---
_id: '15033'
abstract:
- lang: eng
  text: The GNOM (GN) Guanine nucleotide Exchange Factor for ARF small GTPases (ARF-GEF)
    is among the best studied trafficking regulators in plants, playing crucial and
    unique developmental roles in patterning and polarity. The current models place
    GN at the Golgi apparatus (GA), where it mediates secretion/recycling, and at
    the plasma membrane (PM) presumably contributing to clathrin-mediated endocytosis
    (CME). The mechanistic basis of the developmental function of GN, distinct from
    the other ARF-GEFs including its closest homologue GNOM-LIKE1 (GNL1), remains
    elusive. Insights from this study largely extend the current notions of GN function.
    We show that GN, but not GNL1, localizes to the cell periphery at long-lived structures
    distinct from clathrin-coated pits, while CME and secretion proceed normally in
    <jats:italic>gn</jats:italic> knockouts. The functional GN mutant variant GN<jats:sup>fewerroots</jats:sup>,
    absent from the GA, suggests that the cell periphery is the major site of GN action
    responsible for its developmental function. Following inhibition by Brefeldin
    A, GN, but not GNL1, relocates to the PM likely on exocytic vesicles, suggesting
    selective molecular associations en route to the cell periphery. A study of GN-GNL1
    chimeric ARF-GEFs indicates that all GN domains contribute to the specific GN
    function in a partially redundant manner. Together, this study offers significant
    steps toward the elucidation of the mechanism underlying unique cellular and development
    functions of GNOM.
acknowledgement: "The authors would like to gratefully acknowledge Dr Xixi Zhang for
  cloning the GNL1/pDONR221 construct and for useful discussions.H2020 European Research\r\nCouncil
  Advanced Grant ETAP742985 to Jiří Friml, Austrian Science Fund I 3630-B25 to Jiří
  Friml"
article_processing_charge: Yes
article_type: original
author:
- first_name: Maciek
  full_name: Adamowski, Maciek
  id: 45F536D2-F248-11E8-B48F-1D18A9856A87
  last_name: Adamowski
  orcid: 0000-0001-6463-5257
- first_name: Ivana
  full_name: Matijevic, Ivana
  id: 83c17ce3-15b2-11ec-abd3-f486545870bd
  last_name: Matijevic
- first_name: Jiří
  full_name: Friml, Jiří
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: Adamowski M, Matijevic I, Friml J. Developmental patterning function of GNOM
    ARF-GEF mediated from the cell periphery. <i>eLife</i>. 2024;13. doi:<a href="https://doi.org/10.7554/elife.68993">10.7554/elife.68993</a>
  apa: Adamowski, M., Matijevic, I., &#38; Friml, J. (2024). Developmental patterning
    function of GNOM ARF-GEF mediated from the cell periphery. <i>ELife</i>. eLife
    Sciences Publications. <a href="https://doi.org/10.7554/elife.68993">https://doi.org/10.7554/elife.68993</a>
  chicago: Adamowski, Maciek, Ivana Matijevic, and Jiří Friml. “Developmental Patterning
    Function of GNOM ARF-GEF Mediated from the Cell Periphery.” <i>ELife</i>. eLife
    Sciences Publications, 2024. <a href="https://doi.org/10.7554/elife.68993">https://doi.org/10.7554/elife.68993</a>.
  ieee: M. Adamowski, I. Matijevic, and J. Friml, “Developmental patterning function
    of GNOM ARF-GEF mediated from the cell periphery,” <i>eLife</i>, vol. 13. eLife
    Sciences Publications, 2024.
  ista: Adamowski M, Matijevic I, Friml J. 2024. Developmental patterning function
    of GNOM ARF-GEF mediated from the cell periphery. eLife. 13.
  mla: Adamowski, Maciek, et al. “Developmental Patterning Function of GNOM ARF-GEF
    Mediated from the Cell Periphery.” <i>ELife</i>, vol. 13, eLife Sciences Publications,
    2024, doi:<a href="https://doi.org/10.7554/elife.68993">10.7554/elife.68993</a>.
  short: M. Adamowski, I. Matijevic, J. Friml, ELife 13 (2024).
date_created: 2024-02-27T07:10:11Z
date_published: 2024-02-21T00:00:00Z
date_updated: 2024-02-28T12:29:43Z
day: '21'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.7554/elife.68993
ec_funded: 1
has_accepted_license: '1'
intvolume: '        13'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.7554/eLife.68993
month: '02'
oa: 1
oa_version: Published Version
project:
- _id: 261099A6-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '742985'
  name: Tracing Evolution of Auxin Transport and Polarity in Plants
- _id: 26538374-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I03630
  name: Molecular mechanisms of endocytic cargo recognition in plants
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: epub_ahead
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2024'
...
---
_id: '11448'
abstract:
- lang: eng
  text: Studies of protein fitness landscapes reveal biophysical constraints guiding
    protein evolution and empower prediction of functional proteins. However, generalisation
    of these findings is limited due to scarceness of systematic data on fitness landscapes
    of proteins with a defined evolutionary relationship. We characterized the fitness
    peaks of four orthologous fluorescent proteins with a broad range of sequence
    divergence. While two of the four studied fitness peaks were sharp, the other
    two were considerably flatter, being almost entirely free of epistatic interactions.
    Mutationally robust proteins, characterized by a flat fitness peak, were not optimal
    templates for machine-learning-driven protein design – instead, predictions were
    more accurate for fragile proteins with epistatic landscapes. Our work paves insights
    for practical application of fitness landscape heterogeneity in protein engineering.
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
acknowledgement: "We thank Ondřej Draganov, Rodrigo Redondo, Bor Kavčič, Mia Juračić
  and Andrea Pauli for discussion and technical advice. We thank Anita Testa Salmazo
  for advice on resin protein purification, Dmitry Bolotin and the Milaboratory (milaboratory.com)
  for access to computing and storage infrastructure, and Josef Houser and Eva Fujdiarova
  for technical assistance and data interpretation. Core facility Biomolecular Interactions
  and Crystallization of CEITEC Masaryk University is gratefully acknowledged for
  the obtaining of the scientific data presented in this paper. This research was
  supported by the Scientific Service Units (SSU) of IST-Austria\r\nthrough resources
  provided by the Bioimaging Facility (BIF), and the Life Science Facility (LSF).
  MiSeq and HiSeq NGS sequencing was performed by the Next Generation Sequencing Facility
  at Vienna BioCenter Core Facilities (VBCF), member of the Vienna BioCenter (VBC),
  Austria. FACS was performed at the BioOptics Facility of the Institute of Molecular
  Pathology (IMP), Austria. We also thank the Biomolecular Crystallography Facility
  in the Vanderbilt University Center for Structural Biology. We are grateful to Joel
  M Harp for help with X-ray data collection. This work was supported by the ERC Consolidator
  grant to FAK (771209—CharFL). KSS acknowledges support by President’s Grant МК–5405.2021.1.4,
  the Imperial College Research Fellowship and the MRC London Institute of Medical
  Sciences (UKRI MC-A658-5QEA0).\r\nAF is supported by the Marie Skłodowska-Curie
  Fellowship (H2020-MSCA-IF-2019, Grant Agreement No. 898203, Project acronym \"FLINDIP\").
  Experiments were partially carried out using equipment provided by the Institute
  of Bioorganic Chemistry of the Russian Academy of Sciences Сore Facility (CKP IBCH).
  This work was supported by a Russian Science Foundation grant 19-74-10102.This project
  has received funding from the European Union’s Horizon 2020 research and innovation
  programme under the Marie Skłodowska-Curie Grant Agreement No. 665,385."
article_number: '75842'
article_processing_charge: No
article_type: original
author:
- first_name: Louisa
  full_name: Gonzalez Somermeyer, Louisa
  id: 4720D23C-F248-11E8-B48F-1D18A9856A87
  last_name: Gonzalez Somermeyer
  orcid: 0000-0001-9139-5383
- first_name: Aubin
  full_name: Fleiss, Aubin
  last_name: Fleiss
- first_name: Alexander S
  full_name: Mishin, Alexander S
  last_name: Mishin
- first_name: Nina G
  full_name: Bozhanova, Nina G
  last_name: Bozhanova
- first_name: Anna A
  full_name: Igolkina, Anna A
  last_name: Igolkina
- first_name: Jens
  full_name: Meiler, Jens
  last_name: Meiler
- first_name: Maria-Elisenda
  full_name: Alaball Pujol, Maria-Elisenda
  last_name: Alaball Pujol
- first_name: Ekaterina V
  full_name: Putintseva, Ekaterina V
  last_name: Putintseva
- first_name: Karen S
  full_name: Sarkisyan, Karen S
  last_name: Sarkisyan
- first_name: Fyodor
  full_name: Kondrashov, Fyodor
  id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
  last_name: Kondrashov
  orcid: 0000-0001-8243-4694
citation:
  ama: Gonzalez Somermeyer L, Fleiss A, Mishin AS, et al. Heterogeneity of the GFP
    fitness landscape and data-driven protein design. <i>eLife</i>. 2022;11. doi:<a
    href="https://doi.org/10.7554/elife.75842">10.7554/elife.75842</a>
  apa: Gonzalez Somermeyer, L., Fleiss, A., Mishin, A. S., Bozhanova, N. G., Igolkina,
    A. A., Meiler, J., … Kondrashov, F. (2022). Heterogeneity of the GFP fitness landscape
    and data-driven protein design. <i>ELife</i>. eLife Sciences Publications. <a
    href="https://doi.org/10.7554/elife.75842">https://doi.org/10.7554/elife.75842</a>
  chicago: Gonzalez Somermeyer, Louisa, Aubin Fleiss, Alexander S Mishin, Nina G Bozhanova,
    Anna A Igolkina, Jens Meiler, Maria-Elisenda Alaball Pujol, Ekaterina V Putintseva,
    Karen S Sarkisyan, and Fyodor Kondrashov. “Heterogeneity of the GFP Fitness Landscape
    and Data-Driven Protein Design.” <i>ELife</i>. eLife Sciences Publications, 2022.
