0b443ee9d
  last_name: Muhia
- first_name: PingAn
  full_name: YuanXiang, PingAn
  last_name: YuanXiang
- first_name: Jan
  full_name: Sedlacik, Jan
  last_name: Sedlacik
- first_name: Jürgen R.
  full_name: Schwarz, Jürgen R.
  last_name: Schwarz
- first_name: Frank F.
  full_name: Heisler, Frank F.
  last_name: Heisler
- first_name: Kira V.
  full_name: Gromova, Kira V.
  last_name: Gromova
- first_name: Edda
  full_name: Thies, Edda
  last_name: Thies
- first_name: Petra
  full_name: Breiden, Petra
  last_name: Breiden
- first_name: Yvonne
  full_name: Pechmann, Yvonne
  last_name: Pechmann
- first_name: Michael R.
  full_name: Kreutz, Michael R.
  last_name: Kreutz
- first_name: Matthias
  full_name: Kneussel, Matthias
  last_name: Kneussel
citation:
  ama: Muhia MW, YuanXiang P, Sedlacik J, et al. Muskelin regulates actin-dependent
    synaptic changes and intrinsic brain activity relevant to behavioral and cognitive
    processes. <i>Communications Biology</i>. 2022;5. doi:<a href="https://doi.org/10.1038/s42003-022-03446-1">10.1038/s42003-022-03446-1</a>
  apa: Muhia, M. W., YuanXiang, P., Sedlacik, J., Schwarz, J. R., Heisler, F. F.,
    Gromova, K. V., … Kneussel, M. (2022). Muskelin regulates actin-dependent synaptic
    changes and intrinsic brain activity relevant to behavioral and cognitive processes.
    <i>Communications Biology</i>. Springer Nature. <a href="https://doi.org/10.1038/s42003-022-03446-1">https://doi.org/10.1038/s42003-022-03446-1</a>
  chicago: Muhia, Mary W, PingAn YuanXiang, Jan Sedlacik, Jürgen R. Schwarz, Frank
    F. Heisler, Kira V. Gromova, Edda Thies, et al. “Muskelin Regulates Actin-Dependent
    Synaptic Changes and Intrinsic Brain Activity Relevant to Behavioral and Cognitive
    Processes.” <i>Communications Biology</i>. Springer Nature, 2022. <a href="https://doi.org/10.1038/s42003-022-03446-1">https://doi.org/10.1038/s42003-022-03446-1</a>.
  ieee: M. W. Muhia <i>et al.</i>, “Muskelin regulates actin-dependent synaptic changes
    and intrinsic brain activity relevant to behavioral and cognitive processes,”
    <i>Communications Biology</i>, vol. 5. Springer Nature, 2022.
  ista: Muhia MW, YuanXiang P, Sedlacik J, Schwarz JR, Heisler FF, Gromova KV, Thies
    E, Breiden P, Pechmann Y, Kreutz MR, Kneussel M. 2022. Muskelin regulates actin-dependent
    synaptic changes and intrinsic brain activity relevant to behavioral and cognitive
    processes. Communications Biology. 5, 589.
  mla: Muhia, Mary W., et al. “Muskelin Regulates Actin-Dependent Synaptic Changes
    and Intrinsic Brain Activity Relevant to Behavioral and Cognitive Processes.”
    <i>Communications Biology</i>, vol. 5, 589, Springer Nature, 2022, doi:<a href="https://doi.org/10.1038/s42003-022-03446-1">10.1038/s42003-022-03446-1</a>.
  short: M.W. Muhia, P. YuanXiang, J. Sedlacik, J.R. Schwarz, F.F. Heisler, K.V. Gromova,
    E. Thies, P. Breiden, Y. Pechmann, M.R. Kreutz, M. Kneussel, Communications Biology
    5 (2022).
date_created: 2023-01-16T09:48:19Z
date_published: 2022-06-15T00:00:00Z
date_updated: 2023-08-04T09:25:59Z
day: '15'
ddc:
- '570'
department:
- _id: PreCl
doi: 10.1038/s42003-022-03446-1
external_id:
  isi:
  - '000811777900003'
file:
- access_level: open_access
  checksum: bd95be1e77090208b79bc45ea8785d0b
  content_type: application/pdf
  creator: dernst
  date_created: 2023-01-27T08:23:46Z
  date_updated: 2023-01-27T08:23:46Z
  file_id: '12417'
  file_name: 2022_CommBiology_Muhia.pdf
  file_size: 3968356
  relation: main_file
  success: 1
file_date_updated: 2023-01-27T08:23:46Z
has_accepted_license: '1'
intvolume: '         5'
isi: 1
keyword:
- General Agricultural and Biological Sciences
- General Biochemistry
- Genetics and Molecular Biology
- Medicine (miscellaneous)
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: Communications Biology
publication_identifier:
  issn:
  - 2399-3642
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Muskelin regulates actin-dependent synaptic changes and intrinsic brain activity
  relevant to behavioral and cognitive processes
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 5
year: '2022'
...
---
_id: '12238'
abstract:
- lang: eng
  text: Upon the initiation of collective cell migration, the cells at the free edge
    are specified as leader cells; however, the mechanism underlying the leader cell
    specification remains elusive. Here, we show that lamellipodial extension after
    the release from mechanical confinement causes sustained extracellular signal-regulated
    kinase (ERK) activation and underlies the leader cell specification. Live-imaging
    of Madin-Darby canine kidney (MDCK) cells and mouse epidermis through the use
    of Förster resonance energy transfer (FRET)-based biosensors showed that leader
    cells exhibit sustained ERK activation in a hepatocyte growth factor (HGF)-dependent
    manner. Meanwhile, follower cells exhibit oscillatory ERK activation waves in
    an epidermal growth factor (EGF) signaling-dependent manner. Lamellipodial extension
    at the free edge increases the cellular sensitivity to HGF. The HGF-dependent
    ERK activation, in turn, promotes lamellipodial extension, thereby forming a positive
    feedback loop between cell extension and ERK activation and specifying the cells
    at the free edge as the leader cells. Our findings show that the integration of
    physical and biochemical cues underlies the leader cell specification during collective
    cell migration.
acknowledgement: We thank the members of the Matsuda Laboratory for their helpful
  discussion and encouragement, and we thank K. Hirano and K. Takakura for their technical
  assistance. This work was supported by the Kyoto University Live Imaging Center.
  Financial support was provided in the form of JSPS KAKENHI grants (nos. 17J02107
  and 20K22653 to N.H., and 20H05898 and 19H00993 to M.M.), a JST CREST grant (no.
  JPMJCR1654 to M.M.), a Moonshot R&D grant (no. JPMJPS2022-11 to M.M.), Generalitat
  de Catalunya and the CERCA Programme (no. SGR-2017-01602 to X.T.), MICCINN/FEDER
  (no. PGC2018-099645-B-I00 to X.T.), and European Research Council (no. Adv-883739
  to X.T.). IBEC is a recipient of a Severo Ochoa Award of Excellence from the MINECO.
  This work was partly supported by an Extramural Collaborative Research Grant of
  Cancer Research Institute, Kanazawa University.
article_processing_charge: No
article_type: original
author:
- first_name: Naoya
  full_name: Hino, Naoya
  id: 5299a9ce-7679-11eb-a7bc-d1e62b936307
  last_name: Hino
- first_name: Kimiya
  full_name: Matsuda, Kimiya
  last_name: Matsuda
- first_name: Yuya
  full_name: Jikko, Yuya
  last_name: Jikko
- first_name: Gembu
  full_name: Maryu, Gembu
  last_name: Maryu
- first_name: Katsuya
  full_name: Sakai, Katsuya
  last_name: Sakai
- first_name: Ryu
  full_name: Imamura, Ryu
  last_name: Imamura
- first_name: Shinya
  full_name: Tsukiji, Shinya
  last_name: Tsukiji
- first_name: Kazuhiro
  full_name: Aoki, Kazuhiro
  last_name: Aoki
- first_name: Kenta
  full_name: Terai, Kenta
  last_name: Terai
- first_name: Tsuyoshi
  full_name: Hirashima, Tsuyoshi
  last_name: Hirashima
- first_name: Xavier
  full_name: Trepat, Xavier
  last_name: Trepat
- first_name: Michiyuki
  full_name: Matsuda, Michiyuki
  last_name: Matsuda
citation:
  ama: Hino N, Matsuda K, Jikko Y, et al. A feedback loop between lamellipodial extension
    and HGF-ERK signaling specifies leader cells during collective cell migration.
    <i>Developmental Cell</i>. 2022;57(19):2290-2304.e7. doi:<a href="https://doi.org/10.1016/j.devcel.2022.09.003">10.1016/j.devcel.2022.09.003</a>
  apa: Hino, N., Matsuda, K., Jikko, Y., Maryu, G., Sakai, K., Imamura, R., … Matsuda,
    M. (2022). A feedback loop between lamellipodial extension and HGF-ERK signaling
    specifies leader cells during collective cell migration. <i>Developmental Cell</i>.
    Elsevier. <a href="https://doi.org/10.1016/j.devcel.2022.09.003">https://doi.org/10.1016/j.devcel.2022.09.003</a>
  chicago: Hino, Naoya, Kimiya Matsuda, Yuya Jikko, Gembu Maryu, Katsuya Sakai, Ryu
    Imamura, Shinya Tsukiji, et al. “A Feedback Loop between Lamellipodial Extension
    and HGF-ERK Signaling Specifies Leader Cells during Collective Cell Migration.”
    <i>Developmental Cell</i>. Elsevier, 2022. <a href="https://doi.org/10.1016/j.devcel.2022.09.003">https://doi.org/10.1016/j.devcel.2022.09.003</a>.
  ieee: N. Hino <i>et al.</i>, “A feedback loop between lamellipodial extension and
    HGF-ERK signaling specifies leader cells during collective cell migration,” <i>Developmental
    Cell</i>, vol. 57, no. 19. Elsevier, p. 2290–2304.e7, 2022.
  ista: Hino N, Matsuda K, Jikko Y, Maryu G, Sakai K, Imamura R, Tsukiji S, Aoki K,
    Terai K, Hirashima T, Trepat X, Matsuda M. 2022. A feedback loop between lamellipodial
    extension and HGF-ERK signaling specifies leader cells during collective cell
    migration. Developmental Cell. 57(19), 2290–2304.e7.
  mla: Hino, Naoya, et al. “A Feedback Loop between Lamellipodial Extension and HGF-ERK
    Signaling Specifies Leader Cells during Collective Cell Migration.” <i>Developmental
    Cell</i>, vol. 57, no. 19, Elsevier, 2022, p. 2290–2304.e7, doi:<a href="https://doi.org/10.1016/j.devcel.2022.09.003">10.1016/j.devcel.2022.09.003</a>.
  short: N. Hino, K. Matsuda, Y. Jikko, G. Maryu, K. Sakai, R. Imamura, S. Tsukiji,
    K. Aoki, K. Terai, T. Hirashima, X. Trepat, M. Matsuda, Developmental Cell 57
    (2022) 2290–2304.e7.
date_created: 2023-01-16T09:51:39Z
date_published: 2022-10-01T00:00:00Z
date_updated: 2023-08-04T09:38:53Z
day: '01'
department:
- _id: CaHe
doi: 10.1016/j.devcel.2022.09.003
external_id:
  isi:
  - '000898428700006'
  pmid:
  - '36174555'
intvolume: '        57'
isi: 1
issue: '19'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '10'
oa_version: None
page: 2290-2304.e7
pmid: 1
publication: Developmental Cell
publication_identifier:
  issn:
  - 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A feedback loop between lamellipodial extension and HGF-ERK signaling specifies
  leader cells during collective cell migration
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 57
year: '2022'
...
---
_id: '12261'
abstract:
- lang: eng
  text: 'Dose–response relationships are a general concept for quantitatively describing
    biological systems across multiple scales, from the molecular to the whole-cell
    level. A clinically relevant example is the bacterial growth response to antibiotics,
    which is routinely characterized by dose–response curves. The shape of the dose–response
    curve varies drastically between antibiotics and plays a key role in treatment,
    drug interactions, and resistance evolution. However, the mechanisms shaping the
    dose–response curve remain largely unclear. Here, we show in Escherichia coli
    that the distinctively shallow dose–response curve of the antibiotic trimethoprim
    is caused by a negative growth-mediated feedback loop: Trimethoprim slows growth,
    which in turn weakens the effect of this antibiotic. At the molecular level, this
    feedback is caused by the upregulation of the drug target dihydrofolate reductase
    (FolA/DHFR). We show that this upregulation is not a specific response to trimethoprim
    but follows a universal trend line that depends primarily on the growth rate,
    irrespective of its cause. Rewiring the feedback loop alters the dose–response
    curve in a predictable manner, which we corroborate using a mathematical model
    of cellular resource allocation and growth. Our results indicate that growth-mediated
    feedback loops may shape drug responses more generally and could be exploited
    to design evolutionary traps that enable selection against drug resistance.'
acknowledged_ssus:
- _id: M-Shop
acknowledgement: This work was in part supported by Human Frontier Science Program
  GrantRGP0042/2013, Marie Curie Career Integration Grant303507, AustrianScience Fund
  (FWF) Grant P27201-B22, and German Research Foundation(DFG) Collaborative Research
  Center (SFB)1310to TB. SAA was supportedby the European Union’s Horizon2020Research
  and Innovation Programunder the Marie Skłodowska-Curie Grant agreement No707352.
  We wouldlike to thank the Bollenbach group for regular fruitful discussions. We
  areparticularly thankful for the technical assistance of Booshini Fernando andfor
  discussions of the theoretical aspects with Gerrit Ansmann. We areindebted to Bor
  Kavˇciˇc for invaluable advice, help with setting up theluciferase-based growth
  monitoring system, and for sharing plasmids. Weacknowledge the IST Austria Miba
  Machine Shop for their support inbuilding a housing for the stacker of the plate
  reader, which enabled thehigh-throughput luciferase-based experiments. We are grateful
  to RosalindAllen, Bor Kavˇciˇc and Dor Russ for feedback on the manuscript. Open
  Accessfunding enabled and organized by Projekt DEAL.
article_number: e10490
article_processing_charge: No
article_type: original
author:
- first_name: Andreas
  full_name: Angermayr, Andreas
  id: 4677C796-F248-11E8-B48F-1D18A9856A87
  last_name: Angermayr
  orcid: 0000-0001-8619-2223
- first_name: Tin Yau
  full_name: Pang, Tin Yau
  last_name: Pang
- first_name: Guillaume
  full_name: Chevereau, Guillaume
  last_name: Chevereau
- first_name: Karin
  full_name: Mitosch, Karin
  id: 39B66846-F248-11E8-B48F-1D18A9856A87
  last_name: Mitosch
- first_name: Martin J
  full_name: Lercher, Martin J
  last_name: Lercher
- first_name: Mark Tobias
  full_name: Bollenbach, Mark Tobias
  id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
  last_name: Bollenbach
  orcid: 0000-0003-4398-476X
citation:
  ama: Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. Growth‐mediated
    negative feedback shapes quantitative antibiotic response. <i>Molecular Systems
    Biology</i>. 2022;18(9). doi:<a href="https://doi.org/10.15252/msb.202110490">10.15252/msb.202110490</a>
  apa: Angermayr, A., Pang, T. Y., Chevereau, G., Mitosch, K., Lercher, M. J., &#38;
    Bollenbach, M. T. (2022). Growth‐mediated negative feedback shapes quantitative
    antibiotic response. <i>Molecular Systems Biology</i>. Embo Press. <a href="https://doi.org/10.15252/msb.202110490">https://doi.org/10.15252/msb.202110490</a>
  chicago: Angermayr, Andreas, Tin Yau Pang, Guillaume Chevereau, Karin Mitosch, Martin
    J Lercher, and Mark Tobias Bollenbach. “Growth‐mediated Negative Feedback Shapes
    Quantitative Antibiotic Response.” <i>Molecular Systems Biology</i>. Embo Press,
    2022. <a href="https://doi.org/10.15252/msb.202110490">https://doi.org/10.15252/msb.202110490</a>.
  ieee: A. Angermayr, T. Y. Pang, G. Chevereau, K. Mitosch, M. J. Lercher, and M.
    T. Bollenbach, “Growth‐mediated negative feedback shapes quantitative antibiotic
    response,” <i>Molecular Systems Biology</i>, vol. 18, no. 9. Embo Press, 2022.
  ista: Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. 2022.
    Growth‐mediated negative feedback shapes quantitative antibiotic response. Molecular
    Systems Biology. 18(9), e10490.
  mla: Angermayr, Andreas, et al. “Growth‐mediated Negative Feedback Shapes Quantitative
    Antibiotic Response.” <i>Molecular Systems Biology</i>, vol. 18, no. 9, e10490,
    Embo Press, 2022, doi:<a href="https://doi.org/10.15252/msb.202110490">10.15252/msb.202110490</a>.
  short: A. Angermayr, T.Y. Pang, G. Chevereau, K. Mitosch, M.J. Lercher, M.T. Bollenbach,
    Molecular Systems Biology 18 (2022).
date_created: 2023-01-16T09:58:34Z
date_published: 2022-09-01T00:00:00Z
date_updated: 2023-08-04T09:51:49Z
day: '01'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.15252/msb.202110490
external_id:
  isi:
  - '000856482800001'
file:
- access_level: open_access
  checksum: 8b1d8f5ea20c8408acf466435fb6ae01
  content_type: application/pdf
  creator: dernst
  date_created: 2023-01-30T09:49:55Z
  date_updated: 2023-01-30T09:49:55Z
  file_id: '12446'
  file_name: 2022_MolecularSystemsBio_Angermayr.pdf
  file_size: 1098812
  relation: main_file
  success: 1
file_date_updated: 2023-01-30T09:49:55Z
has_accepted_license: '1'
intvolume: '        18'
isi: 1
issue: '9'
keyword:
- Applied Mathematics
- Computational Theory and Mathematics
- General Agricultural and Biological Sciences
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- Information Systems
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: Molecular Systems Biology
publication_identifier:
  eissn:
  - 1744-4292
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Growth‐mediated negative feedback shapes quantitative antibiotic response
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 18
year: '2022'
...
---
_id: '12288'
abstract:
- lang: eng
  text: To understand the function of neuronal circuits, it is crucial to disentangle
    the connectivity patterns within the network. However, most tools currently used
    to explore connectivity have low throughput, low selectivity, or limited accessibility.
    Here, we report the development of an improved packaging system for the production
    of the highly neurotropic RVdGenvA-CVS-N2c rabies viral vectors, yielding titers
    orders of magnitude higher with no background contamination, at a fraction of
    the production time, while preserving the efficiency of transsynaptic labeling.
    Along with the production pipeline, we developed suites of ‘starter’ AAV and bicistronic
    RVdG-CVS-N2c vectors, enabling retrograde labeling from a wide range of neuronal
    populations, tailored for diverse experimental requirements. We demonstrate the
    power and flexibility of the new system by uncovering hidden local and distal
    inhibitory connections in the mouse hippocampal formation and by imaging the functional
    properties of a cortical microcircuit across weeks. Our novel production pipeline
    provides a convenient approach to generate new rabies vectors, while our toolkit
    flexibly and efficiently expands the current capacity to label, manipulate and
    image the neuronal activity of interconnected neuronal circuits in vitro and in
    vivo.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We thank F Marr for technical assistance, A Murray for RVdG-CVS-N2c
  viruses and Neuro2A packaging cell-lines and J Watson for reading the manuscript.
  This research was supported by the Scientific Service Units (SSU) of IST-Austria
  through resources provided by the Imaging and Optics Facility (IOF) and the Preclinical
  Facility (PCF). This project was funded by the European Research Council (ERC) under
  the European Union’s Horizon 2020 research and innovation programme (ERC advanced
  grant No 692692, PJ, ERC starting grant No 756502, MJ), the Fond zur Förderung der
  Wissenschaftlichen Forschung (Z 312-B27, Wittgenstein award, PJ), the Human Frontier
  Science Program (LT000256/2018-L, AS) and EMBO (ALTF 1098-2017, AS).
article_number: '79848'
article_processing_charge: No
article_type: original
author:
- first_name: Anton L
  full_name: Sumser, Anton L
  id: 3320A096-F248-11E8-B48F-1D18A9856A87
  last_name: Sumser
  orcid: 0000-0002-4792-1881
- first_name: Maximilian A
  full_name: Jösch, Maximilian A
  id: 2BD278E6-F248-11E8-B48F-1D18A9856A87
  last_name: Jösch
  orcid: 0000-0002-3937-1330
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
- first_name: Yoav
  full_name: Ben Simon, Yoav
  id: 43DF3136-F248-11E8-B48F-1D18A9856A87
  last_name: Ben Simon
citation:
  ama: Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. Fast, high-throughput production
    of improved rabies viral vectors for specific, efficient and versatile transsynaptic
    retrograde labeling. <i>eLife</i>. 2022;11. doi:<a href="https://doi.org/10.7554/elife.79848">10.7554/elife.79848</a>
  apa: Sumser, A. L., Jösch, M. A., Jonas, P. M., &#38; Ben Simon, Y. (2022). Fast,
    high-throughput production of improved rabies viral vectors for specific, efficient
    and versatile transsynaptic retrograde labeling. <i>ELife</i>. eLife Sciences
    Publications. <a href="https://doi.org/10.7554/elife.79848">https://doi.org/10.7554/elife.79848</a>
  chicago: Sumser, Anton L, Maximilian A Jösch, Peter M Jonas, and Yoav Ben Simon.
    “Fast, High-Throughput Production of Improved Rabies Viral Vectors for Specific,
    Efficient and Versatile Transsynaptic Retrograde Labeling.” <i>ELife</i>. eLife
    Sciences Publications, 2022. <a href="https://doi.org/10.7554/elife.79848">https://doi.org/10.7554/elife.79848</a>.
  ieee: A. L. Sumser, M. A. Jösch, P. M. Jonas, and Y. Ben Simon, “Fast, high-throughput
    production of improved rabies viral vectors for specific, efficient and versatile
    transsynaptic retrograde labeling,” <i>eLife</i>, vol. 11. eLife Sciences Publications,
    2022.
  ista: Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. 2022. Fast, high-throughput production
    of improved rabies viral vectors for specific, efficient and versatile transsynaptic
    retrograde labeling. eLife. 11, 79848.
  mla: Sumser, Anton L., et al. “Fast, High-Throughput Production of Improved Rabies
    Viral Vectors for Specific, Efficient and Versatile Transsynaptic Retrograde Labeling.”
    <i>ELife</i>, vol. 11, 79848, eLife Sciences Publications, 2022, doi:<a href="https://doi.org/10.7554/elife.79848">10.7554/elife.79848</a>.
  short: A.L. Sumser, M.A. Jösch, P.M. Jonas, Y. Ben Simon, ELife 11 (2022).
date_created: 2023-01-16T10:04:15Z
date_published: 2022-09-15T00:00:00Z
date_updated: 2023-08-04T10:29:48Z
day: '15'
ddc:
- '570'
department:
- _id: MaJö
- _id: PeJo
doi: 10.7554/elife.79848
ec_funded: 1
external_id:
  isi:
  - '000892204300001'
  pmid:
  - '36040301'
file:
- access_level: open_access
  checksum: 5a2a65e3e7225090c3d8199f3bbd7b7b
  content_type: application/pdf
  creator: dernst
  date_created: 2023-01-30T11:50:53Z
  date_updated: 2023-01-30T11:50:53Z
  file_id: '12463'
  file_name: 2022_eLife_Sumser.pdf
  file_size: 8506811
  relation: main_file
  success: 1
file_date_updated: 2023-01-30T11:50:53Z
has_accepted_license: '1'
intvolume: '        11'
isi: 1
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '692692'
  name: Biophysics and circuit function of a giant cortical glumatergic synapse
- _id: 2634E9D2-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '756502'
  name: Circuits of Visual Attention
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: Z00312
  name: The Wittgenstein Prize
- _id: 266D407A-B435-11E9-9278-68D0E5697425
  grant_number: LT000256
  name: Neuronal networks of salience and spatial detection in the murine superior
    colliculus
- _id: 264FEA02-B435-11E9-9278-68D0E5697425
  grant_number: ALTF 1098-2017
  name: Connecting sensory with motor processing in the superior colliculus
publication: eLife
publication_identifier:
  eissn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Fast, high-throughput production of improved rabies viral vectors for specific,
  efficient and versatile transsynaptic retrograde labeling
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '12670'
abstract:
- lang: eng
  text: DNA methylation plays essential homeostatic functions in eukaryotic genomes.
    In animals, DNA methylation is also developmentally regulated and, in turn, regulates
    development. In the past two decades, huge research effort has endorsed the understanding
    that DNA methylation plays a similar role in plant development, especially during
    sexual reproduction. The power of whole-genome sequencing and cell isolation techniques,
    as well as bioinformatics tools, have enabled recent studies to reveal dynamic
    changes in DNA methylation during germline development. Furthermore, the combination
    of these technological advances with genetics, developmental biology and cell
    biology tools has revealed functional methylation reprogramming events that control
    gene and transposon activities in flowering plant germlines. In this review, we
    discuss the major advances in our knowledge of DNA methylation dynamics during
    male and female germline development in flowering plants.
article_processing_charge: No
article_type: review
author:
- first_name: Shengbo
  full_name: He, Shengbo
  last_name: He
- first_name: Xiaoqi
  full_name: Feng, Xiaoqi
  id: e0164712-22ee-11ed-b12a-d80fcdf35958
  last_name: Feng
  orcid: 0000-0002-4008-1234
citation:
  ama: He S, Feng X. DNA methylation dynamics during germline development. <i>Journal
    of Integrative Plant Biology</i>. 2022;64(12):2240-2251. doi:<a href="https://doi.org/10.1111/jipb.13422">10.1111/jipb.13422</a>
  apa: He, S., &#38; Feng, X. (2022). DNA methylation dynamics during germline development.