    <a href="https://doi.org/10.7554/elife.75842">https://doi.org/10.7554/elife.75842</a>.
  ieee: L. Gonzalez Somermeyer <i>et al.</i>, “Heterogeneity of the GFP fitness landscape
    and data-driven protein design,” <i>eLife</i>, vol. 11. eLife Sciences Publications,
    2022.
  ista: Gonzalez Somermeyer L, Fleiss A, Mishin AS, Bozhanova NG, Igolkina AA, Meiler
    J, Alaball Pujol M-E, Putintseva EV, Sarkisyan KS, Kondrashov F. 2022. Heterogeneity
    of the GFP fitness landscape and data-driven protein design. eLife. 11, 75842.
  mla: Gonzalez Somermeyer, Louisa, et al. “Heterogeneity of the GFP Fitness Landscape
    and Data-Driven Protein Design.” <i>ELife</i>, vol. 11, 75842, eLife Sciences
    Publications, 2022, doi:<a href="https://doi.org/10.7554/elife.75842">10.7554/elife.75842</a>.
  short: L. Gonzalez Somermeyer, A. Fleiss, A.S. Mishin, N.G. Bozhanova, A.A. Igolkina,
    J. Meiler, M.-E. Alaball Pujol, E.V. Putintseva, K.S. Sarkisyan, F. Kondrashov,
    ELife 11 (2022).
date_created: 2022-06-18T09:06:59Z
date_published: 2022-05-05T00:00:00Z
date_updated: 2023-08-03T07:20:15Z
day: '05'
ddc:
- '570'
department:
- _id: GradSch
- _id: FyKo
doi: 10.7554/elife.75842
ec_funded: 1
external_id:
  isi:
  - '000799197200001'
file:
- access_level: open_access
  checksum: 7573c28f44028ab0cc81faef30039e44
  content_type: application/pdf
  creator: dernst
  date_created: 2022-06-20T07:44:19Z
  date_updated: 2022-06-20T07:44:19Z
  file_id: '11454'
  file_name: 2022_eLife_Somermeyer.pdf
  file_size: 5297213
  relation: main_file
  success: 1
file_date_updated: 2022-06-20T07:44:19Z
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: '05'
oa: 1
oa_version: Published Version
project:
- _id: 26580278-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '771209'
  name: Characterizing the fitness landscape on population and global scales
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '665385'
  name: International IST Doctoral Program
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Heterogeneity of the GFP fitness landscape and data-driven protein design
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: '9283'
abstract:
- lang: eng
  text: Gene expression levels are influenced by multiple coexisting molecular mechanisms.
    Some of these interactions such as those of transcription factors and promoters
    have been studied extensively. However, predicting phenotypes of gene regulatory
    networks (GRNs) remains a major challenge. Here, we use a well-defined synthetic
    GRN to study in Escherichia coli how network phenotypes depend on local genetic
    context, i.e. the genetic neighborhood of a transcription factor and its relative
    position. We show that one GRN with fixed topology can display not only quantitatively
    but also qualitatively different phenotypes, depending solely on the local genetic
    context of its components. Transcriptional read-through is the main molecular
    mechanism that places one transcriptional unit (TU) within two separate regulons
    without the need for complex regulatory sequences. We propose that relative order
    of individual TUs, with its potential for combinatorial complexity, plays an important
    role in shaping phenotypes of GRNs.
acknowledgement: "We thank J Bollback, L Hurst, M Lagator, C Nizak, O Rivoire, M Savageau,
  G Tkacik, and B Vicozo\r\nfor helpful discussions; A Dolinar and A Greshnova for
  technical assistance; T Bollenbach for supplying the strain JW0336; C Rusnac, and
  members of the Guet lab for comments. The research leading to these results has
  received funding from the People Programme (Marie Curie Actions) of the European
  Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement n˚\r\n628377
  (ANS) and an Austrian Science Fund (FWF) grant n˚ I 3901-B32 (CCG)."
article_number: e65993
article_processing_charge: Yes
article_type: original
author:
- first_name: Anna A
  full_name: Nagy-Staron, Anna A
  id: 3ABC5BA6-F248-11E8-B48F-1D18A9856A87
  last_name: Nagy-Staron
  orcid: 0000-0002-1391-8377
- first_name: Kathrin
  full_name: Tomasek, Kathrin
  id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
  last_name: Tomasek
  orcid: 0000-0003-3768-877X
- first_name: Caroline
  full_name: Caruso Carter, Caroline
  last_name: Caruso Carter
- first_name: Elisabeth
  full_name: Sonnleitner, Elisabeth
  last_name: Sonnleitner
- first_name: Bor
  full_name: Kavcic, Bor
  id: 350F91D2-F248-11E8-B48F-1D18A9856A87
  last_name: Kavcic
  orcid: 0000-0001-6041-254X
- first_name: Tiago
  full_name: Paixão, Tiago
  last_name: Paixão
- first_name: Calin C
  full_name: Guet, Calin C
  id: 47F8433E-F248-11E8-B48F-1D18A9856A87
  last_name: Guet
  orcid: 0000-0001-6220-2052
citation:
  ama: Nagy-Staron AA, Tomasek K, Caruso Carter C, et al. Local genetic context shapes
    the function of a gene regulatory network. <i>eLife</i>. 2021;10. doi:<a href="https://doi.org/10.7554/elife.65993">10.7554/elife.65993</a>
  apa: Nagy-Staron, A. A., Tomasek, K., Caruso Carter, C., Sonnleitner, E., Kavcic,
    B., Paixão, T., &#38; Guet, C. C. (2021). Local genetic context shapes the function
    of a gene regulatory network. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.65993">https://doi.org/10.7554/elife.65993</a>
  chicago: Nagy-Staron, Anna A, Kathrin Tomasek, Caroline Caruso Carter, Elisabeth
    Sonnleitner, Bor Kavcic, Tiago Paixão, and Calin C Guet. “Local Genetic Context
    Shapes the Function of a Gene Regulatory Network.” <i>ELife</i>. eLife Sciences
    Publications, 2021. <a href="https://doi.org/10.7554/elife.65993">https://doi.org/10.7554/elife.65993</a>.
  ieee: A. A. Nagy-Staron <i>et al.</i>, “Local genetic context shapes the function
    of a gene regulatory network,” <i>eLife</i>, vol. 10. eLife Sciences Publications,
    2021.
  ista: Nagy-Staron AA, Tomasek K, Caruso Carter C, Sonnleitner E, Kavcic B, Paixão
    T, Guet CC. 2021. Local genetic context shapes the function of a gene regulatory
    network. eLife. 10, e65993.
  mla: Nagy-Staron, Anna A., et al. “Local Genetic Context Shapes the Function of
    a Gene Regulatory Network.” <i>ELife</i>, vol. 10, e65993, eLife Sciences Publications,
    2021, doi:<a href="https://doi.org/10.7554/elife.65993">10.7554/elife.65993</a>.
  short: A.A. Nagy-Staron, K. Tomasek, C. Caruso Carter, E. Sonnleitner, B. Kavcic,
    T. Paixão, C.C. Guet, ELife 10 (2021).
date_created: 2021-03-23T10:11:46Z
date_published: 2021-03-08T00:00:00Z
date_updated: 2024-02-21T12:41:57Z
day: '08'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.7554/elife.65993
ec_funded: 1
external_id:
  isi:
  - '000631050900001'
file:
- access_level: open_access
  checksum: 3c2f44058c2dd45a5a1027f09d263f8e
  content_type: application/pdf
  creator: bkavcic
  date_created: 2021-03-23T10:12:58Z
  date_updated: 2021-03-23T10:12:58Z
  file_id: '9284'
  file_name: elife-65993-v2.pdf
  file_size: 1390469
  relation: main_file
  success: 1
file_date_updated: 2021-03-23T10:12:58Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
keyword:
- Genetics and Molecular Biology
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 2517526A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '628377'
  name: 'The Systems Biology of Transcriptional Read-Through in Bacteria: from Synthetic
    Networks to Genomic Studies'
- _id: 268BFA92-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I03901
  name: 'CyberCircuits: Cybergenetic circuits to test composability of gene networks'
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
  record:
  - id: '8951'
    relation: research_data
    status: public
status: public
title: Local genetic context shapes the function of a gene regulatory network
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: '10270'
abstract:
- lang: eng
  text: Plants develop new organs to adjust their bodies to dynamic changes in the
    environment. How independent organs achieve anisotropic shapes and polarities
    is poorly understood. To address this question, we constructed a mechano-biochemical
    model for Arabidopsis root meristem growth that integrates biologically plausible
    principles. Computer model simulations demonstrate how differential growth of
    neighboring tissues results in the initial symmetry-breaking leading to anisotropic
    root growth. Furthermore, the root growth feeds back on a polar transport network
    of the growth regulator auxin. Model, predictions are in close agreement with
    in vivo patterns of anisotropic growth, auxin distribution, and cell polarity,
    as well as several root phenotypes caused by chemical, mechanical, or genetic
    perturbations. Our study demonstrates that the combination of tissue mechanics
    and polar auxin transport organizes anisotropic root growth and cell polarities
    during organ outgrowth. Therefore, a mobile auxin signal transported through immobile
    cells drives polarity and growth mechanics to coordinate complex organ development.
acknowledgement: 'e are grateful Richard Smith, Anne-Lise Routier, Crisanto Gutierrez
  and Juergen Kleine-Vehn for providing critical comments on the manuscript. Funding:
  This work was supported by the Programa de Atraccion de Talento 2017 (Comunidad
  de Madrid, 2017-T1/BIO-5654 to KW), Severo Ochoa (SO) Programme for Centres of Excellence
  in R&D from the Agencia Estatal de Investigacion of Spain (grant SEV-2016–0672 (2017–2021)
  to KW via the CBGP). In the frame of SEV-2016–0672 funding MM is supported with
  a postdoctoral contract. KW was supported by Programa Estatal de Generacion del
  Conocimiento y Fortalecimiento Cientıfico y Tecnologico del Sistema de I + D + I
  2019 (PGC2018-093387-A-I00) from MICIU (to KW). MG is recipient of an IST Interdisciplinary
  Project (IC1022IPC03).'
article_number: '72132'
article_processing_charge: Yes
article_type: original
author:
- first_name: Marco
  full_name: Marconi, Marco
  last_name: Marconi
- first_name: Marçal
  full_name: Gallemi, Marçal
  id: 460C6802-F248-11E8-B48F-1D18A9856A87
  last_name: Gallemi
  orcid: 0000-0003-4675-6893
- first_name: Eva
  full_name: Benková, Eva
  id: 38F4F166-F248-11E8-B48F-1D18A9856A87
  last_name: Benková
  orcid: 0000-0002-8510-9739
- first_name: Krzysztof
  full_name: Wabnik, Krzysztof
  last_name: Wabnik
citation:
  ama: Marconi M, Gallemi M, Benková E, Wabnik K. A coupled mechano-biochemical model
    for cell polarity guided anisotropic root growth. <i>eLife</i>. 2021;10. doi:<a
    href="https://doi.org/10.7554/elife.72132">10.7554/elife.72132</a>
  apa: Marconi, M., Gallemi, M., Benková, E., &#38; Wabnik, K. (2021). A coupled mechano-biochemical
    model for cell polarity guided anisotropic root growth. <i>ELife</i>. eLife Sciences
    Publications. <a href="https://doi.org/10.7554/elife.72132">https://doi.org/10.7554/elife.72132</a>
  chicago: Marconi, Marco, Marçal Gallemi, Eva Benková, and Krzysztof Wabnik. “A Coupled
    Mechano-Biochemical Model for Cell Polarity Guided Anisotropic Root Growth.” <i>ELife</i>.
    eLife Sciences Publications, 2021. <a href="https://doi.org/10.7554/elife.72132">https://doi.org/10.7554/elife.72132</a>.
  ieee: M. Marconi, M. Gallemi, E. Benková, and K. Wabnik, “A coupled mechano-biochemical
    model for cell polarity guided anisotropic root growth,” <i>eLife</i>, vol. 10.
    eLife Sciences Publications, 2021.
  ista: Marconi M, Gallemi M, Benková E, Wabnik K. 2021. A coupled mechano-biochemical
    model for cell polarity guided anisotropic root growth. eLife. 10, 72132.
  mla: Marconi, Marco, et al. “A Coupled Mechano-Biochemical Model for Cell Polarity
    Guided Anisotropic Root Growth.” <i>ELife</i>, vol. 10, 72132, eLife Sciences
    Publications, 2021, doi:<a href="https://doi.org/10.7554/elife.72132">10.7554/elife.72132</a>.
  short: M. Marconi, M. Gallemi, E. Benková, K. Wabnik, ELife 10 (2021).
date_created: 2021-11-11T10:05:18Z
date_published: 2021-11-01T00:00:00Z
date_updated: 2023-08-14T11:49:23Z
day: '01'
ddc:
- '570'
department:
- _id: EvBe
doi: 10.7554/elife.72132
external_id:
  isi:
  - '000734671200001'
  pmid:
  - '34723798'
file:
- access_level: open_access
  checksum: fad13c509b53bb7a2bef9c946a7ca60a
  content_type: application/pdf
  creator: dernst
  date_created: 2022-05-13T09:00:29Z
  date_updated: 2022-05-13T09:00:29Z
  file_id: '11372'
  file_name: 2021_eLife_Marconi.pdf
  file_size: 14137503
  relation: main_file
  success: 1
file_date_updated: 2022-05-13T09:00:29Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: A coupled mechano-biochemical model for cell polarity guided anisotropic root
  growth
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: '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: '10533'
abstract:
- lang: eng
  text: Flowering plants utilize small RNA molecules to guide DNA methyltransferases
    to genomic sequences. This RNA-directed DNA methylation (RdDM) pathway preferentially
    targets euchromatic transposable elements. However, RdDM is thought to be recruited
    by methylation of histone H3 at lysine 9 (H3K9me), a hallmark of heterochromatin.
    How RdDM is targeted to euchromatin despite an affinity for H3K9me is unclear.
    Here we show that loss of histone H1 enhances heterochromatic RdDM, preferentially
    at nucleosome linker DNA. Surprisingly, this does not require SHH1, the RdDM component
    that binds H3K9me. Furthermore, H3K9me is dispensable for RdDM, as is CG DNA methylation.
    Instead, we find that non-CG methylation is specifically associated with small
    RNA biogenesis, and without H1 small RNA production quantitatively expands to
    non-CG methylated loci. Our results demonstrate that H1 enforces the separation
    of euchromatic and heterochromatic DNA methylation pathways by excluding the small
    RNA-generating branch of RdDM from non-CG methylated heterochromatin.
acknowledgement: We thank X Feng for helpful comments on the manuscript. This work
  was supported by a European Research Council grant MaintainMeth (725746) to DZ.
article_number: e72676
article_processing_charge: No
article_type: original
author:
- first_name: Jaemyung
  full_name: Choi, Jaemyung
  last_name: Choi
- first_name: David B
  full_name: Lyons, David B
  last_name: Lyons
- first_name: Daniel
  full_name: Zilberman, Daniel
  id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
  last_name: Zilberman
  orcid: 0000-0002-0123-8649
citation:
  ama: Choi J, Lyons DB, Zilberman D. Histone H1 prevents non-CG methylation-mediated
    small RNA biogenesis in Arabidopsis heterochromatin. <i>eLife</i>. 2021;10. doi:<a
    href="https://doi.org/10.7554/elife.72676">10.7554/elife.72676</a>
  apa: Choi, J., Lyons, D. B., &#38; Zilberman, D. (2021). Histone H1 prevents non-CG
    methylation-mediated small RNA biogenesis in Arabidopsis heterochromatin. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.72676">https://doi.org/10.7554/elife.72676</a>
  chicago: Choi, Jaemyung, David B Lyons, and Daniel Zilberman. “Histone H1 Prevents
    Non-CG Methylation-Mediated Small RNA Biogenesis in Arabidopsis Heterochromatin.”
    <i>ELife</i>. eLife Sciences Publications, 2021. <a href="https://doi.org/10.7554/elife.72676">https://doi.org/10.7554/elife.72676</a>.
  ieee: J. Choi, D. B. Lyons, and D. Zilberman, “Histone H1 prevents non-CG methylation-mediated
    small RNA biogenesis in Arabidopsis heterochromatin,” <i>eLife</i>, vol. 10. eLife
    Sciences Publications, 2021.
  ista: Choi J, Lyons DB, Zilberman D. 2021. Histone H1 prevents non-CG methylation-mediated
    small RNA biogenesis in Arabidopsis heterochromatin. eLife. 10, e72676.
  mla: Choi, Jaemyung, et al. “Histone H1 Prevents Non-CG Methylation-Mediated Small
    RNA Biogenesis in Arabidopsis Heterochromatin.” <i>ELife</i>, vol. 10, e72676,
    eLife Sciences Publications, 2021, doi:<a href="https://doi.org/10.7554/elife.72676">10.7554/elife.72676</a>.
  short: J. Choi, D.B. Lyons, D. Zilberman, ELife 10 (2021).
date_created: 2021-12-10T13:12:08Z
date_published: 2021-12-01T00:00:00Z
date_updated: 2023-08-17T06:21:08Z
day: '01'
ddc:
- '570'
department:
- _id: DaZi
doi: 10.7554/elife.72676
ec_funded: 1
external_id:
  isi:
  - '000754832000001'
  pmid:
  - '34850679'
file:
- access_level: open_access
  checksum: 22ed4c55fb550f6da02ae55c359be651
  content_type: application/pdf
  creator: dernst
  date_created: 2022-05-16T10:42:22Z
  date_updated: 2022-05-16T10:42:22Z
  file_id: '11384'
  file_name: 2021_eLife_Choi.pdf
  file_size: 2715200
  relation: main_file
  success: 1
file_date_updated: 2022-05-16T10:42:22Z
has_accepted_license: '1'
intvolume: '        10'
isi: 1
keyword:
- genetics and molecular biology
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 62935a00-2b32-11ec-9570-eff30fa39068
  call_identifier: H2020
  grant_number: '725746'
  name: Quantitative analysis of DNA methylation maintenance with chromatin
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Histone H1 prevents non-CG methylation-mediated small RNA biogenesis in Arabidopsis
  heterochromatin
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: '11055'
abstract:
- lang: eng
  text: Vascular dysfunctions are a common feature of multiple age-related diseases.