    <i>Journal of Integrative Plant Biology</i>. Wiley. <a href="https://doi.org/10.1111/jipb.13422">https://doi.org/10.1111/jipb.13422</a>
  chicago: He, Shengbo, and Xiaoqi Feng. “DNA Methylation Dynamics during Germline
    Development.” <i>Journal of Integrative Plant Biology</i>. Wiley, 2022. <a href="https://doi.org/10.1111/jipb.13422">https://doi.org/10.1111/jipb.13422</a>.
  ieee: S. He and X. Feng, “DNA methylation dynamics during germline development,”
    <i>Journal of Integrative Plant Biology</i>, vol. 64, no. 12. Wiley, pp. 2240–2251,
    2022.
  ista: He S, Feng X. 2022. DNA methylation dynamics during germline development.
    Journal of Integrative Plant Biology. 64(12), 2240–2251.
  mla: He, Shengbo, and Xiaoqi Feng. “DNA Methylation Dynamics during Germline Development.”
    <i>Journal of Integrative Plant Biology</i>, vol. 64, no. 12, Wiley, 2022, pp.
    2240–51, doi:<a href="https://doi.org/10.1111/jipb.13422">10.1111/jipb.13422</a>.
  short: S. He, X. Feng, Journal of Integrative Plant Biology 64 (2022) 2240–2251.
date_created: 2023-02-23T09:15:57Z
date_published: 2022-12-07T00:00:00Z
date_updated: 2023-05-08T10:59:00Z
day: '07'
department:
- _id: XiFe
doi: 10.1111/jipb.13422
extern: '1'
external_id:
  pmid:
  - '36478632'
intvolume: '        64'
issue: '12'
keyword:
- Plant Science
- General Biochemistry
- Genetics and Molecular Biology
- Biochemistry
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1111/jipb.13422
month: '12'
oa: 1
oa_version: Published Version
page: 2240-2251
pmid: 1
publication: Journal of Integrative Plant Biology
publication_identifier:
  eissn:
  - 1744-7909
  issn:
  - 1672-9072
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: DNA methylation dynamics during germline development
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 64
year: '2022'
...
---
_id: '10834'
abstract:
- lang: eng
  text: Hematopoietic-specific protein 1 (Hem1) is an essential subunit of the WAVE
    regulatory complex (WRC) in immune cells. WRC is crucial for Arp2/3 complex activation
    and the protrusion of branched actin filament networks. Moreover, Hem1 loss of
    function in immune cells causes autoimmune diseases in humans. Here, we show that
    genetic removal of Hem1 in macrophages diminishes frequency and efficacy of phagocytosis
    as well as phagocytic cup formation in addition to defects in lamellipodial protrusion
    and migration. Moreover, Hem1-null macrophages displayed strong defects in cell
    adhesion despite unaltered podosome formation and concomitant extracellular matrix
    degradation. Specifically, dynamics of both adhesion and de-adhesion as well as
    concomitant phosphorylation of paxillin and focal adhesion kinase (FAK) were significantly
    compromised. Accordingly, disruption of WRC function in non-hematopoietic cells
    coincided with both defects in adhesion turnover and altered FAK and paxillin
    phosphorylation. Consistently, platelets exhibited reduced adhesion and diminished
    integrin αIIbβ3 activation upon WRC removal. Interestingly, adhesion phenotypes,
    but not lamellipodia formation, were partially rescued by small molecule activation
    of FAK. A full rescue of the phenotype, including lamellipodia formation, required
    not only the presence of WRCs but also their binding to and activation by Rac.
    Collectively, our results uncover that WRC impacts on integrin-dependent processes
    in a FAK-dependent manner, controlling formation and dismantling of adhesions,
    relevant for properly grabbing onto extracellular surfaces and particles during
    cell edge expansion, like in migration or phagocytosis.
acknowledgement: We are grateful to Silvia Prettin, Ina Schleicher, and Petra Hagendorff
  for expert technical assistance; David Dettbarn for animal keeping and breeding;
  and Lothar Gröbe and Maria Höxter for cell sorting. We also thank Werner Tegge for
  peptides and Giorgio Scita for antibodies. This work was supported, in part, by
  the Deutsche Forschungsgemeinschaft (DFG), Priority Programm SPP1150 (to T.E.B.S.,
  K.R., and M. Sixt), and by DFG grant GRK2223/1 (to K.R.). T.E.B.S. acknowledges
  support by the Helmholtz Society through HGF impulse fund W2/W3-066 and M. Schnoor
  by the Mexican Council for Science and Technology (CONACyT, 284292 ), Fund SEP-Cinvestav
  ( 108 ), and the Royal Society, UK (Newton Advanced Fellowship, NAF/R1/180017 ).
article_processing_charge: No
article_type: original
author:
- first_name: Stephanie
  full_name: Stahnke, Stephanie
  last_name: Stahnke
- first_name: Hermann
  full_name: Döring, Hermann
  last_name: Döring
- first_name: Charly
  full_name: Kusch, Charly
  last_name: Kusch
- first_name: David J.J.
  full_name: de Gorter, David J.J.
  last_name: de Gorter
- first_name: Sebastian
  full_name: Dütting, Sebastian
  last_name: Dütting
- first_name: Aleks
  full_name: Guledani, Aleks
  last_name: Guledani
- first_name: Irina
  full_name: Pleines, Irina
  last_name: Pleines
- first_name: Michael
  full_name: Schnoor, Michael
  last_name: Schnoor
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Robert
  full_name: Geffers, Robert
  last_name: Geffers
- first_name: Manfred
  full_name: Rohde, Manfred
  last_name: Rohde
- first_name: Mathias
  full_name: Müsken, Mathias
  last_name: Müsken
- first_name: Frieda
  full_name: Kage, Frieda
  last_name: Kage
- first_name: Anika
  full_name: Steffen, Anika
  last_name: Steffen
- first_name: Jan
  full_name: Faix, Jan
  last_name: Faix
- first_name: Bernhard
  full_name: Nieswandt, Bernhard
  last_name: Nieswandt
- first_name: Klemens
  full_name: Rottner, Klemens
  last_name: Rottner
- first_name: Theresia E.B.
  full_name: Stradal, Theresia E.B.
  last_name: Stradal
citation:
  ama: Stahnke S, Döring H, Kusch C, et al. Loss of Hem1 disrupts macrophage function
    and impacts migration, phagocytosis, and integrin-mediated adhesion. <i>Current
    Biology</i>. 2021;31(10):2051-2064.e8. doi:<a href="https://doi.org/10.1016/j.cub.2021.02.043">10.1016/j.cub.2021.02.043</a>
  apa: Stahnke, S., Döring, H., Kusch, C., de Gorter, D. J. J., Dütting, S., Guledani,
    A., … Stradal, T. E. B. (2021). Loss of Hem1 disrupts macrophage function and
    impacts migration, phagocytosis, and integrin-mediated adhesion. <i>Current Biology</i>.
    Elsevier. <a href="https://doi.org/10.1016/j.cub.2021.02.043">https://doi.org/10.1016/j.cub.2021.02.043</a>
  chicago: Stahnke, Stephanie, Hermann Döring, Charly Kusch, David J.J. de Gorter,
    Sebastian Dütting, Aleks Guledani, Irina Pleines, et al. “Loss of Hem1 Disrupts
    Macrophage Function and Impacts Migration, Phagocytosis, and Integrin-Mediated
    Adhesion.” <i>Current Biology</i>. Elsevier, 2021. <a href="https://doi.org/10.1016/j.cub.2021.02.043">https://doi.org/10.1016/j.cub.2021.02.043</a>.
  ieee: S. Stahnke <i>et al.</i>, “Loss of Hem1 disrupts macrophage function and impacts
    migration, phagocytosis, and integrin-mediated adhesion,” <i>Current Biology</i>,
    vol. 31, no. 10. Elsevier, p. 2051–2064.e8, 2021.
  ista: Stahnke S, Döring H, Kusch C, de Gorter DJJ, Dütting S, Guledani A, Pleines
    I, Schnoor M, Sixt MK, Geffers R, Rohde M, Müsken M, Kage F, Steffen A, Faix J,
    Nieswandt B, Rottner K, Stradal TEB. 2021. Loss of Hem1 disrupts macrophage function
    and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology.
    31(10), 2051–2064.e8.
  mla: Stahnke, Stephanie, et al. “Loss of Hem1 Disrupts Macrophage Function and Impacts
    Migration, Phagocytosis, and Integrin-Mediated Adhesion.” <i>Current Biology</i>,
    vol. 31, no. 10, Elsevier, 2021, p. 2051–2064.e8, doi:<a href="https://doi.org/10.1016/j.cub.2021.02.043">10.1016/j.cub.2021.02.043</a>.
  short: S. Stahnke, H. Döring, C. Kusch, D.J.J. de Gorter, S. Dütting, A. Guledani,
    I. Pleines, M. Schnoor, M.K. Sixt, R. Geffers, M. Rohde, M. Müsken, F. Kage, A.
    Steffen, J. Faix, B. Nieswandt, K. Rottner, T.E.B. Stradal, Current Biology 31
    (2021) 2051–2064.e8.
date_created: 2022-03-08T07:51:04Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2023-08-17T07:01:14Z
day: '24'
department:
- _id: MiSi
doi: 10.1016/j.cub.2021.02.043
external_id:
  isi:
  - '000654652200002'
  pmid:
  - '33711252'
intvolume: '        31'
isi: 1
issue: '10'
keyword:
- General Agricultural and Biological Sciences
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1101/2020.03.24.005835
month: '05'
oa: 1
oa_version: Preprint
page: 2051-2064.e8
pmid: 1
publication: Current Biology
publication_identifier:
  issn:
  - 0960-9822
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis,
  and integrin-mediated adhesion
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 31
year: '2021'
...
---
_id: '11052'
abstract:
- lang: eng
  text: In order to combat molecular damage, most cellular proteins undergo rapid
    turnover. We have previously identified large nuclear protein assemblies that
    can persist for years in post-mitotic tissues and are subject to age-related decline.
    Here, we report that mitochondria can be long lived in the mouse brain and reveal
    that specific mitochondrial proteins have half-lives longer than the average proteome.
    These mitochondrial long-lived proteins (mitoLLPs) are core components of the
    electron transport chain (ETC) and display increased longevity in respiratory
    supercomplexes. We find that COX7C, a mitoLLP that forms a stable contact site
    between complexes I and IV, is required for complex IV and supercomplex assembly.
    Remarkably, even upon depletion of COX7C transcripts, ETC function is maintained
    for days, effectively uncoupling mitochondrial function from ongoing transcription
    of its mitoLLPs. Our results suggest that modulating protein longevity within
    the ETC is critical for mitochondrial proteome maintenance and the robustness
    of mitochondrial function.
article_processing_charge: No
article_type: original
author:
- first_name: Shefali
  full_name: Krishna, Shefali
  last_name: Krishna
- first_name: Rafael
  full_name: Arrojo e Drigo, Rafael
  last_name: Arrojo e Drigo
- first_name: Juliana S.
  full_name: Capitanio, Juliana S.
  last_name: Capitanio
- first_name: Ranjan
  full_name: Ramachandra, Ranjan
  last_name: Ramachandra
- first_name: Mark
  full_name: Ellisman, Mark
  last_name: Ellisman
- first_name: Martin W
  full_name: HETZER, Martin W
  id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
  last_name: HETZER
  orcid: 0000-0002-2111-992X
citation:
  ama: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
    M. Identification of long-lived proteins in the mitochondria reveals increased
    stability of the electron transport chain. <i>Developmental Cell</i>. 2021;56(21):P2952-2965.e9.
    doi:<a href="https://doi.org/10.1016/j.devcel.2021.10.008">10.1016/j.devcel.2021.10.008</a>
  apa: Krishna, S., Arrojo e Drigo, R., Capitanio, J. S., Ramachandra, R., Ellisman,
    M., &#38; Hetzer, M. (2021). Identification of long-lived proteins in the mitochondria
    reveals increased stability of the electron transport chain. <i>Developmental
    Cell</i>. Elsevier. <a href="https://doi.org/10.1016/j.devcel.2021.10.008">https://doi.org/10.1016/j.devcel.2021.10.008</a>
  chicago: Krishna, Shefali, Rafael Arrojo e Drigo, Juliana S. Capitanio, Ranjan Ramachandra,
    Mark Ellisman, and Martin Hetzer. “Identification of Long-Lived Proteins in the
    Mitochondria Reveals Increased Stability of the Electron Transport Chain.” <i>Developmental
    Cell</i>. Elsevier, 2021. <a href="https://doi.org/10.1016/j.devcel.2021.10.008">https://doi.org/10.1016/j.devcel.2021.10.008</a>.
  ieee: S. Krishna, R. Arrojo e Drigo, J. S. Capitanio, R. Ramachandra, M. Ellisman,
    and M. Hetzer, “Identification of long-lived proteins in the mitochondria reveals
    increased stability of the electron transport chain,” <i>Developmental Cell</i>,
    vol. 56, no. 21. Elsevier, p. P2952–2965.e9, 2021.
  ista: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
    M. 2021. Identification of long-lived proteins in the mitochondria reveals increased
    stability of the electron transport chain. Developmental Cell. 56(21), P2952–2965.e9.
  mla: Krishna, Shefali, et al. “Identification of Long-Lived Proteins in the Mitochondria
    Reveals Increased Stability of the Electron Transport Chain.” <i>Developmental
    Cell</i>, vol. 56, no. 21, Elsevier, 2021, p. P2952–2965.e9, doi:<a href="https://doi.org/10.1016/j.devcel.2021.10.008">10.1016/j.devcel.2021.10.008</a>.
  short: S. Krishna, R. Arrojo e Drigo, J.S. Capitanio, R. Ramachandra, M. Ellisman,
    M. Hetzer, Developmental Cell 56 (2021) P2952–2965.e9.
date_created: 2022-04-07T07:43:14Z
date_published: 2021-11-08T00:00:00Z
date_updated: 2022-07-18T08:26:38Z
day: '08'
doi: 10.1016/j.devcel.2021.10.008
extern: '1'
external_id:
  pmid:
  - '34715012'
intvolume: '        56'
issue: '21'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa_version: None
page: P2952-2965.e9
pmid: 1
publication: Developmental Cell
publication_identifier:
  issn:
  - 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Identification of long-lived proteins in the mitochondria reveals increased
  stability of the electron transport chain
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 56
year: '2021'
...