    However, modeling healthy and pathological aging of the human vasculature represents
    an unresolved experimental challenge. Here, we generated induced vascular endothelial
    cells (iVECs) and smooth muscle cells (iSMCs) by direct reprogramming of healthy
    human fibroblasts from donors of different ages and Hutchinson-Gilford Progeria
    Syndrome (HGPS) patients. iVECs induced from old donors revealed upregulation
    of GSTM1 and PALD1, genes linked to oxidative stress, inflammation and endothelial
    junction stability, as vascular aging markers. A functional assay performed on
    PALD1 KD VECs demonstrated a recovery in vascular permeability. We found that
    iSMCs from HGPS donors overexpressed bone morphogenetic protein (BMP)−4, which
    plays a key role in both vascular calcification and endothelial barrier damage
    observed in HGPS. Strikingly, BMP4 concentrations are higher in serum from HGPS
    vs. age-matched mice. Furthermore, targeting BMP4 with blocking antibody recovered
    the functionality of the vascular barrier in vitro, hence representing a potential
    future therapeutic strategy to limit cardiovascular dysfunction in HGPS. These
    results show that iVECs and iSMCs retain disease-related signatures, allowing
    modeling of vascular aging and HGPS in vitro.
article_number: e54383
article_processing_charge: No
article_type: original
author:
- first_name: Simone
  full_name: Bersini, Simone
  last_name: Bersini
- first_name: Roberta
  full_name: Schulte, Roberta
  last_name: Schulte
- first_name: Ling
  full_name: Huang, Ling
  last_name: Huang
- first_name: Hannah
  full_name: Tsai, Hannah
  last_name: Tsai
- 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: Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. Direct reprogramming of human
    smooth muscle and vascular endothelial cells reveals defects associated with aging
    and Hutchinson-Gilford progeria syndrome. <i>eLife</i>. 2020;9. doi:<a href="https://doi.org/10.7554/elife.54383">10.7554/elife.54383</a>
  apa: Bersini, S., Schulte, R., Huang, L., Tsai, H., &#38; Hetzer, M. (2020). Direct
    reprogramming of human smooth muscle and vascular endothelial cells reveals defects
    associated with aging and Hutchinson-Gilford progeria syndrome. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.54383">https://doi.org/10.7554/elife.54383</a>
  chicago: Bersini, Simone, Roberta Schulte, Ling Huang, Hannah Tsai, and Martin Hetzer.
    “Direct Reprogramming of Human Smooth Muscle and Vascular Endothelial Cells Reveals
    Defects Associated with Aging and Hutchinson-Gilford Progeria Syndrome.” <i>ELife</i>.
    eLife Sciences Publications, 2020. <a href="https://doi.org/10.7554/elife.54383">https://doi.org/10.7554/elife.54383</a>.
  ieee: S. Bersini, R. Schulte, L. Huang, H. Tsai, and M. Hetzer, “Direct reprogramming
    of human smooth muscle and vascular endothelial cells reveals defects associated
    with aging and Hutchinson-Gilford progeria syndrome,” <i>eLife</i>, vol. 9. eLife
    Sciences Publications, 2020.
  ista: Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. 2020. Direct reprogramming
    of human smooth muscle and vascular endothelial cells reveals defects associated
    with aging and Hutchinson-Gilford progeria syndrome. eLife. 9, e54383.
  mla: Bersini, Simone, et al. “Direct Reprogramming of Human Smooth Muscle and Vascular
    Endothelial Cells Reveals Defects Associated with Aging and Hutchinson-Gilford
    Progeria Syndrome.” <i>ELife</i>, vol. 9, e54383, eLife Sciences Publications,
    2020, doi:<a href="https://doi.org/10.7554/elife.54383">10.7554/elife.54383</a>.
  short: S. Bersini, R. Schulte, L. Huang, H. Tsai, M. Hetzer, ELife 9 (2020).
date_created: 2022-04-07T07:43:48Z
date_published: 2020-09-08T00:00:00Z
date_updated: 2022-07-18T08:30:37Z
day: '08'
ddc:
- '570'
doi: 10.7554/elife.54383
extern: '1'
external_id:
  pmid:
  - '32896271'
file:
- access_level: open_access
  checksum: f8b3821349a194050be02570d8fe7d4b
  content_type: application/pdf
  creator: dernst
  date_created: 2022-04-08T06:53:10Z
  date_updated: 2022-04-08T06:53:10Z
  file_id: '11132'
  file_name: 2020_eLife_Bersini.pdf
  file_size: 4399825
  relation: main_file
  success: 1
file_date_updated: 2022-04-08T06:53:10Z
has_accepted_license: '1'
intvolume: '         9'
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
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Direct reprogramming of human smooth muscle and vascular endothelial cells
  reveals defects associated with aging and Hutchinson-Gilford progeria syndrome
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: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 9
year: '2020'
...
---
_id: '7793'
abstract:
- lang: eng
  text: Hormonal signalling in animals often involves direct transcription factor-hormone
    interactions that modulate gene expression. In contrast, plant hormone signalling
    is most commonly based on de-repression via the degradation of transcriptional
    repressors. Recently, we uncovered a non-canonical signalling mechanism for the
    plant hormone auxin whereby auxin directly affects the activity of the atypical
    auxin response factor (ARF), ETTIN towards target genes without the requirement
    for protein degradation. Here we show that ETTIN directly binds auxin, leading
    to dissociation from co-repressor proteins of the TOPLESS/TOPLESS-RELATED family
    followed by histone acetylation and induction of gene expression. This mechanism
    is reminiscent of animal hormone signalling as it affects the activity towards
    regulation of target genes and provides the first example of a DNA-bound hormone
    receptor in plants. Whilst auxin affects canonical ARFs indirectly by facilitating
    degradation of Aux/IAA repressors, direct ETTIN-auxin interactions allow switching
    between repressive and de-repressive chromatin states in an instantly-reversible
    manner.
article_number: e51787
article_processing_charge: No
article_type: original
author:
- first_name: André
  full_name: Kuhn, André
  last_name: Kuhn
- first_name: Sigurd
  full_name: Ramans Harborough, Sigurd
  last_name: Ramans Harborough
- first_name: Heather M
  full_name: McLaughlin, Heather M
  last_name: McLaughlin
- first_name: Bhavani
  full_name: Natarajan, Bhavani
  last_name: Natarajan
- first_name: Inge
  full_name: Verstraeten, Inge
  id: 362BF7FE-F248-11E8-B48F-1D18A9856A87
  last_name: Verstraeten
  orcid: 0000-0001-7241-2328
- first_name: Jiří
  full_name: Friml, Jiří
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
- first_name: Stefan
  full_name: Kepinski, Stefan
  last_name: Kepinski
- first_name: Lars
  full_name: Østergaard, Lars
  last_name: Østergaard
citation:
  ama: Kuhn A, Ramans Harborough S, McLaughlin HM, et al. Direct ETTIN-auxin interaction
    controls chromatin states in gynoecium development. <i>eLife</i>. 2020;9. doi:<a
    href="https://doi.org/10.7554/elife.51787">10.7554/elife.51787</a>
  apa: Kuhn, A., Ramans Harborough, S., McLaughlin, H. M., Natarajan, B., Verstraeten,
    I., Friml, J., … Østergaard, L. (2020). Direct ETTIN-auxin interaction controls
    chromatin states in gynoecium development. <i>ELife</i>. eLife Sciences Publications.
    <a href="https://doi.org/10.7554/elife.51787">https://doi.org/10.7554/elife.51787</a>
  chicago: Kuhn, André, Sigurd Ramans Harborough, Heather M McLaughlin, Bhavani Natarajan,
    Inge Verstraeten, Jiří Friml, Stefan Kepinski, and Lars Østergaard. “Direct ETTIN-Auxin
    Interaction Controls Chromatin States in Gynoecium Development.” <i>ELife</i>.
    eLife Sciences Publications, 2020. <a href="https://doi.org/10.7554/elife.51787">https://doi.org/10.7554/elife.51787</a>.
  ieee: A. Kuhn <i>et al.</i>, “Direct ETTIN-auxin interaction controls chromatin
    states in gynoecium development,” <i>eLife</i>, vol. 9. eLife Sciences Publications,
    2020.
  ista: Kuhn A, Ramans Harborough S, McLaughlin HM, Natarajan B, Verstraeten I, Friml
    J, Kepinski S, Østergaard L. 2020. Direct ETTIN-auxin interaction controls chromatin
    states in gynoecium development. eLife. 9, e51787.
  mla: Kuhn, André, et al. “Direct ETTIN-Auxin Interaction Controls Chromatin States
    in Gynoecium Development.” <i>ELife</i>, vol. 9, e51787, eLife Sciences Publications,
    2020, doi:<a href="https://doi.org/10.7554/elife.51787">10.7554/elife.51787</a>.
  short: A. Kuhn, S. Ramans Harborough, H.M. McLaughlin, B. Natarajan, I. Verstraeten,
    J. Friml, S. Kepinski, L. Østergaard, ELife 9 (2020).
date_created: 2020-05-04T08:50:47Z
date_published: 2020-04-08T00:00:00Z
date_updated: 2023-08-21T06:17:12Z
day: '08'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.7554/elife.51787
external_id:
  isi:
  - '000527752200001'
  pmid:
  - '32267233'
file:
- access_level: open_access
  checksum: 15d740de1a741fdcc6ec128c48eed017
  content_type: application/pdf
  creator: dernst
  date_created: 2020-05-04T09:06:43Z
  date_updated: 2020-07-14T12:48:03Z
  file_id: '7794'
  file_name: 2020_eLife_Kuhn.pdf
  file_size: 2893082
  relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
has_accepted_license: '1'
intvolume: '         9'
isi: 1
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Direct ETTIN-auxin interaction controls chromatin states in gynoecium 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: 9
year: '2020'
...
---
_id: '7888'
abstract:
- lang: eng
  text: Embryonic stem cell cultures are thought to self-organize into embryoid bodies,
    able to undergo symmetry-breaking, germ layer specification and even morphogenesis.
    Yet, it is unclear how to reconcile this remarkable self-organization capacity
    with classical experiments demonstrating key roles for extrinsic biases by maternal
    factors and/or extraembryonic tissues in embryogenesis. Here, we show that zebrafish
    embryonic tissue explants, prepared prior to germ layer induction and lacking
    extraembryonic tissues, can specify all germ layers and form a seemingly complete
    mesendoderm anlage. Importantly, explant organization requires polarized inheritance
    of maternal factors from dorsal-marginal regions of the blastoderm. Moreover,
    induction of endoderm and head-mesoderm, which require peak Nodal-signaling levels,
    is highly variable in explants, reminiscent of embryos with reduced Nodal signals
    from the extraembryonic tissues. Together, these data suggest that zebrafish explants
    do not undergo bona fide self-organization, but rather display features of genetically
    encoded self-assembly, where intrinsic genetic programs control the emergence
    of order.
article_number: e55190
article_processing_charge: No
article_type: original
author:
- first_name: Alexandra
  full_name: Schauer, Alexandra
  id: 30A536BA-F248-11E8-B48F-1D18A9856A87
  last_name: Schauer
  orcid: 0000-0001-7659-9142
- first_name: Diana C
  full_name: Nunes Pinheiro, Diana C
  id: 2E839F16-F248-11E8-B48F-1D18A9856A87
  last_name: Nunes Pinheiro
  orcid: 0000-0003-4333-7503
- first_name: Robert
  full_name: Hauschild, Robert
  id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
  last_name: Hauschild
  orcid: 0000-0001-9843-3522
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Schauer A, Nunes Pinheiro DC, Hauschild R, Heisenberg C-PJ. Zebrafish embryonic
    explants undergo genetically encoded self-assembly. <i>eLife</i>. 2020;9. doi:<a
    href="https://doi.org/10.7554/elife.55190">10.7554/elife.55190</a>
  apa: Schauer, A., Nunes Pinheiro, D. C., Hauschild, R., &#38; Heisenberg, C.-P.
    J. (2020). Zebrafish embryonic explants undergo genetically encoded self-assembly.
    <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.55190">https://doi.org/10.7554/elife.55190</a>
  chicago: Schauer, Alexandra, Diana C Nunes Pinheiro, Robert Hauschild, and Carl-Philipp
    J Heisenberg. “Zebrafish Embryonic Explants Undergo Genetically Encoded Self-Assembly.”
    <i>ELife</i>. eLife Sciences Publications, 2020. <a href="https://doi.org/10.7554/elife.55190">https://doi.org/10.7554/elife.55190</a>.
  ieee: A. Schauer, D. C. Nunes Pinheiro, R. Hauschild, and C.-P. J. Heisenberg, “Zebrafish
    embryonic explants undergo genetically encoded self-assembly,” <i>eLife</i>, vol.
    9. eLife Sciences Publications, 2020.
  ista: Schauer A, Nunes Pinheiro DC, Hauschild R, Heisenberg C-PJ. 2020. Zebrafish
    embryonic explants undergo genetically encoded self-assembly. eLife. 9, e55190.
  mla: Schauer, Alexandra, et al. “Zebrafish Embryonic Explants Undergo Genetically
    Encoded Self-Assembly.” <i>ELife</i>, vol. 9, e55190, eLife Sciences Publications,
    2020, doi:<a href="https://doi.org/10.7554/elife.55190">10.7554/elife.55190</a>.
  short: A. Schauer, D.C. Nunes Pinheiro, R. Hauschild, C.-P.J. Heisenberg, ELife
    9 (2020).
date_created: 2020-05-25T15:01:40Z
date_published: 2020-04-06T00:00:00Z
date_updated: 2023-08-21T06:25:49Z
day: '06'
ddc:
- '570'
department:
- _id: CaHe
- _id: Bio
doi: 10.7554/elife.55190
ec_funded: 1
external_id:
  isi:
  - '000531544400001'
  pmid:
  - '32250246'
file:
- access_level: open_access
  checksum: f6aad884cf706846ae9357fcd728f8b5
  content_type: application/pdf
  creator: dernst
  date_created: 2020-05-25T15:15:43Z
  date_updated: 2020-07-14T12:48:04Z
  file_id: '7890'
  file_name: 2020_eLife_Schauer.pdf
  file_size: 7744848
  relation: main_file
file_date_updated: 2020-07-14T12:48:04Z
has_accepted_license: '1'
intvolume: '         9'
isi: 1
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '742573'
  name: Interaction and feedback between cell mechanics and fate specification in
    vertebrate gastrulation
- _id: 26B1E39C-B435-11E9-9278-68D0E5697425
  grant_number: '25239'
  name: 'Mesendoderm specification in zebrafish: The role of extraembryonic tissues'
- _id: 26520D1E-B435-11E9-9278-68D0E5697425
  grant_number: ALTF 850-2017
  name: Coordination of mesendoderm cell fate specification and internalization during
    zebrafish gastrulation
- _id: 266BC5CE-B435-11E9-9278-68D0E5697425
  grant_number: LT000429
  name: Coordination of mesendoderm fate specification and internalization during
    zebrafish gastrulation
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
  record:
  - id: '12891'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Zebrafish embryonic explants undergo genetically encoded self-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: 9
year: '2020'
...
---
_id: '7593'
abstract:
- lang: eng
  text: Heterozygous loss of human PAFAH1B1 (coding for LIS1) results in the disruption
    of neurogenesis and neuronal migration via dysregulation of microtubule (MT) stability
    and dynein motor function/localization that alters mitotic spindle orientation,
    chromosomal segregation, and nuclear migration. Recently, human induced pluripotent
    stem cell (iPSC) models revealed an important role for LIS1 in controlling the
    length of terminal cell divisions of outer radial glial (oRG) progenitors, suggesting
    cellular functions of LIS1 in regulating neural progenitor cell (NPC) daughter
    cell separation. Here we examined the late mitotic stages NPCs in vivo and mouse
    embryonic fibroblasts (MEFs) in vitro from Pafah1b1-deficient mutants. Pafah1b1-deficient
    neocortical NPCs and MEFs similarly exhibited cleavage plane displacement with
    mislocalization of furrow-associated markers, associated with actomyosin dysfunction
    and cell membrane hyper-contractility. Thus, it suggests LIS1 acts as a key molecular
    link connecting MTs/dynein and actomyosin, ensuring that cell membrane contractility
    is tightly controlled to execute proper daughter cell separation.
article_number: '51512'
article_processing_charge: No
article_type: original
author:
- first_name: Hyang Mi
  full_name: Moon, Hyang Mi
  last_name: Moon
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
- first_name: Liqun
  full_name: Luo, Liqun
  last_name: Luo
- first_name: Anthony
  full_name: Wynshaw-Boris, Anthony
  last_name: Wynshaw-Boris
citation:
  ama: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. LIS1 determines cleavage plane
    positioning by regulating actomyosin-mediated cell membrane contractility. <i>eLife</i>.
    2020;9. doi:<a href="https://doi.org/10.7554/elife.51512">10.7554/elife.51512</a>
  apa: Moon, H. M., Hippenmeyer, S., Luo, L., &#38; Wynshaw-Boris, A. (2020). LIS1
    determines cleavage plane positioning by regulating actomyosin-mediated cell membrane
    contractility. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.51512">https://doi.org/10.7554/elife.51512</a>
  chicago: Moon, Hyang Mi, Simon Hippenmeyer, Liqun Luo, and Anthony Wynshaw-Boris.
    “LIS1 Determines Cleavage Plane Positioning by Regulating Actomyosin-Mediated
    Cell Membrane Contractility.” <i>ELife</i>. eLife Sciences Publications, 2020.