---
_id: '13356'
abstract:
- lang: eng
  text: 'Self-assembly of nanoparticles can be mediated by polymers, but has so far
    led almost exclusively to nanoparticle aggregates that are amorphous. Here, we
    employed Coulombic interactions to generate a range of composite materials from
    mixtures of charged nanoparticles and oppositely charged polymers. The assembly
    behavior of these nanoparticle/polymer composites depends on their order of addition:
    polymers added to nanoparticles give rise to stable aggregates, but nanoparticles
    added to polymers disassemble the initially formed aggregates. The amorphous aggregates
    were transformed into crystalline ones by transiently increasing the ionic strength
    of the solution. The morphology of the resulting crystals depended on the length
    of the polymer: short polymer chains mediated the self-assembly of nanoparticles
    into strongly faceted crystals, whereas long chains led to pseudospherical nanoparticle/polymer
    assemblies, within which the crystalline order of nanoparticles was retained.'
article_processing_charge: No
article_type: original
author:
- first_name: Tong
  full_name: Bian, Tong
  last_name: Bian
- first_name: Rafal
  full_name: Klajn, Rafal
  id: 8e84690e-1e48-11ed-a02b-a1e6fb8bb53b
  last_name: Klajn
citation:
  ama: Bian T, Klajn R. Morphology control in crystalline nanoparticle–polymer aggregates.
    <i>Annals of the New York Academy of Sciences</i>. 2021;1505(1):191-201. doi:<a
    href="https://doi.org/10.1111/nyas.14674">10.1111/nyas.14674</a>
  apa: Bian, T., &#38; Klajn, R. (2021). Morphology control in crystalline nanoparticle–polymer
    aggregates. <i>Annals of the New York Academy of Sciences</i>. Wiley. <a href="https://doi.org/10.1111/nyas.14674">https://doi.org/10.1111/nyas.14674</a>
  chicago: Bian, Tong, and Rafal Klajn. “Morphology Control in Crystalline Nanoparticle–Polymer
    Aggregates.” <i>Annals of the New York Academy of Sciences</i>. Wiley, 2021. <a
    href="https://doi.org/10.1111/nyas.14674">https://doi.org/10.1111/nyas.14674</a>.
  ieee: T. Bian and R. Klajn, “Morphology control in crystalline nanoparticle–polymer
    aggregates,” <i>Annals of the New York Academy of Sciences</i>, vol. 1505, no.
    1. Wiley, pp. 191–201, 2021.
  ista: Bian T, Klajn R. 2021. Morphology control in crystalline nanoparticle–polymer
    aggregates. Annals of the New York Academy of Sciences. 1505(1), 191–201.
  mla: Bian, Tong, and Rafal Klajn. “Morphology Control in Crystalline Nanoparticle–Polymer
    Aggregates.” <i>Annals of the New York Academy of Sciences</i>, vol. 1505, no.
    1, Wiley, 2021, pp. 191–201, doi:<a href="https://doi.org/10.1111/nyas.14674">10.1111/nyas.14674</a>.
  short: T. Bian, R. Klajn, Annals of the New York Academy of Sciences 1505 (2021)
    191–201.
date_created: 2023-08-01T09:33:39Z
date_published: 2021-12-01T00:00:00Z
date_updated: 2023-08-07T10:01:10Z
day: '01'
ddc:
- '540'
doi: 10.1111/nyas.14674
extern: '1'
external_id:
  pmid:
  - '34427923'
intvolume: '      1505'
issue: '1'
keyword:
- History and Philosophy of Science
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1111/nyas.14674
month: '12'
oa: 1
oa_version: Published Version
page: 191-201
pmid: 1
publication: Annals of the New York Academy of Sciences
publication_identifier:
  eissn:
  - 1749-6632
  issn:
  - 0077-8923
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Morphology control in crystalline nanoparticle–polymer aggregates
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1505
year: '2021'
...
---
_id: '9387'
abstract:
- lang: eng
  text: We report the complete analysis of a deterministic model of deleterious mutations
    and negative selection against them at two haploid loci without recombination.
    As long as mutation is a weaker force than selection, mutant alleles remain rare
    at the only stable equilibrium, and otherwise, a variety of dynamics are possible.
    If the mutation-free genotype is absent, generally the only stable equilibrium
    is the one that corresponds to fixation of the mutant allele at the locus where
    it is less deleterious. This result suggests that fixation of a deleterious allele
    that follows a click of the Muller’s ratchet is governed by natural selection,
    instead of random drift.
acknowledgement: This work was supported by the Russian Science Foundation grant N
  16-14-10173.
article_number: '110729'
article_processing_charge: No
article_type: original
author:
- first_name: Kseniia
  full_name: Khudiakova, Kseniia
  id: 4E6DC800-AE37-11E9-AC72-31CAE5697425
  last_name: Khudiakova
  orcid: 0000-0002-6246-1465
- first_name: Tatiana Yu.
  full_name: Neretina, Tatiana Yu.
  last_name: Neretina
- first_name: Alexey S.
  full_name: Kondrashov, Alexey S.
  last_name: Kondrashov
citation:
  ama: Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection
    balance and Muller’s ratchet. <i>Journal of Theoretical Biology</i>. 2021;524.
    doi:<a href="https://doi.org/10.1016/j.jtbi.2021.110729">10.1016/j.jtbi.2021.110729</a>
  apa: Khudiakova, K., Neretina, T. Y., &#38; Kondrashov, A. S. (2021). Two linked
    loci under mutation-selection balance and Muller’s ratchet. <i>Journal of Theoretical
    Biology</i>. Elsevier . <a href="https://doi.org/10.1016/j.jtbi.2021.110729">https://doi.org/10.1016/j.jtbi.2021.110729</a>
  chicago: Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two
    Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” <i>Journal
    of Theoretical Biology</i>. Elsevier , 2021. <a href="https://doi.org/10.1016/j.jtbi.2021.110729">https://doi.org/10.1016/j.jtbi.2021.110729</a>.
  ieee: K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under
    mutation-selection balance and Muller’s ratchet,” <i>Journal of Theoretical Biology</i>,
    vol. 524. Elsevier , 2021.
  ista: Khudiakova K, Neretina TY, Kondrashov AS. 2021. Two linked loci under mutation-selection
    balance and Muller’s ratchet. Journal of Theoretical Biology. 524, 110729.
  mla: Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance
    and Muller’s Ratchet.” <i>Journal of Theoretical Biology</i>, vol. 524, 110729,
    Elsevier , 2021, doi:<a href="https://doi.org/10.1016/j.jtbi.2021.110729">10.1016/j.jtbi.2021.110729</a>.
  short: K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology
    524 (2021).
date_created: 2021-05-12T05:58:42Z
date_published: 2021-04-24T00:00:00Z
date_updated: 2023-08-08T13:32:40Z
day: '24'
department:
- _id: GradSch
doi: 10.1016/j.jtbi.2021.110729
external_id:
  isi:
  - '000659161500002'
intvolume: '       524'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- Modelling and Simulation
- Statistics and Probability
- General Immunology and Microbiology
- Applied Mathematics
- General Agricultural and Biological Sciences
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.biorxiv.org/content/10.1101/477489v1
month: '04'
oa: 1
oa_version: Preprint
publication: Journal of Theoretical Biology
publication_identifier:
  issn:
  - 0022-5193
publication_status: published
publisher: 'Elsevier '
quality_controlled: '1'
status: public
title: Two linked loci under mutation-selection balance and Muller’s ratchet
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 524
year: '2021'
...
---
_id: '9429'
abstract:
- lang: eng
  text: De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3
    lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency
    leads to motor coordination deficits as well as ASD-relevant social and cognitive
    impairments. However, induction of Cul3 haploinsufficiency later in life does
    not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during
    a critical developmental window. Here we show that Cul3 is essential to regulate
    neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice
    display cortical lamination abnormalities. At the molecular level, we found that
    Cul3 controls neuronal migration by tightly regulating the amount of Plastin3
    (Pls3), a previously unrecognized player of neural migration. Furthermore, we
    found that Pls3 cell-autonomously regulates cell migration by regulating actin
    cytoskeleton organization, and its levels are inversely proportional to neural
    migration speed. Finally, we provide evidence that cellular phenotypes associated
    with autism-linked gene haploinsufficiency can be rescued by transcriptional activation
    of the intact allele in vitro, offering a proof of concept for a potential therapeutic
    approach for ASDs.
acknowledged_ssus:
- _id: PreCl
acknowledgement: We thank A. Coll Manzano, F. Freeman, M. Ladron de Guevara, and A.
  Ç. Yahya for technical assistance, S. Deixler, A. Lepold, and A. Schlerka for the
  management of our animal colony, as well as M. Schunn and the Preclinical Facility
  team for technical assistance. We thank K. Heesom and her team at the University
  of Bristol Proteomics Facility for the proteomics sample preparation, data generation,
  and analysis support. We thank Y. B. Simon for kindly providing the plasmid for
  lentiviral labeling. Further, we thank M. Sixt for his advice regarding cell migration
  and the fruitful discussions. This work was supported by the ISTPlus postdoctoral
  fellowship (Grant Agreement No. 754411) to B.B., by the European Union’s Horizon
  2020 research and innovation program (ERC) grant 715508 (REVERSEAUTISM), and by
  the Austrian Science Fund (FWF) to G.N. (DK W1232-B24 and SFB F7807-B) and to J.G.D
  (I3600-B27).
article_number: '3058'
article_processing_charge: No
article_type: original
author:
- first_name: Jasmin
  full_name: Morandell, Jasmin
  id: 4739D480-F248-11E8-B48F-1D18A9856A87
  last_name: Morandell
- first_name: Lena A
  full_name: Schwarz, Lena A
  id: 29A8453C-F248-11E8-B48F-1D18A9856A87
  last_name: Schwarz
- first_name: Bernadette
  full_name: Basilico, Bernadette
  id: 36035796-5ACA-11E9-A75E-7AF2E5697425
  last_name: Basilico
  orcid: 0000-0003-1843-3173
- first_name: Saren
  full_name: Tasciyan, Saren
  id: 4323B49C-F248-11E8-B48F-1D18A9856A87
  last_name: Tasciyan
  orcid: 0000-0003-1671-393X
- first_name: Georgi A
  full_name: Dimchev, Georgi A
  id: 38C393BE-F248-11E8-B48F-1D18A9856A87
  last_name: Dimchev
  orcid: 0000-0001-8370-6161
- first_name: Armel
  full_name: Nicolas, Armel
  id: 2A103192-F248-11E8-B48F-1D18A9856A87
  last_name: Nicolas
- first_name: Christoph M
  full_name: Sommer, Christoph M
  id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
  last_name: Sommer
  orcid: 0000-0003-1216-9105
- first_name: Caroline
  full_name: Kreuzinger, Caroline
  id: 382077BA-F248-11E8-B48F-1D18A9856A87
  last_name: Kreuzinger
- first_name: Christoph
  full_name: Dotter, Christoph
  id: 4C66542E-F248-11E8-B48F-1D18A9856A87
  last_name: Dotter
  orcid: 0000-0002-9033-9096
- first_name: Lisa
  full_name: Knaus, Lisa
  id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87
  last_name: Knaus
- first_name: Zoe
  full_name: Dobler, Zoe
  id: D23090A2-9057-11EA-883A-A8396FC7A38F
  last_name: Dobler
- first_name: Emanuele
  full_name: Cacci, Emanuele
  last_name: Cacci
- first_name: Florian KM
  full_name: Schur, Florian KM
  id: 48AD8942-F248-11E8-B48F-1D18A9856A87
  last_name: Schur
  orcid: 0000-0003-4790-8078
- first_name: Johann G
  full_name: Danzl, Johann G
  id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
  last_name: Danzl
  orcid: 0000-0001-8559-3973
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
citation:
  ama: Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein
    homeostasis and cell migration during a critical window of brain development.