    <a href="https://doi.org/10.7554/elife.51512">https://doi.org/10.7554/elife.51512</a>.
  ieee: H. M. Moon, S. Hippenmeyer, L. Luo, and A. Wynshaw-Boris, “LIS1 determines
    cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility,”
    <i>eLife</i>, vol. 9. eLife Sciences Publications, 2020.
  ista: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. 2020. LIS1 determines cleavage
    plane positioning by regulating actomyosin-mediated cell membrane contractility.
    eLife. 9, 51512.
  mla: Moon, Hyang Mi, et al. “LIS1 Determines Cleavage Plane Positioning by Regulating
    Actomyosin-Mediated Cell Membrane Contractility.” <i>ELife</i>, vol. 9, 51512,
    eLife Sciences Publications, 2020, doi:<a href="https://doi.org/10.7554/elife.51512">10.7554/elife.51512</a>.
  short: H.M. Moon, S. Hippenmeyer, L. Luo, A. Wynshaw-Boris, ELife 9 (2020).
date_created: 2020-03-20T13:16:41Z
date_published: 2020-03-11T00:00:00Z
date_updated: 2023-08-18T07:06:31Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/elife.51512
external_id:
  isi:
  - '000522835800001'
  pmid:
  - '32159512'
file:
- access_level: open_access
  checksum: 396ceb2dd10b102ef4e699666b9342c3
  content_type: application/pdf
  creator: dernst
  date_created: 2020-09-24T07:03:20Z
  date_updated: 2020-09-24T07:03:20Z
  file_id: '8567'
  file_name: 2020_elife_Moon.pdf
  file_size: 15089438
  relation: main_file
  success: 1
file_date_updated: 2020-09-24T07:03:20Z
has_accepted_license: '1'
intvolume: '         9'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1101/751958
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: LIS1 determines cleavage plane positioning by regulating actomyosin-mediated
  cell membrane contractility
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: 9
year: '2020'
...
---
_id: '11060'
abstract:
- lang: eng
  text: The inner nuclear membrane (INM) is a subdomain of the endoplasmic reticulum
    (ER) that is gated by the nuclear pore complex. It is unknown whether proteins
    of the INM and ER are degraded through shared or distinct pathways in mammalian
    cells. We applied dynamic proteomics to profile protein half-lives and report
    that INM and ER residents turn over at similar rates, indicating that the INM’s
    unique topology is not a barrier to turnover. Using a microscopy approach, we
    observed that the proteasome can degrade INM proteins in situ. However, we also
    uncovered evidence for selective, vesicular transport-mediated turnover of a single
    INM protein, emerin, that is potentiated by ER stress. Emerin is rapidly cleared
    from the INM by a mechanism that requires emerin’s LEM domain to mediate vesicular
    trafficking to lysosomes. This work demonstrates that the INM can be dynamically
    remodeled in response to environmental inputs.
article_number: e49796
article_processing_charge: No
article_type: original
author:
- first_name: Abigail
  full_name: Buchwalter, Abigail
  last_name: Buchwalter
- first_name: Roberta
  full_name: Schulte, Roberta
  last_name: Schulte
- first_name: Hsiao
  full_name: Tsai, Hsiao
  last_name: Tsai
- first_name: Juliana
  full_name: Capitanio, Juliana
  last_name: Capitanio
- 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: Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. Selective clearance
    of the inner nuclear membrane protein emerin by vesicular transport during ER
    stress. <i>eLife</i>. 2019;8. doi:<a href="https://doi.org/10.7554/elife.49796">10.7554/elife.49796</a>
  apa: Buchwalter, A., Schulte, R., Tsai, H., Capitanio, J., &#38; Hetzer, M. (2019).
    Selective clearance of the inner nuclear membrane protein emerin by vesicular
    transport during ER stress. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.49796">https://doi.org/10.7554/elife.49796</a>
  chicago: Buchwalter, Abigail, Roberta Schulte, Hsiao Tsai, Juliana Capitanio, and
    Martin Hetzer. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin
    by Vesicular Transport during ER Stress.” <i>ELife</i>. eLife Sciences Publications,
    2019. <a href="https://doi.org/10.7554/elife.49796">https://doi.org/10.7554/elife.49796</a>.
  ieee: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, and M. Hetzer, “Selective
    clearance of the inner nuclear membrane protein emerin by vesicular transport
    during ER stress,” <i>eLife</i>, vol. 8. eLife Sciences Publications, 2019.
  ista: Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. 2019. Selective clearance
    of the inner nuclear membrane protein emerin by vesicular transport during ER
    stress. eLife. 8, e49796.
  mla: Buchwalter, Abigail, et al. “Selective Clearance of the Inner Nuclear Membrane
    Protein Emerin by Vesicular Transport during ER Stress.” <i>ELife</i>, vol. 8,
    e49796, eLife Sciences Publications, 2019, doi:<a href="https://doi.org/10.7554/elife.49796">10.7554/elife.49796</a>.
  short: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, M. Hetzer, ELife 8 (2019).
date_created: 2022-04-07T07:45:02Z
date_published: 2019-10-10T00:00:00Z
date_updated: 2023-05-31T06:36:22Z
day: '10'
ddc:
- '570'
doi: 10.7554/elife.49796
extern: '1'
external_id:
  pmid:
  - '31599721'
file:
- access_level: open_access
  checksum: 1e8672a1e9c3dc0a2d3d0dad89673616
  content_type: application/pdf
  creator: dernst
  date_created: 2022-04-08T08:18:01Z
  date_updated: 2022-04-08T08:18:01Z
  file_id: '11138'
  file_name: 2019_eLife_Buchwalter.pdf
  file_size: 6984654
  relation: main_file
  success: 1
file_date_updated: 2022-04-08T08:18:01Z
has_accepted_license: '1'
intvolume: '         8'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
  record:
  - id: '13079'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: Selective clearance of the inner nuclear membrane protein emerin by vesicular
  transport during ER stress
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: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 8
year: '2019'
...
---
_id: '7405'
abstract:
- lang: eng
  text: Biophysical modeling of neuronal networks helps to integrate and interpret
    rapidly growing and disparate experimental datasets at multiple scales. The NetPyNE
    tool (www.netpyne.org) provides both programmatic and graphical interfaces to
    develop data-driven multiscale network models in NEURON. NetPyNE clearly separates
    model parameters from implementation code. Users provide specifications at a high
    level via a standardized declarative language, for example connectivity rules,
    to create millions of cell-to-cell connections. NetPyNE then enables users to
    generate the NEURON network, run efficiently parallelized simulations, optimize
    and explore network parameters through automated batch runs, and use built-in
    functions for visualization and analysis – connectivity matrices, voltage traces,
    spike raster plots, local field potentials, and information theoretic measures.
    NetPyNE also facilitates model sharing by exporting and importing standardized
    formats (NeuroML and SONATA). NetPyNE is already being used to teach computational
    neuroscience students and by modelers to investigate brain regions and phenomena.
article_number: e44494
article_processing_charge: No
article_type: original
author:
- first_name: Salvador
  full_name: Dura-Bernal, Salvador
  last_name: Dura-Bernal
- first_name: Benjamin
  full_name: Suter, Benjamin
  id: 4952F31E-F248-11E8-B48F-1D18A9856A87
  last_name: Suter
  orcid: 0000-0002-9885-6936
- first_name: Padraig
  full_name: Gleeson, Padraig
  last_name: Gleeson
- first_name: Matteo
  full_name: Cantarelli, Matteo
  last_name: Cantarelli
- first_name: Adrian
  full_name: Quintana, Adrian
  last_name: Quintana
- first_name: Facundo
  full_name: Rodriguez, Facundo
  last_name: Rodriguez
- first_name: David J
  full_name: Kedziora, David J
  last_name: Kedziora
- first_name: George L
  full_name: Chadderdon, George L
  last_name: Chadderdon
- first_name: Cliff C
  full_name: Kerr, Cliff C
  last_name: Kerr
- first_name: Samuel A
  full_name: Neymotin, Samuel A
  last_name: Neymotin
- first_name: Robert A
  full_name: McDougal, Robert A
  last_name: McDougal
- first_name: Michael
  full_name: Hines, Michael
  last_name: Hines
- first_name: Gordon MG
  full_name: Shepherd, Gordon MG
  last_name: Shepherd
- first_name: William W
  full_name: Lytton, William W
  last_name: Lytton
citation:
  ama: Dura-Bernal S, Suter B, Gleeson P, et al. NetPyNE, a tool for data-driven multiscale
    modeling of brain circuits. <i>eLife</i>. 2019;8. doi:<a href="https://doi.org/10.7554/elife.44494">10.7554/elife.44494</a>
  apa: Dura-Bernal, S., Suter, B., Gleeson, P., Cantarelli, M., Quintana, A., Rodriguez,
    F., … Lytton, W. W. (2019). NetPyNE, a tool for data-driven multiscale modeling
    of brain circuits. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.44494">https://doi.org/10.7554/elife.44494</a>
  chicago: Dura-Bernal, Salvador, Benjamin Suter, Padraig Gleeson, Matteo Cantarelli,
    Adrian Quintana, Facundo Rodriguez, David J Kedziora, et al. “NetPyNE, a Tool
    for Data-Driven Multiscale Modeling of Brain Circuits.” <i>ELife</i>. eLife Sciences
    Publications, 2019. <a href="https://doi.org/10.7554/elife.44494">https://doi.org/10.7554/elife.44494</a>.
  ieee: S. Dura-Bernal <i>et al.</i>, “NetPyNE, a tool for data-driven multiscale
    modeling of brain circuits,” <i>eLife</i>, vol. 8. eLife Sciences Publications,
    2019.
  ista: Dura-Bernal S, Suter B, Gleeson P, Cantarelli M, Quintana A, Rodriguez F,
    Kedziora DJ, Chadderdon GL, Kerr CC, Neymotin SA, McDougal RA, Hines M, Shepherd
    GM, Lytton WW. 2019. NetPyNE, a tool for data-driven multiscale modeling of brain
    circuits. eLife. 8, e44494.