    <i>Nature Communications</i>. 2021;12(1). doi:<a href="https://doi.org/10.1038/s41467-021-23123-x">10.1038/s41467-021-23123-x</a>
  apa: Morandell, J., Schwarz, L. A., Basilico, B., Tasciyan, S., Dimchev, G. A.,
    Nicolas, A., … Novarino, G. (2021). Cul3 regulates cytoskeleton protein homeostasis
    and cell migration during a critical window of brain development. <i>Nature Communications</i>.
    Springer Nature. <a href="https://doi.org/10.1038/s41467-021-23123-x">https://doi.org/10.1038/s41467-021-23123-x</a>
  chicago: Morandell, Jasmin, Lena A Schwarz, Bernadette Basilico, Saren Tasciyan,
    Georgi A Dimchev, Armel Nicolas, Christoph M Sommer, et al. “Cul3 Regulates Cytoskeleton
    Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.”
    <i>Nature Communications</i>. Springer Nature, 2021. <a href="https://doi.org/10.1038/s41467-021-23123-x">https://doi.org/10.1038/s41467-021-23123-x</a>.
  ieee: J. Morandell <i>et al.</i>, “Cul3 regulates cytoskeleton protein homeostasis
    and cell migration during a critical window of brain development,” <i>Nature Communications</i>,
    vol. 12, no. 1. Springer Nature, 2021.
  ista: Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev GA, Nicolas A, Sommer
    CM, Kreuzinger C, Dotter C, Knaus L, Dobler Z, Cacci E, Schur FK, Danzl JG, Novarino
    G. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during
    a critical window of brain development. Nature Communications. 12(1), 3058.
  mla: Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis
    and Cell Migration during a Critical Window of Brain Development.” <i>Nature Communications</i>,
    vol. 12, no. 1, 3058, Springer Nature, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-23123-x">10.1038/s41467-021-23123-x</a>.
  short: J. Morandell, L.A. Schwarz, B. Basilico, S. Tasciyan, G.A. Dimchev, A. Nicolas,
    C.M. Sommer, C. Kreuzinger, C. Dotter, L. Knaus, Z. Dobler, E. Cacci, F.K. Schur,
    J.G. Danzl, G. Novarino, Nature Communications 12 (2021).
date_created: 2021-05-28T11:49:46Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2024-09-10T12:04:26Z
day: '24'
ddc:
- '572'
department:
- _id: GaNo
- _id: JoDa
- _id: FlSc
- _id: MiSi
- _id: LifeSc
- _id: Bio
doi: 10.1038/s41467-021-23123-x
ec_funded: 1
external_id:
  isi:
  - '000658769900010'
file:
- access_level: open_access
  checksum: 337e0f7959c35ec959984cacdcb472ba
  content_type: application/pdf
  creator: kschuh
  date_created: 2021-05-28T12:39:43Z
  date_updated: 2021-05-28T12:39:43Z
  file_id: '9430'
  file_name: 2021_NatureCommunications_Morandell.pdf
  file_size: 9358599
  relation: main_file
  success: 1
file_date_updated: 2021-05-28T12:39:43Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '754411'
  name: ISTplus - Postdoctoral Fellowships
- _id: 25444568-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '715508'
  name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
    and in vitro Models
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: W1232-B24
  name: Molecular Drug Targets
- _id: 05A0D778-7A3F-11EA-A408-12923DDC885E
  grant_number: F07807
  name: Neural stem cells in autism and epilepsy
- _id: 265CB4D0-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I03600
  name: Optical control of synaptic function via adhesion molecules
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
  link:
  - relation: press_release
    url: https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/
  record:
  - id: '7800'
    relation: earlier_version
    status: public
  - id: '12401'
    relation: dissertation_contains
    status: public
status: public
title: Cul3 regulates cytoskeleton protein homeostasis and cell migration during a
  critical window of brain development
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '9431'
abstract:
- lang: eng
  text: Inositol hexakisphosphate (IP6) is an assembly cofactor for HIV-1. We report
    here that IP6 is also used for assembly of Rous sarcoma virus (RSV), a retrovirus
    from a different genus. IP6 is ~100-fold more potent at promoting RSV mature capsid
    protein (CA) assembly than observed for HIV-1 and removal of IP6 in cells reduces
    infectivity by 100-fold. Here, visualized by cryo-electron tomography and subtomogram
    averaging, mature capsid-like particles show an IP6-like density in the CA hexamer,
    coordinated by rings of six lysines and six arginines. Phosphate and IP6 have
    opposing effects on CA in vitro assembly, inducing formation of T = 1 icosahedrons
    and tubes, respectively, implying that phosphate promotes pentamer and IP6 hexamer
    formation. Subtomogram averaging and classification optimized for analysis of
    pleomorphic retrovirus particles reveal that the heterogeneity of mature RSV CA
    polyhedrons results from an unexpected, intrinsic CA hexamer flexibility. In contrast,
    the CA pentamer forms rigid units organizing the local architecture. These different
    features of hexamers and pentamers determine the structural mechanism to form
    CA polyhedrons of variable shape in mature RSV particles.
acknowledged_ssus:
- _id: ScienComp
- _id: LifeSc
- _id: EM-Fac
acknowledgement: This work was funded by the National Institute of Allergy and Infectious
  Diseases under awards R01AI147890 to R.A.D., R01AI150454 to V.M.V, R35GM136258 in
  support of J-P.R.F, and the Austrian Science Fund (FWF) grant P31445 to F.K.M.S.
  Access to high-resolution cryo-ET data acquisition at EMBL Heidelberg was supported
  by iNEXT (grant no. 653706), funded by the Horizon 2020 program of the European
  Union (PID 4246). We thank Wim Hagen and Felix Weis at EMBL Heidelberg for support
  in cryo-ET data acquisition. This work made use of the Cornell Center for Materials
  Research Shared Facilities, which are supported through the NSF MRSEC program (DMR-179875).
  This research was also supported by the Scientific Service Units (SSUs) of IST Austria
  through resources provided by Scientific Computing (SciComp), the Life Science Facility
  (LSF), and the Electron Microscopy Facility (EMF).
article_number: '3226'
article_processing_charge: No
article_type: original
author:
- first_name: Martin
  full_name: Obr, Martin
  id: 4741CA5A-F248-11E8-B48F-1D18A9856A87
  last_name: Obr
- first_name: Clifton L.
  full_name: Ricana, Clifton L.
  last_name: Ricana
- first_name: Nadia
  full_name: Nikulin, Nadia
  last_name: Nikulin
- first_name: Jon-Philip R.
  full_name: Feathers, Jon-Philip R.
  last_name: Feathers
- first_name: Marco
  full_name: Klanschnig, Marco
  last_name: Klanschnig
- first_name: Andreas
  full_name: Thader, Andreas
  id: 3A18A7B8-F248-11E8-B48F-1D18A9856A87
  last_name: Thader
- first_name: Marc C.
  full_name: Johnson, Marc C.
  last_name: Johnson
- first_name: Volker M.
  full_name: Vogt, Volker M.
  last_name: Vogt
- first_name: Florian KM
  full_name: Schur, Florian KM
  id: 48AD8942-F248-11E8-B48F-1D18A9856A87
  last_name: Schur
  orcid: 0000-0003-4790-8078
- first_name: Robert A.
  full_name: Dick, Robert A.
  last_name: Dick
citation:
  ama: Obr M, Ricana CL, Nikulin N, et al. Structure of the mature Rous sarcoma virus
    lattice reveals a role for IP6 in the formation of the capsid hexamer. <i>Nature
    Communications</i>. 2021;12(1). doi:<a href="https://doi.org/10.1038/s41467-021-23506-0">10.1038/s41467-021-23506-0</a>
  apa: Obr, M., Ricana, C. L., Nikulin, N., Feathers, J.-P. R., Klanschnig, M., Thader,
    A., … Dick, R. A. (2021). Structure of the mature Rous sarcoma virus lattice reveals
    a role for IP6 in the formation of the capsid hexamer. <i>Nature Communications</i>.
    Nature Research. <a href="https://doi.org/10.1038/s41467-021-23506-0">https://doi.org/10.1038/s41467-021-23506-0</a>
  chicago: Obr, Martin, Clifton L. Ricana, Nadia Nikulin, Jon-Philip R. Feathers,
    Marco Klanschnig, Andreas Thader, Marc C. Johnson, Volker M. Vogt, Florian KM
    Schur, and Robert A. Dick. “Structure of the Mature Rous Sarcoma Virus Lattice
    Reveals a Role for IP6 in the Formation of the Capsid Hexamer.” <i>Nature Communications</i>.
    Nature Research, 2021. <a href="https://doi.org/10.1038/s41467-021-23506-0">https://doi.org/10.1038/s41467-021-23506-0</a>.
  ieee: M. Obr <i>et al.</i>, “Structure of the mature Rous sarcoma virus lattice
    reveals a role for IP6 in the formation of the capsid hexamer,” <i>Nature Communications</i>,
    vol. 12, no. 1. Nature Research, 2021.
  ista: Obr M, Ricana CL, Nikulin N, Feathers J-PR, Klanschnig M, Thader A, Johnson
    MC, Vogt VM, Schur FK, Dick RA. 2021. Structure of the mature Rous sarcoma virus
    lattice reveals a role for IP6 in the formation of the capsid hexamer. Nature
    Communications. 12(1), 3226.
  mla: Obr, Martin, et al. “Structure of the Mature Rous Sarcoma Virus Lattice Reveals
    a Role for IP6 in the Formation of the Capsid Hexamer.” <i>Nature Communications</i>,
    vol. 12, no. 1, 3226, Nature Research, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-23506-0">10.1038/s41467-021-23506-0</a>.
  short: M. Obr, C.L. Ricana, N. Nikulin, J.-P.R. Feathers, M. Klanschnig, A. Thader,
    M.C. Johnson, V.M. Vogt, F.K. Schur, R.A. Dick, Nature Communications 12 (2021).
date_created: 2021-05-28T14:25:50Z
date_published: 2021-05-28T00:00:00Z
date_updated: 2023-08-08T13:53:53Z
day: '28'
ddc:
- '570'
department:
- _id: FlSc
doi: 10.1038/s41467-021-23506-0
external_id:
  isi:
  - '000659145000011'
file:
- access_level: open_access
  checksum: 53ccc53d09a9111143839dbe7784e663
  content_type: application/pdf
  creator: kschuh
  date_created: 2021-06-09T15:21:14Z
  date_updated: 2021-06-09T15:21:14Z
  file_id: '9538'
  file_name: 2021_NatureCommunications_Obr.pdf
  file_size: 6166295
  relation: main_file
  success: 1
file_date_updated: 2021-06-09T15:21:14Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 26736D6A-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P31445
  name: Structural conservation and diversity in retroviral capsid
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Nature Research
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/how-retroviruses-become-infectious/
scopus_import: '1'
status: public
title: Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in
  the formation of the capsid hexamer
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '9540'
abstract:
- lang: eng
  text: The hexameric AAA-ATPase Drg1 is a key factor in eukaryotic ribosome biogenesis
    and initiates cytoplasmic maturation of the large ribosomal subunit by releasing
    the shuttling maturation factor Rlp24. Drg1 monomers contain two AAA-domains (D1
    and D2) that act in a concerted manner. Rlp24 release is inhibited by the drug
    diazaborine which blocks ATP hydrolysis in D2. The mode of inhibition was unknown.
    Here we show the first cryo-EM structure of Drg1 revealing the inhibitory mechanism.
    Diazaborine forms a covalent bond to the 2′-OH of the nucleotide in D2, explaining
    its specificity for this site. As a consequence, the D2 domain is locked in a
    rigid, inactive state, stalling the whole Drg1 hexamer. Resistance mechanisms
    identified include abolished drug binding and altered positioning of the nucleotide.
    Our results suggest nucleotide-modifying compounds as potential novel inhibitors
    for AAA-ATPases.
acknowledged_ssus:
- _id: EM-Fac
acknowledgement: We are deeply grateful to the late Gregor Högenauer who built the
  foundation for this study with his visionary work on the inhibitor diazaborine and
  its bacterial target. We thank Rolf Breinbauer for insightful discussions on boron
  chemistry. We thank Anton Meinhart and Tim Clausen for the valuable discussion of
  the manuscript. We are indebted to Thomas Köcher for the MS measurement of the diazaborine-ATPγS
  adduct. We thank the team of the VBCF for support during early phases of this work
  and the IST Austria Electron Microscopy Facility for providing equipment. The lab
  of D.H. is supported by Boehringer Ingelheim. The work was funded by FWF projects
  P32536 and P32977 (to H.B.).
article_number: '3483'
article_processing_charge: No
article_type: original
author:
- first_name: Michael
  full_name: Prattes, Michael
  last_name: Prattes
- first_name: Irina
  full_name: Grishkovskaya, Irina
  last_name: Grishkovskaya
- first_name: Victor-Valentin
  full_name: Hodirnau, Victor-Valentin
  id: 3661B498-F248-11E8-B48F-1D18A9856A87
  last_name: Hodirnau
- first_name: Ingrid
  full_name: Rössler, Ingrid
  last_name: Rössler
- first_name: Isabella
  full_name: Klein, Isabella
  last_name: Klein
- first_name: Christina
  full_name: Hetzmannseder, Christina
  last_name: Hetzmannseder
- first_name: Gertrude
  full_name: Zisser, Gertrude
  last_name: Zisser
- first_name: Christian C.
  full_name: Gruber, Christian C.
  last_name: Gruber
- first_name: Karl
  full_name: Gruber, Karl
  last_name: Gruber
- first_name: David
  full_name: Haselbach, David
  last_name: Haselbach
- first_name: Helmut
  full_name: Bergler, Helmut
  last_name: Bergler
citation:
  ama: Prattes M, Grishkovskaya I, Hodirnau V-V, et al. Structural basis for inhibition
    of the AAA-ATPase Drg1 by diazaborine. <i>Nature Communications</i>. 2021;12(1).
    doi:<a href="https://doi.org/10.1038/s41467-021-23854-x">10.1038/s41467-021-23854-x</a>
  apa: Prattes, M., Grishkovskaya, I., Hodirnau, V.-V., Rössler, I., Klein, I., Hetzmannseder,
    C., … Bergler, H. (2021). Structural basis for inhibition of the AAA-ATPase Drg1
    by diazaborine. <i>Nature Communications</i>. Springer Nature. <a href="https://doi.org/10.1038/s41467-021-23854-x">https://doi.org/10.1038/s41467-021-23854-x</a>
  chicago: Prattes, Michael, Irina Grishkovskaya, Victor-Valentin Hodirnau, Ingrid
    Rössler, Isabella Klein, Christina Hetzmannseder, Gertrude Zisser, et al. “Structural
    Basis for Inhibition of the AAA-ATPase Drg1 by Diazaborine.” <i>Nature Communications</i>.
    Springer Nature, 2021. <a href="https://doi.org/10.1038/s41467-021-23854-x">https://doi.org/10.1038/s41467-021-23854-x</a>.
  ieee: M. Prattes <i>et al.</i>, “Structural basis for inhibition of the AAA-ATPase
    Drg1 by diazaborine,” <i>Nature Communications</i>, vol. 12, no. 1. Springer Nature,
    2021.
  ista: Prattes M, Grishkovskaya I, Hodirnau V-V, Rössler I, Klein I, Hetzmannseder
    C, Zisser G, Gruber CC, Gruber K, Haselbach D, Bergler H. 2021. Structural basis
    for inhibition of the AAA-ATPase Drg1 by diazaborine. Nature Communications. 12(1),
    3483.
  mla: Prattes, Michael, et al. “Structural Basis for Inhibition of the AAA-ATPase
    Drg1 by Diazaborine.” <i>Nature Communications</i>, vol. 12, no. 1, 3483, Springer
    Nature, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-23854-x">10.1038/s41467-021-23854-x</a>.
  short: M. Prattes, I. Grishkovskaya, V.-V. Hodirnau, I. Rössler, I. Klein, C. Hetzmannseder,
    G. Zisser, C.C. Gruber, K. Gruber, D. Haselbach, H. Bergler, Nature Communications
    12 (2021).
date_created: 2021-06-10T14:57:45Z
date_published: 2021-06-09T00:00:00Z
date_updated: 2023-08-08T14:05:26Z
day: '09'
ddc:
- '570'
department:
- _id: EM-Fac
doi: 10.1038/s41467-021-23854-x
external_id:
  isi:
  - '000664874700014'
  pmid:
  - '34108481'
file:
- access_level: open_access
  checksum: 40fc24c1310930990b52a8ad1142ee97
  content_type: application/pdf
  creator: cziletti
  date_created: 2021-06-15T18:55:59Z
  date_updated: 2021-06-15T18:55:59Z
  file_id: '9556'
  file_name: 2021_NatureComm_Prattes.pdf
  file_size: 3397292
  relation: main_file
  success: 1
file_date_updated: 2021-06-15T18:55:59Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Structural basis for inhibition of the AAA-ATPase Drg1 by diazaborine
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '10163'
abstract:
- lang: eng
  text: The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol
    II) is a regulatory hub for transcription and RNA processing. Here, we identify
    PHD-finger protein 3 (PHF3) as a regulator of transcription and mRNA stability
    that docks onto Pol II CTD through its SPOC domain. We characterize SPOC as a
    CTD reader domain that preferentially binds two phosphorylated Serine-2 marks
    in adjacent CTD repeats. PHF3 drives liquid-liquid phase separation of phosphorylated
    Pol II, colocalizes with Pol II clusters and tracks with Pol II across the length
    of genes. PHF3 knock-out or SPOC deletion in human cells results in increased
    Pol II stalling, reduced elongation rate and an increase in mRNA stability, with
    marked derepression of neuronal genes. Key neuronal genes are aberrantly expressed
    in Phf3 knock-out mouse embryonic stem cells, resulting in impaired neuronal differentiation.
    Our data suggest that PHF3 acts as a prominent effector of neuronal gene regulation
    by bridging transcription with mRNA decay.
acknowledgement: 'D.S. thanks Claudine Kraft, Renée Schroeder, Verena Jantsch, Franz
  Klein and Peter Schlögelhofer for support. We thank Anita Testa Salmazo for help
  with purifying Pol II; Matthias Geyer and Robert Düster for sharing DYRK1A kinase;
  Felix Hartmann and Clemens Plaschka for help with mass photometry; Goran Kokic for
  design of the arrest assay sequences; Petra van der Lelij for help with generating
  mESC KO; Maximilian Freilinger for help with the purification of mEGFP-CTD; Stefan
  Ameres, Nina Fasching and Brian Reichholf for advice on SLAM-seq and for sharing
  reagents; Laura Gallego Valle for advice regarding LLPS assays; Krzysztof Chylinski
  for advice regarding CRISPR/Cas9 methodology; VBCF Protein Technologies facility
  for purifying PHF3 and providing gRNAs and Cas9; VBCF NGS facility for sequencing;
  Monoclonal antibody facility at the Helmholtz center for Pol II antibodies; Friedrich
  Propst and Elzbieta Kowalska for advice and for sharing materials; Egon Ogris for
  sharing materials; Martin Eilers for recommending a ChIP-grade TFIIS antibody; Susanne
  Opravil, Otto Hudecz, Markus Hartl and Natascha Hartl for mass spectrometry analysis;
  staff of the X-ray beamlines at the ESRF in Grenoble for their excellent support;
  Christa Bücker, Anton Meinhart, Clemens Plaschka and members of the Slade lab for
  critical comments on the manuscript; Life Science Editors for editing assistance.
  M.B. and D.S. acknowledge support by the FWF-funded DK ‘Chromosome Dynamics’. T.K.
  is a recipient of the DOC fellowship from the Austrian Academy of Sciences. U.S.
  is supported by the L’Oreal for Women in Science Austria Fellowship and the Austrian
  Science Fund (FWF T 795-B30). M.L is supported by the Vienna Science and Technology
  Fund (WWTF, VRG14-006). R.S. is supported by the Czech Science Foundation (15-17670 S
  and 21-24460 S), Ministry of Education, Youths and Sports of the Czech Republic
  (CEITEC 2020 project (LQ1601)), and the European Research Council (ERC) under the
  European Union’s Horizon 2020 research and innovation programme (Grant agreement
  no. 649030); this publication reflects only the author’s view and the Research Executive
  Agency is not responsible for any use that may be made of the information it contains.
  M.S. is supported by the Czech Science Foundation (GJ20-21581Y). K.D.C. research
  is supported by the Austrian Science Fund (FWF) Projects I525 and I1593, P22276,
  P19060, and W1221, Federal Ministry of Economy, Family and Youth through the initiative
  ‘Laura Bassi Centres of Expertise’, funding from the Centre of Optimized Structural
  Studies No. 253275, the Wellcome Trust Collaborative Award (201543/Z/16), COST action
  BM1405 Non-globular proteins - from sequence to structure, function and application
  in molecular physiopathology (NGP-NET), the Vienna Science and Technology Fund (WWTF
  LS17-008), and by the University of Vienna. This project was funded by the MFPL
  start-up grant, the Vienna Science and Technology Fund (WWTF LS14-001), and the
  Austrian Science Fund (P31546-B28 and W1258 “DK: Integrative Structural Biology”)
  to D.S.'
article_number: '6078'
article_processing_charge: No
article_type: original
author:
- first_name: Lisa-Marie
  full_name: Appel, Lisa-Marie
  last_name: Appel
- first_name: Vedran
  full_name: Franke, Vedran
  last_name: Franke
- first_name: Melania
  full_name: Bruno, Melania
  last_name: Bruno
- first_name: Irina
  full_name: Grishkovskaya, Irina
  last_name: Grishkovskaya
- first_name: Aiste
  full_name: Kasiliauskaite, Aiste
  last_name: Kasiliauskaite
- first_name: Tanja
  full_name: Kaufmann, Tanja
  last_name: Kaufmann
- first_name: Ursula E.
  full_name: Schoeberl, Ursula E.
  last_name: Schoeberl
- first_name: Martin G.
  full_name: Puchinger, Martin G.
  last_name: Puchinger
- first_name: Sebastian
  full_name: Kostrhon, Sebastian
  last_name: Kostrhon
- first_name: Carmen
  full_name: Ebenwaldner, Carmen
  last_name: Ebenwaldner
- first_name: Marek
  full_name: Sebesta, Marek
  last_name: Sebesta
- first_name: Etienne
  full_name: Beltzung, Etienne
  last_name: Beltzung
- first_name: Karl
  full_name: Mechtler, Karl
  last_name: Mechtler
- first_name: Gen
  full_name: Lin, Gen
  last_name: Lin
- first_name: Anna
  full_name: Vlasova, Anna
  last_name: Vlasova
- first_name: Martin
  full_name: Leeb, Martin
  last_name: Leeb
- first_name: Rushad
  full_name: Pavri, Rushad
  last_name: Pavri
- first_name: Alexander
  full_name: Stark, Alexander
  last_name: Stark
- first_name: Altuna
  full_name: Akalin, Altuna
  last_name: Akalin
- first_name: Richard
  full_name: Stefl, Richard
  last_name: Stefl
- first_name: Carrie A
  full_name: Bernecky, Carrie A
  id: 2CB9DFE2-F248-11E8-B48F-1D18A9856A87
  last_name: Bernecky
  orcid: 0000-0003-0893-7036
- first_name: Kristina
  full_name: Djinovic-Carugo, Kristina
  last_name: Djinovic-Carugo
- first_name: Dea
  full_name: Slade, Dea
  last_name: Slade
citation:
  ama: Appel L-M, Franke V, Bruno M, et al. PHF3 regulates neuronal gene expression
    through the Pol II CTD reader domain SPOC. <i>Nature Communications</i>. 2021;12(1).
    doi:<a href="https://doi.org/10.1038/s41467-021-26360-2">10.1038/s41467-021-26360-2</a>
  apa: Appel, L.-M., Franke, V., Bruno, M., Grishkovskaya, I., Kasiliauskaite, A.,
    Kaufmann, T., … Slade, D. (2021). PHF3 regulates neuronal gene expression through
    the Pol II CTD reader domain SPOC. <i>Nature Communications</i>. Springer Nature.
    <a href="https://doi.org/10.1038/s41467-021-26360-2">https://doi.org/10.1038/s41467-021-26360-2</a>
  chicago: Appel, Lisa-Marie, Vedran Franke, Melania Bruno, Irina Grishkovskaya, Aiste
    Kasiliauskaite, Tanja Kaufmann, Ursula E. Schoeberl, et al. “PHF3 Regulates Neuronal
    Gene Expression through the Pol II CTD Reader Domain SPOC.” <i>Nature Communications</i>.
    Springer Nature, 2021. <a href="https://doi.org/10.1038/s41467-021-26360-2">https://doi.org/10.1038/s41467-021-26360-2</a>.
  ieee: L.-M. Appel <i>et al.</i>, “PHF3 regulates neuronal gene expression through
    the Pol II CTD reader domain SPOC,” <i>Nature Communications</i>, vol. 12, no.
    1. Springer Nature, 2021.
  ista: Appel L-M, Franke V, Bruno M, Grishkovskaya I, Kasiliauskaite A, Kaufmann
    T, Schoeberl UE, Puchinger MG, Kostrhon S, Ebenwaldner C, Sebesta M, Beltzung
    E, Mechtler K, Lin G, Vlasova A, Leeb M, Pavri R, Stark A, Akalin A, Stefl R,
    Bernecky C, Djinovic-Carugo K, Slade D. 2021. PHF3 regulates neuronal gene expression
    through the Pol II CTD reader domain SPOC. Nature Communications. 12(1), 6078.
  mla: Appel, Lisa-Marie, et al. “PHF3 Regulates Neuronal Gene Expression through
    the Pol II CTD Reader Domain SPOC.” <i>Nature Communications</i>, vol. 12, no.
    1, 6078, Springer Nature, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-26360-2">10.1038/s41467-021-26360-2</a>.
  short: L.-M. Appel, V. Franke, M. Bruno, I. Grishkovskaya, A. Kasiliauskaite, T.