  mla: Dura-Bernal, Salvador, et al. “NetPyNE, a Tool for Data-Driven Multiscale Modeling
    of Brain Circuits.” <i>ELife</i>, vol. 8, e44494, eLife Sciences Publications,
    2019, doi:<a href="https://doi.org/10.7554/elife.44494">10.7554/elife.44494</a>.
  short: S. Dura-Bernal, B. Suter, P. Gleeson, M. Cantarelli, A. Quintana, F. Rodriguez,
    D.J. Kedziora, G.L. Chadderdon, C.C. Kerr, S.A. Neymotin, R.A. McDougal, M. Hines,
    G.M. Shepherd, W.W. Lytton, ELife 8 (2019).
date_created: 2020-01-30T09:08:01Z
date_published: 2019-05-31T00:00:00Z
date_updated: 2023-09-07T14:27:52Z
day: '31'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.7554/elife.44494
external_id:
  isi:
  - '000468968400001'
  pmid:
  - '31025934'
file:
- access_level: open_access
  checksum: 7014189c11c10a12feeeae37f054871d
  content_type: application/pdf
  creator: dernst
  date_created: 2020-02-04T08:41:47Z
  date_updated: 2020-07-14T12:47:57Z
  file_id: '7444'
  file_name: 2019_eLife_DuraBernal.pdf
  file_size: 6182359
  relation: main_file
file_date_updated: 2020-07-14T12:47:57Z
has_accepted_license: '1'
intvolume: '         8'
isi: 1
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: NetPyNE, a tool for data-driven multiscale modeling of brain circuits
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 8
year: '2019'
...
---
_id: '6187'
abstract:
- lang: eng
  text: Aberrant display of the truncated core1 O-glycan T-antigen is a common feature
    of human cancer cells that correlates with metastasis. Here we show that T-antigen
    in Drosophila melanogaster macrophages is involved in their developmentally programmed
    tissue invasion. Higher macrophage T-antigen levels require an atypical major
    facilitator superfamily (MFS) member that we named Minerva which enables macrophage
    dissemination and invasion. We characterize for the first time the T and Tn glycoform
    O-glycoproteome of the Drosophila melanogaster embryo, and determine that Minerva
    increases the presence of T-antigen on proteins in pathways previously linked
    to cancer, most strongly on the sulfhydryl oxidase Qsox1 which we show is required
    for macrophage tissue entry. Minerva’s vertebrate ortholog, MFSD1, rescues the
    minerva mutant’s migration and T-antigen glycosylation defects. We thus identify
    a key conserved regulator that orchestrates O-glycosylation on a protein subset
    to activate a program governing migration steps important for both development
    and cancer metastasis.
acknowledged_ssus:
- _id: LifeSc
article_number: e41801
article_processing_charge: No
author:
- first_name: Katarina
  full_name: Valosková, Katarina
  id: 46F146FC-F248-11E8-B48F-1D18A9856A87
  last_name: Valosková
- first_name: Julia
  full_name: Biebl, Julia
  id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
  last_name: Biebl
- first_name: Marko
  full_name: Roblek, Marko
  id: 3047D808-F248-11E8-B48F-1D18A9856A87
  last_name: Roblek
  orcid: 0000-0001-9588-1389
- first_name: Shamsi
  full_name: Emtenani, Shamsi
  id: 49D32318-F248-11E8-B48F-1D18A9856A87
  last_name: Emtenani
  orcid: 0000-0001-6981-6938
- first_name: Attila
  full_name: György, Attila
  id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
  last_name: György
  orcid: 0000-0002-1819-198X
- first_name: Michaela
  full_name: Misova, Michaela
  id: 495A3C32-F248-11E8-B48F-1D18A9856A87
  last_name: Misova
  orcid: 0000-0003-2427-6856
- first_name: Aparna
  full_name: Ratheesh, Aparna
  id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
  last_name: Ratheesh
  orcid: 0000-0001-7190-0776
- first_name: Patricia
  full_name: Rodrigues, Patricia
  id: 2CE4065A-F248-11E8-B48F-1D18A9856A87
  last_name: Rodrigues
- first_name: Katerina
  full_name: Shkarina, Katerina
  last_name: Shkarina
- first_name: Ida Signe Bohse
  full_name: Larsen, Ida Signe Bohse
  last_name: Larsen
- first_name: Sergey Y
  full_name: Vakhrushev, Sergey Y
  last_name: Vakhrushev
- first_name: Henrik
  full_name: Clausen, Henrik
  last_name: Clausen
- first_name: Daria E
  full_name: Siekhaus, Daria E
  id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
  last_name: Siekhaus
  orcid: 0000-0001-8323-8353
citation:
  ama: Valosková K, Bicher J, Roblek M, et al. A conserved major facilitator superfamily
    member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion.
    <i>eLife</i>. 2019;8. doi:<a href="https://doi.org/10.7554/elife.41801">10.7554/elife.41801</a>
  apa: Valosková, K., Bicher, J., Roblek, M., Emtenani, S., György, A., Misova, M.,
    … Siekhaus, D. E. (2019). A conserved major facilitator superfamily member orchestrates
    a subset of O-glycosylation to aid macrophage tissue invasion. <i>ELife</i>. eLife
    Sciences Publications. <a href="https://doi.org/10.7554/elife.41801">https://doi.org/10.7554/elife.41801</a>
  chicago: Valosková, Katarina, Julia Bicher, Marko Roblek, Shamsi Emtenani, Attila
    György, Michaela Misova, Aparna Ratheesh, et al. “A Conserved Major Facilitator
    Superfamily Member Orchestrates a Subset of O-Glycosylation to Aid Macrophage
    Tissue Invasion.” <i>ELife</i>. eLife Sciences Publications, 2019. <a href="https://doi.org/10.7554/elife.41801">https://doi.org/10.7554/elife.41801</a>.
  ieee: K. Valosková <i>et al.</i>, “A conserved major facilitator superfamily member
    orchestrates a subset of O-glycosylation to aid macrophage tissue invasion,” <i>eLife</i>,
    vol. 8. eLife Sciences Publications, 2019.
  ista: Valosková K, Bicher J, Roblek M, Emtenani S, György A, Misova M, Ratheesh
    A, Rodrigues P, Shkarina K, Larsen ISB, Vakhrushev SY, Clausen H, Siekhaus DE.
    2019. A conserved major facilitator superfamily member orchestrates a subset of
    O-glycosylation to aid macrophage tissue invasion. eLife. 8, e41801.
  mla: Valosková, Katarina, et al. “A Conserved Major Facilitator Superfamily Member
    Orchestrates a Subset of O-Glycosylation to Aid Macrophage Tissue Invasion.” <i>ELife</i>,
    vol. 8, e41801, eLife Sciences Publications, 2019, doi:<a href="https://doi.org/10.7554/elife.41801">10.7554/elife.41801</a>.
  short: K. Valosková, J. Bicher, M. Roblek, S. Emtenani, A. György, M. Misova, A.
    Ratheesh, P. Rodrigues, K. Shkarina, I.S.B. Larsen, S.Y. Vakhrushev, H. Clausen,
    D.E. Siekhaus, ELife 8 (2019).
date_created: 2019-03-28T13:37:45Z
date_published: 2019-03-26T00:00:00Z
date_updated: 2024-03-25T23:30:15Z
day: '26'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.7554/elife.41801
ec_funded: 1
external_id:
  isi:
  - '000462530200001'
file:
- access_level: open_access
  checksum: cc0d1a512559d52e7e7cb0e9b9854b40
  content_type: application/pdf
  creator: dernst
  date_created: 2019-03-28T14:00:41Z
  date_updated: 2020-07-14T12:47:23Z
  file_id: '6188'
  file_name: 2019_eLife_Valoskova.pdf
  file_size: 4496017
  relation: main_file
file_date_updated: 2020-07-14T12:47:23Z
has_accepted_license: '1'
intvolume: '         8'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 253CDE40-B435-11E9-9278-68D0E5697425
  grant_number: '24283'
  name: Examination of the role of a MFS transporter in the migration of Drosophila
    immune cells
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P29638
  name: The role of Drosophila TNF alpha in immune cell invasion
- _id: 2536F660-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '334077'
  name: Investigating the role of transporters in invasive migration through junctions
- _id: 25388084-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '329540'
  name: 'Breaking barriers: Investigating the junctional and mechanobiological changes
    underlying the ability of Drosophila immune cells to invade an epithelium'
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '665385'
  name: International IST Doctoral Program
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/new-gene-potentially-involved-in-metastasis-identified/
  record:
  - id: '6530'
    relation: dissertation_contains
  - id: '8983'
    relation: dissertation_contains
    status: public
  - id: '6546'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation
  to aid macrophage tissue invasion
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: 8
year: '2019'
...