    Kaufmann, U.E. Schoeberl, M.G. Puchinger, S. Kostrhon, C. Ebenwaldner, M. Sebesta,
    E. Beltzung, K. Mechtler, G. Lin, A. Vlasova, M. Leeb, R. Pavri, A. Stark, A.
    Akalin, R. Stefl, C. Bernecky, K. Djinovic-Carugo, D. Slade, Nature Communications
    12 (2021).
date_created: 2021-10-20T14:40:32Z
date_published: 2021-10-19T00:00:00Z
date_updated: 2023-08-14T08:02:31Z
day: '19'
ddc:
- '610'
department:
- _id: CaBe
doi: 10.1038/s41467-021-26360-2
external_id:
  isi:
  - '000709050300001'
file:
- access_level: open_access
  checksum: d99fcd51aebde19c21314e3de0148007
  content_type: application/pdf
  creator: cchlebak
  date_created: 2021-10-21T13:51:49Z
  date_updated: 2021-10-21T13:51:49Z
  file_id: '10169'
  file_name: 2021_NatComm_Appel.pdf
  file_size: 5111706
  relation: main_file
  success: 1
file_date_updated: 2021-10-21T13:51:49Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- general physics and astronomy
- general biochemistry
- genetics and molecular biology
- general chemistry
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  eissn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
  link:
  - description: 'Preprint '
    relation: earlier_version
    url: https://www.biorxiv.org/content/10.1101/2020.02.11.943159
status: public
title: PHF3 regulates neuronal gene expression through the Pol II CTD reader domain
  SPOC
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '10301'
abstract:
- lang: eng
  text: De novo protein synthesis is required for synapse modifications underlying
    stable memory encoding. Yet neurons are highly compartmentalized cells and how
    protein synthesis can be regulated at the synapse level is unknown. Here, we characterize
    neuronal signaling complexes formed by the postsynaptic scaffold GIT1, the mechanistic
    target of rapamycin (mTOR) kinase, and Raptor that couple synaptic stimuli to
    mTOR-dependent protein synthesis; and identify NMDA receptors containing GluN3A
    subunits as key negative regulators of GIT1 binding to mTOR. Disruption of GIT1/mTOR
    complexes by enhancing GluN3A expression or silencing GIT1 inhibits synaptic mTOR
    activation and restricts the mTOR-dependent translation of specific activity-regulated
    mRNAs. Conversely, GluN3A removal enables complex formation, potentiates mTOR-dependent
    protein synthesis, and facilitates the consolidation of associative and spatial
    memories in mice. The memory enhancement becomes evident with light or spaced
    training, can be achieved by selectively deleting GluN3A from excitatory neurons
    during adulthood, and does not compromise other aspects of cognition such as memory
    flexibility or extinction. Our findings provide mechanistic insight into synaptic
    translational control and reveal a potentially selective target for cognitive
    enhancement.
acknowledgement: We thank Stuart Lipton and Nobuki Nakanishi for providing the Grin3a
  knockout mice, Beverly Davidson for the AAV-caRheb, Jose Esteban for help with behavioral
  and biochemical experiments, and Noelia Campillo, Rebeca Martínez-Turrillas, and
  Ana Navarro for expert technical help. Work was funded by the UTE project CIMA;
  fellowships from the Fundación Tatiana Pérez de Guzmán el Bueno, FEBS, and IBRO
  (to M.J.C.D.), Generalitat Valenciana (to O.E.-Z.), Juan de la Cierva (to L.G.R.),
  FPI-MINECO (to E.R.V., to S.N.) and Intertalentum postdoctoral program (to V.B.);
  ANR (GluBrain3A) and ERC Advanced Grants (#693021) (to P.P.); Ramón y Cajal program
  RYC2014-15784, RETOS-MINECO SAF2016-76565-R, ERANET-Neuron JTC 2019 ISCIII AC19/00077
  FEDER funds (to R.A.); RETOS-MINECO SAF2017-87928-R (to A.B.); an NIH grant (NS76637)
  and UTHSC College of Medicine funds (to S.J.T.); and NARSAD Independent Investigator
  Award and grants from the MINECO (CSD2008-00005, SAF2013-48983R, SAF2016-80895-R),
  Generalitat Valenciana (PROMETEO 2019/020)(to I.P.O.) and Severo-Ochoa Excellence
  Awards (SEV-2013-0317, SEV-2017-0723).
article_number: e71575
article_processing_charge: No
article_type: original
author:
- first_name: María J
  full_name: Conde-Dusman, María J
  last_name: Conde-Dusman
- first_name: Partha N
  full_name: Dey, Partha N
  last_name: Dey
- first_name: Óscar
  full_name: Elía-Zudaire, Óscar
  last_name: Elía-Zudaire
- first_name: Luis E
  full_name: Garcia Rabaneda, Luis E
  id: 33D1B084-F248-11E8-B48F-1D18A9856A87
  last_name: Garcia Rabaneda
- first_name: Carmen
  full_name: García-Lira, Carmen
  last_name: García-Lira
- first_name: Teddy
  full_name: Grand, Teddy
  last_name: Grand
- first_name: Victor
  full_name: Briz, Victor
  last_name: Briz
- first_name: Eric R
  full_name: Velasco, Eric R
  last_name: Velasco
- first_name: Raül
  full_name: Andero Galí, Raül
  last_name: Andero Galí
- first_name: Sergio
  full_name: Niñerola, Sergio
  last_name: Niñerola
- first_name: Angel
  full_name: Barco, Angel
  last_name: Barco
- first_name: Pierre
  full_name: Paoletti, Pierre
  last_name: Paoletti
- first_name: John F
  full_name: Wesseling, John F
  last_name: Wesseling
- first_name: Fabrizio
  full_name: Gardoni, Fabrizio
  last_name: Gardoni
- first_name: Steven J
  full_name: Tavalin, Steven J
  last_name: Tavalin
- first_name: Isabel
  full_name: Perez-Otaño, Isabel
  last_name: Perez-Otaño
citation:
  ama: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, et al. Control of protein synthesis
    and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
    <i>eLife</i>. 2021;10. doi:<a href="https://doi.org/10.7554/elife.71575">10.7554/elife.71575</a>
  apa: Conde-Dusman, M. J., Dey, P. N., Elía-Zudaire, Ó., Garcia Rabaneda, L. E.,
    García-Lira, C., Grand, T., … Perez-Otaño, I. (2021). Control of protein synthesis
    and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
    <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.71575">https://doi.org/10.7554/elife.71575</a>
  chicago: Conde-Dusman, María J, Partha N Dey, Óscar Elía-Zudaire, Luis E Garcia
    Rabaneda, Carmen García-Lira, Teddy Grand, Victor Briz, et al. “Control of Protein
    Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1
    Assembly.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href="https://doi.org/10.7554/elife.71575">https://doi.org/10.7554/elife.71575</a>.
  ieee: M. J. Conde-Dusman <i>et al.</i>, “Control of protein synthesis and memory
    by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” <i>eLife</i>,
    vol. 10. eLife Sciences Publications, 2021.
  ista: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, Garcia Rabaneda LE, García-Lira C,
    Grand T, Briz V, Velasco ER, Andero Galí R, Niñerola S, Barco A, Paoletti P, Wesseling
    JF, Gardoni F, Tavalin SJ, Perez-Otaño I. 2021. Control of protein synthesis and
    memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. eLife.
    10, e71575.
  mla: Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by
    GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” <i>ELife</i>,
    vol. 10, e71575, eLife Sciences Publications, 2021, doi:<a href="https://doi.org/10.7554/elife.71575">10.7554/elife.71575</a>.
  short: M.J. Conde-Dusman, P.N. Dey, Ó. Elía-Zudaire, L.E. Garcia Rabaneda, C. García-Lira,
    T. Grand, V. Briz, E.R. Velasco, R. Andero Galí, S. Niñerola, A. Barco, P. Paoletti,
    J.F. Wesseling, F. Gardoni, S.J. Tavalin, I. Perez-Otaño, ELife 10 (2021).
date_created: 2021-11-18T06:59:45Z
date_published: 2021-11-17T00:00:00Z
date_updated: 2023-08-14T11:50:50Z
day: '17'
ddc:
- '570'
department:
- _id: GaNo
doi: 10.7554/elife.71575
external_id:
  isi:
  - '000720945900001'
file:
- access_level: open_access
  checksum: 59318e9e41507cec83c2f4070e6ad540
  content_type: application/pdf
  creator: lgarciar
  date_created: 2021-11-18T07:02:02Z
  date_updated: 2021-11-18T07:02:02Z
  file_id: '10302'
  file_name: elife-71575-v1.pdf
  file_size: 2477302
  relation: main_file
  success: 1
file_date_updated: 2021-11-18T07:02:02Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
keyword:
- general immunology and microbiology
- general biochemistry
- genetics and molecular biology
- general medicine
- general neuroscience
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition
  of GIT1/mTORC1 assembly
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '10310'
abstract:
- lang: eng
  text: A high-resolution structure of trimeric cyanobacterial Photosystem I (PSI)
    from Thermosynechococcus elongatus was reported as the first atomic model of PSI
    almost 20 years ago. However, the monomeric PSI structure has not yet been reported
    despite long-standing interest in its structure and extensive spectroscopic characterization
    of the loss of red chlorophylls upon monomerization. Here, we describe the structure
    of monomeric PSI from Thermosynechococcus elongatus BP-1. Comparison with the
    trimer structure gave detailed insights into monomerization-induced changes in
    both the central trimerization domain and the peripheral regions of the complex.
    Monomerization-induced loss of red chlorophylls is assigned to a cluster of chlorophylls
    adjacent to PsaX. Based on our findings, we propose a role of PsaX in the stabilization
    of red chlorophylls and that lipids of the surrounding membrane present a major
    source of thermal energy for uphill excitation energy transfer from red chlorophylls
    to P700.
acknowledgement: We are grateful for additional support and valuable scientific input
  for this project by Yuko Misumi, Jiannan Li, Hisako Kubota-Kawai, Takeshi Kawabata,
  Mian Wu, Eiki Yamashita, Atsushi Nakagawa, Volker Hartmann, Melanie Völkel and Matthias
  Rögner. Parts of this research were funded by the German Research Council (DFG)
  within the framework of GRK 2341 (Microbial Substrate Conversion) to M.M.N., the
  Platform Project for Supporting Drug Discovery and Life Science Research [Basis
  for Supporting Innovative Drug Discovery and Life Science Research (BINDS)] from
  AMED under grant number JP20am0101117 (K.N.), JP16K07266 to Atsunori Oshima and
  C.G., a Grants-in-Aid for Scientific Research under grant number JP 25000013 (K.N.),
  17H03647 (C.G.) and 16H06560 (G.K.) from MEXT-KAKENHI, the International Joint Research
  Promotion Program from Osaka University to M.M.N., C.G. and G.K., and the Cyclic
  Innovation for Clinical Empowerment (CiCLE) Grant Number JP17pc0101020 from AMED
  to K.N. and G.K.
article_number: '304'
article_processing_charge: No
article_type: original
author:
- first_name: Mehmet Orkun
  full_name: Çoruh, Mehmet Orkun
  id: d25163e5-8d53-11eb-a251-e6dd8ea1b8ef
  last_name: Çoruh
  orcid: 0000-0002-3219-2022
- first_name: Anna
  full_name: Frank, Anna
  last_name: Frank
- first_name: Hideaki
  full_name: Tanaka, Hideaki
  last_name: Tanaka
- first_name: Akihiro
  full_name: Kawamoto, Akihiro
  last_name: Kawamoto
- first_name: Eithar
  full_name: El-Mohsnawy, Eithar
  last_name: El-Mohsnawy
- first_name: Takayuki
  full_name: Kato, Takayuki
  last_name: Kato
- first_name: Keiichi
  full_name: Namba, Keiichi
  last_name: Namba
- first_name: Christoph
  full_name: Gerle, Christoph
  last_name: Gerle
- first_name: Marc M.
  full_name: Nowaczyk, Marc M.
  last_name: Nowaczyk
- first_name: Genji
  full_name: Kurisu, Genji
  last_name: Kurisu
citation:
  ama: Çoruh MO, Frank A, Tanaka H, et al. Cryo-EM structure of a functional monomeric
    Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster.
    <i>Communications Biology</i>. 2021;4(1). doi:<a href="https://doi.org/10.1038/s42003-021-01808-9">10.1038/s42003-021-01808-9</a>
  apa: Çoruh, M. O., Frank, A., Tanaka, H., Kawamoto, A., El-Mohsnawy, E., Kato, T.,
    … Kurisu, G. (2021). Cryo-EM structure of a functional monomeric Photosystem I
    from Thermosynechococcus elongatus reveals red chlorophyll cluster. <i>Communications
    Biology</i>. Springer . <a href="https://doi.org/10.1038/s42003-021-01808-9">https://doi.org/10.1038/s42003-021-01808-9</a>
  chicago: Çoruh, Mehmet Orkun, Anna Frank, Hideaki Tanaka, Akihiro Kawamoto, Eithar
    El-Mohsnawy, Takayuki Kato, Keiichi Namba, Christoph Gerle, Marc M. Nowaczyk,
    and Genji Kurisu. “Cryo-EM Structure of a Functional Monomeric Photosystem I from
    Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” <i>Communications
    Biology</i>. Springer , 2021. <a href="https://doi.org/10.1038/s42003-021-01808-9">https://doi.org/10.1038/s42003-021-01808-9</a>.
  ieee: M. O. Çoruh <i>et al.</i>, “Cryo-EM structure of a functional monomeric Photosystem
    I from Thermosynechococcus elongatus reveals red chlorophyll cluster,” <i>Communications
    Biology</i>, vol. 4, no. 1. Springer , 2021.
  ista: Çoruh MO, Frank A, Tanaka H, Kawamoto A, El-Mohsnawy E, Kato T, Namba K, Gerle
    C, Nowaczyk MM, Kurisu G. 2021. Cryo-EM structure of a functional monomeric Photosystem
    I from Thermosynechococcus elongatus reveals red chlorophyll cluster. Communications
    Biology. 4(1), 304.
  mla: Çoruh, Mehmet Orkun, et al. “Cryo-EM Structure of a Functional Monomeric Photosystem
    I from Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” <i>Communications
    Biology</i>, vol. 4, no. 1, 304, Springer , 2021, doi:<a href="https://doi.org/10.1038/s42003-021-01808-9">10.1038/s42003-021-01808-9</a>.
  short: M.O. Çoruh, A. Frank, H. Tanaka, A. Kawamoto, E. El-Mohsnawy, T. Kato, K.
    Namba, C. Gerle, M.M. Nowaczyk, G. Kurisu, Communications Biology 4 (2021).
date_created: 2021-11-19T11:37:29Z
date_published: 2021-03-08T00:00:00Z
date_updated: 2023-08-14T11:51:19Z
day: '08'
ddc:
- '570'
department:
- _id: LeSa
doi: 10.1038/s42003-021-01808-9
external_id:
  isi:
  - '000627440700001'
  pmid:
  - '33686186'
file:
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  checksum: 8ffd39f2bba7152a2441802ff313bf0b
  content_type: application/pdf
  creator: cchlebak
  date_created: 2021-11-19T15:09:18Z
  date_updated: 2021-11-19T15:09:18Z
  file_id: '10318'
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  success: 1
file_date_updated: 2021-11-19T15:09:18Z
has_accepted_license: '1'
intvolume: '         4'
isi: 1
issue: '1'
keyword:
- general agricultural and biological Sciences
- general biochemistry
- genetics and molecular biology
- medicine (miscellaneous)
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: Communications Biology
publication_identifier:
  issn:
  - 2399-3642
publication_status: published
publisher: 'Springer '
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus
  elongatus reveals red chlorophyll cluster
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 4
year: '2021'
...
---
_id: '12585'
abstract:
- lang: eng
  text: Glaciers in High Mountain Asia generate meltwater that supports the water
    needs of 250 million people, but current knowledge of annual accumulation and
    ablation is limited to sparse field measurements biased in location and glacier
    size. Here, we present altitudinally-resolved specific mass balances (surface,
    internal, and basal combined) for 5527 glaciers in High Mountain Asia for 2000–2016,
    derived by correcting observed glacier thinning patterns for mass redistribution
    due to ice flow. We find that 41% of glaciers accumulated mass over less than
    20% of their area, and only 60% ± 10% of regional annual ablation was compensated
    by accumulation. Even without 21st century warming, 21% ± 1% of ice volume will
    be lost by 2100 due to current climatic-geometric imbalance, representing a reduction
    in glacier ablation into rivers of 28% ± 1%. The ablation of glaciers in the Himalayas
    and Tien Shan was mostly unsustainable and ice volume in these regions will reduce
    by at least 30% by 2100. The most important and vulnerable glacier-fed river basins
    (Amu Darya, Indus, Syr Darya, Tarim Interior) were supplied with >50% sustainable
    glacier ablation but will see long-term reductions in ice mass and glacier meltwater
    supply regardless of the Karakoram Anomaly.
article_number: '2868'
article_processing_charge: No
article_type: original
author:
- first_name: Evan
  full_name: Miles, Evan
  last_name: Miles
- first_name: Michael
  full_name: McCarthy, Michael
  last_name: McCarthy
- first_name: Amaury
  full_name: Dehecq, Amaury
  last_name: Dehecq
- first_name: Marin
  full_name: Kneib, Marin
  last_name: Kneib
- first_name: Stefan
  full_name: Fugger, Stefan
  last_name: Fugger
- first_name: Francesca
  full_name: Pellicciotti, Francesca
  id: b28f055a-81ea-11ed-b70c-a9fe7f7b0e70
  last_name: Pellicciotti
citation:
  ama: Miles E, McCarthy M, Dehecq A, Kneib M, Fugger S, Pellicciotti F. Health and
    sustainability of glaciers in High Mountain Asia. <i>Nature Communications</i>.
    2021;12. doi:<a href="https://doi.org/10.1038/s41467-021-23073-4">10.1038/s41467-021-23073-4</a>
  apa: Miles, E., McCarthy, M., Dehecq, A., Kneib, M., Fugger, S., &#38; Pellicciotti,
    F. (2021). Health and sustainability of glaciers in High Mountain Asia. <i>Nature
    Communications</i>. Springer Nature. <a href="https://doi.org/10.1038/s41467-021-23073-4">https://doi.org/10.1038/s41467-021-23073-4</a>
  chicago: Miles, Evan, Michael McCarthy, Amaury Dehecq, Marin Kneib, Stefan Fugger,
    and Francesca Pellicciotti. “Health and Sustainability of Glaciers in High Mountain
    Asia.” <i>Nature Communications</i>. Springer Nature, 2021. <a href="https://doi.org/10.1038/s41467-021-23073-4">https://doi.org/10.1038/s41467-021-23073-4</a>.
  ieee: E. Miles, M. McCarthy, A. Dehecq, M. Kneib, S. Fugger, and F. Pellicciotti,
    “Health and sustainability of glaciers in High Mountain Asia,” <i>Nature Communications</i>,
    vol. 12. Springer Nature, 2021.
  ista: Miles E, McCarthy M, Dehecq A, Kneib M, Fugger S, Pellicciotti F. 2021. Health
    and sustainability of glaciers in High Mountain Asia. Nature Communications. 12,
    2868.
  mla: Miles, Evan, et al. “Health and Sustainability of Glaciers in High Mountain
    Asia.” <i>Nature Communications</i>, vol. 12, 2868, Springer Nature, 2021, doi:<a
    href="https://doi.org/10.1038/s41467-021-23073-4">10.1038/s41467-021-23073-4</a>.
  short: E. Miles, M. McCarthy, A. Dehecq, M. Kneib, S. Fugger, F. Pellicciotti, Nature
    Communications 12 (2021).
date_created: 2023-02-20T08:11:29Z
date_published: 2021-05-17T00:00:00Z
date_updated: 2023-02-28T13:21:51Z
day: '17'
doi: 10.1038/s41467-021-23073-4
extern: '1'
intvolume: '        12'
keyword:
- General Physics and Astronomy
- General Biochemistry
- Genetics and Molecular Biology
- General Chemistry
- Multidisciplinary
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1038/s41467-021-23073-4
month: '05'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Health and sustainability of glaciers in High Mountain Asia
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2021'
...
---
_id: '9778'
abstract:
- lang: eng
  text: The hippocampal mossy fiber synapse is a key synapse of the trisynaptic circuit.
    Post-tetanic potentiation (PTP) is the most powerful form of plasticity at this
    synaptic connection. It is widely believed that mossy fiber PTP is an entirely
    presynaptic phenomenon, implying that PTP induction is input-specific, and requires
    neither activity of multiple inputs nor stimulation of postsynaptic neurons. To
    directly test cooperativity and associativity, we made paired recordings between
    single mossy fiber terminals and postsynaptic CA3 pyramidal neurons in rat brain
    slices. By stimulating non-overlapping mossy fiber inputs converging onto single
    CA3 neurons, we confirm that PTP is input-specific and non-cooperative. Unexpectedly,
    mossy fiber PTP exhibits anti-associative induction properties. EPSCs show only
    minimal PTP after combined pre- and postsynaptic high-frequency stimulation with
    intact postsynaptic Ca2+ signaling, but marked PTP in the absence of postsynaptic
    spiking and after suppression of postsynaptic Ca2+ signaling (10 mM EGTA). PTP
    is largely recovered by inhibitors of voltage-gated R- and L-type Ca2+ channels,
    group II mGluRs, and vacuolar-type H+-ATPase, suggesting the involvement of retrograde
    vesicular glutamate signaling. Transsynaptic regulation of PTP extends the repertoire
    of synaptic computations, implementing a brake on mossy fiber detonation and a
    “smart teacher” function of hippocampal mossy fiber synapses.
acknowledged_ssus:
- _id: SSU
acknowledgement: We thank Drs. Carolina Borges-Merjane and Jose Guzman for critically
  reading the manuscript, and Pablo Castillo for discussions. We are grateful to Alois
  Schlögl for help with analysis, Florian Marr for excellent technical assistance
  and cell reconstruction, Christina Altmutter for technical help, Eleftheria Kralli-Beller
  for manuscript editing, and the Scientific Service Units of IST Austria for support.
  This project received funding from the European Research Council (ERC) under the
  European Union’s Horizon 2020 research and innovation program (grant agreement No
  692692) and the Fond zur Förderung der Wissenschaftlichen Forschung (Z 312-B27,
  Wittgenstein award), both to P.J.
article_number: '2912'
article_processing_charge: No
article_type: original
author:
- first_name: David H
  full_name: Vandael, David H
  id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87
  last_name: Vandael
  orcid: 0000-0001-7577-1676
- first_name: Yuji
  full_name: Okamoto, Yuji
  id: 3337E116-F248-11E8-B48F-1D18A9856A87
  last_name: Okamoto
  orcid: 0000-0003-0408-6094
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Vandael DH, Okamoto Y, Jonas PM. Transsynaptic modulation of presynaptic short-term
    plasticity in hippocampal mossy fiber synapses. <i>Nature Communications</i>.
    2021;12(1). doi:<a href="https://doi.org/10.1038/s41467-021-23153-5">10.1038/s41467-021-23153-5</a>
  apa: Vandael, D. H., Okamoto, Y., &#38; Jonas, P. M. (2021). Transsynaptic modulation
    of presynaptic short-term plasticity in hippocampal mossy fiber synapses. <i>Nature
    Communications</i>. Springer. <a href="https://doi.org/10.1038/s41467-021-23153-5">https://doi.org/10.1038/s41467-021-23153-5</a>
  chicago: Vandael, David H, Yuji Okamoto, and Peter M Jonas. “Transsynaptic Modulation
    of Presynaptic Short-Term Plasticity in Hippocampal Mossy Fiber Synapses.” <i>Nature
    Communications</i>. Springer, 2021. <a href="https://doi.org/10.1038/s41467-021-23153-5">https://doi.org/10.1038/s41467-021-23153-5</a>.
  ieee: D. H. Vandael, Y. Okamoto, and P. M. Jonas, “Transsynaptic modulation of presynaptic
    short-term plasticity in hippocampal mossy fiber synapses,” <i>Nature Communications</i>,
    vol. 12, no. 1. Springer, 2021.
  ista: Vandael DH, Okamoto Y, Jonas PM. 2021. Transsynaptic modulation of presynaptic
    short-term plasticity in hippocampal mossy fiber synapses. Nature Communications.
    12(1), 2912.
  mla: Vandael, David H., et al. “Transsynaptic Modulation of Presynaptic Short-Term
    Plasticity in Hippocampal Mossy Fiber Synapses.” <i>Nature Communications</i>,
    vol. 12, no. 1, 2912, Springer, 2021, doi:<a href="https://doi.org/10.1038/s41467-021-23153-5">10.1038/s41467-021-23153-5</a>.
  short: D.H. Vandael, Y. Okamoto, P.M. Jonas, Nature Communications 12 (2021).
date_created: 2021-08-06T07:22:55Z
date_published: 2021-05-18T00:00:00Z
date_updated: 2023-08-10T14:16:16Z
day: '18'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1038/s41467-021-23153-5
ec_funded: 1
external_id:
  isi:
  - '000655481800014'
file:
- access_level: open_access
  checksum: 6036a8cdae95e1707c2a04d54e325ff4
  content_type: application/pdf
  creator: kschuh
  date_created: 2021-12-17T11:34:50Z
  date_updated: 2021-12-17T11:34:50Z
  file_id: '10563'
  file_name: 2021_NatureCommunications_Vandael.pdf
  file_size: 3108845
  relation: main_file
  success: 1
file_date_updated: 2021-12-17T11:34:50Z
has_accepted_license: '1'
intvolume: '        12'
isi: 1
issue: '1'
keyword:
- general physics and astronomy
- general biochemistry
- genetics and molecular biology
- general chemistry
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '692692'
  name: Biophysics and circuit function of a giant cortical glumatergic synapse
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: Z00312
  name: The Wittgenstein Prize
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/synaptic-transmission-not-a-one-way-street/
scopus_import: '1'
status: public
title: Transsynaptic modulation of presynaptic short-term plasticity in hippocampal
  mossy fiber synapses
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