---
_id: '12192'
abstract:
- lang: eng
  text: Transposable elements (TEs), the movement of which can damage the genome,
    are epigenetically silenced in eukaryotes. Intriguingly, TEs are activated in
    the sperm companion cell – vegetative cell (VC) – of the flowering plant Arabidopsis
    thaliana. However, the extent and mechanism of this activation are unknown. Here
    we show that about 100 heterochromatic TEs are activated in VCs, mostly by DEMETER-catalyzed
    DNA demethylation. We further demonstrate that DEMETER access to some of these
    TEs is permitted by the natural depletion of linker histone H1 in VCs. Ectopically
    expressed H1 suppresses TEs in VCs by reducing DNA demethylation and via a methylation-independent
    mechanism. We demonstrate that H1 is required for heterochromatin condensation
    in plant cells and show that H1 overexpression creates heterochromatic foci in
    the VC progenitor cell. Taken together, our results demonstrate that the natural
    depletion of H1 during male gametogenesis facilitates DEMETER-directed DNA demethylation,
    heterochromatin relaxation, and TE activation.
acknowledgement: We thank David Twell for the pDONR-P4-P1R-pLAT52 and pDONR-P2R-P3-mRFP
  vectors, the John Innes Centre Bioimaging Facility (Elaine Barclay and Grant Calder)
  for their assistance with microscopy, and the Norwich BioScience Institute Partnership
  Computing infrastructure for Science Group for High Performance Computing resources.
  This work was funded by a Biotechnology and Biological Sciences Research Council
  (BBSRC) David Phillips Fellowship (BB/L025043/1; SH, JZ and XF), a European Research
  Council Starting Grant ('SexMeth' 804981; XF) and a Grant to Exceptional Researchers
  by the Gatsby Charitable Foundation (SH and XF).
article_number: '42530'
article_processing_charge: No
article_type: original
author:
- first_name: Shengbo
  full_name: He, Shengbo
  last_name: He
- first_name: Martin
  full_name: Vickers, Martin
  last_name: Vickers
- first_name: Jingyi
  full_name: Zhang, Jingyi
  last_name: Zhang
- 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, Vickers M, Zhang J, Feng X. Natural depletion of histone H1 in sex cells
    causes DNA demethylation, heterochromatin decondensation and transposon activation.
    <i>eLife</i>. 2019;8. doi:<a href="https://doi.org/10.7554/elife.42530">10.7554/elife.42530</a>
  apa: He, S., Vickers, M., Zhang, J., &#38; Feng, X. (2019). Natural depletion of
    histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation
    and transposon activation. <i>ELife</i>. eLife Sciences Publications, Ltd. <a
    href="https://doi.org/10.7554/elife.42530">https://doi.org/10.7554/elife.42530</a>
  chicago: He, Shengbo, Martin Vickers, Jingyi Zhang, and Xiaoqi Feng. “Natural Depletion
    of Histone H1 in Sex Cells Causes DNA Demethylation, Heterochromatin Decondensation
    and Transposon Activation.” <i>ELife</i>. eLife Sciences Publications, Ltd, 2019.
    <a href="https://doi.org/10.7554/elife.42530">https://doi.org/10.7554/elife.42530</a>.
  ieee: S. He, M. Vickers, J. Zhang, and X. Feng, “Natural depletion of histone H1
    in sex cells causes DNA demethylation, heterochromatin decondensation and transposon
    activation,” <i>eLife</i>, vol. 8. eLife Sciences Publications, Ltd, 2019.
  ista: He S, Vickers M, Zhang J, Feng X. 2019. Natural depletion of histone H1 in
    sex cells causes DNA demethylation, heterochromatin decondensation and transposon
    activation. eLife. 8, 42530.
  mla: He, Shengbo, et al. “Natural Depletion of Histone H1 in Sex Cells Causes DNA
    Demethylation, Heterochromatin Decondensation and Transposon Activation.” <i>ELife</i>,
    vol. 8, 42530, eLife Sciences Publications, Ltd, 2019, doi:<a href="https://doi.org/10.7554/elife.42530">10.7554/elife.42530</a>.
  short: S. He, M. Vickers, J. Zhang, X. Feng, ELife 8 (2019).
date_created: 2023-01-16T09:17:21Z
date_published: 2019-05-28T00:00:00Z
date_updated: 2023-05-08T10:54:12Z
day: '28'
ddc:
- '580'
department:
- _id: XiFe
doi: 10.7554/elife.42530
extern: '1'
external_id:
  unknown:
  - '31135340'
file:
- access_level: open_access
  checksum: ea6b89c20d59e5eb3646916fe5d568ad
  content_type: application/pdf
  creator: alisjak
  date_created: 2023-02-07T09:42:46Z
  date_updated: 2023-02-07T09:42:46Z
  file_id: '12525'
  file_name: 2019_elife_He.pdf
  file_size: 2493837
  relation: main_file
  success: 1
file_date_updated: 2023-02-07T09:42:46Z
has_accepted_license: '1'
intvolume: '         8'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594752/
month: '05'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications, Ltd
quality_controlled: '1'
scopus_import: '1'
status: public
title: Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin
  decondensation and transposon activation
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2019'
...
---
_id: '8075'
abstract:
- lang: eng
  text: Ion channel models are the building blocks of computational neuron models.
    Their biological fidelity is therefore crucial for the interpretation of simulations.
    However, the number of published models, and the lack of standardization, make
    the comparison of ion channel models with one another and with experimental data
    difficult. Here, we present a framework for the automated large-scale classification
    of ion channel models. Using annotated metadata and responses to a set of voltage-clamp
    protocols, we assigned 2378 models of voltage- and calcium-gated ion channels
    coded in NEURON to 211 clusters. The IonChannelGenealogy (ICGenealogy) web interface
    provides an interactive resource for the categorization of new and existing models
    and experimental recordings. It enables quantitative comparisons of simulated
    and/or measured ion channel kinetics, and facilitates field-wide standardization
    of experimentally-constrained modeling.
article_number: e22152
article_processing_charge: No
article_type: original
author:
- first_name: William F
  full_name: Podlaski, William F
  last_name: Podlaski
- first_name: Alexander
  full_name: Seeholzer, Alexander
  last_name: Seeholzer
- first_name: Lukas N
  full_name: Groschner, Lukas N
  last_name: Groschner
- first_name: Gero
  full_name: Miesenböck, Gero
  last_name: Miesenböck
- first_name: Rajnish
  full_name: Ranjan, Rajnish
  last_name: Ranjan
- first_name: Tim P
  full_name: Vogels, Tim P
  id: CB6FF8D2-008F-11EA-8E08-2637E6697425
  last_name: Vogels
  orcid: 0000-0003-3295-6181
citation:
  ama: Podlaski WF, Seeholzer A, Groschner LN, Miesenböck G, Ranjan R, Vogels TP.
    Mapping the function of neuronal ion channels in model and experiment. <i>eLife</i>.
    2017;6. doi:<a href="https://doi.org/10.7554/elife.22152">10.7554/elife.22152</a>
  apa: Podlaski, W. F., Seeholzer, A., Groschner, L. N., Miesenböck, G., Ranjan, R.,
    &#38; Vogels, T. P. (2017). Mapping the function of neuronal ion channels in model
    and experiment. <i>ELife</i>. eLife Sciences Publications, Ltd. <a href="https://doi.org/10.7554/elife.22152">https://doi.org/10.7554/elife.22152</a>
  chicago: Podlaski, William F, Alexander Seeholzer, Lukas N Groschner, Gero Miesenböck,
    Rajnish Ranjan, and Tim P Vogels. “Mapping the Function of Neuronal Ion Channels
    in Model and Experiment.” <i>ELife</i>. eLife Sciences Publications, Ltd, 2017.
    <a href="https://doi.org/10.7554/elife.22152">https://doi.org/10.7554/elife.22152</a>.
  ieee: W. F. Podlaski, A. Seeholzer, L. N. Groschner, G. Miesenböck, R. Ranjan, and
    T. P. Vogels, “Mapping the function of neuronal ion channels in model and experiment,”
    <i>eLife</i>, vol. 6. eLife Sciences Publications, Ltd, 2017.
  ista: Podlaski WF, Seeholzer A, Groschner LN, Miesenböck G, Ranjan R, Vogels TP.
    2017. Mapping the function of neuronal ion channels in model and experiment. eLife.
    6, e22152.
  mla: Podlaski, William F., et al. “Mapping the Function of Neuronal Ion Channels
    in Model and Experiment.” <i>ELife</i>, vol. 6, e22152, eLife Sciences Publications,
    Ltd, 2017, doi:<a href="https://doi.org/10.7554/elife.22152">10.7554/elife.22152</a>.
  short: W.F. Podlaski, A. Seeholzer, L.N. Groschner, G. Miesenböck, R. Ranjan, T.P.
    Vogels, ELife 6 (2017).
date_created: 2020-06-30T13:32:18Z
date_published: 2017-03-06T00:00:00Z
date_updated: 2021-01-12T08:16:46Z
day: '06'
ddc:
- '570'
doi: 10.7554/elife.22152
extern: '1'
external_id:
  pmid:
  - '28267430'
file:
- access_level: open_access
  checksum: e5c5a33bcb3ac38ad62df1010ab29040
  content_type: application/pdf
  creator: cziletti
  date_created: 2020-07-16T12:08:40Z
  date_updated: 2020-07-16T12:08:40Z
  file_id: '8124'
  file_name: 2017_elife_Podlaski.pdf
  file_size: 16034505
  relation: main_file
  success: 1
file_date_updated: 2020-07-16T12:08:40Z
has_accepted_license: '1'
intvolume: '         6'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications, Ltd
quality_controlled: '1'
status: public
title: Mapping the function of neuronal ion channels in model and experiment
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: D865714E-FA4E-11E9-B85B-F5C5E5697425
volume: 6
year: '2017'
...
---
_id: '9190'
abstract:
- lang: eng
  text: <jats:p>Plant meristems carry pools of continuously active stem cells, whose
    activity is controlled by developmental and environmental signals. After stem
    cell division, daughter cells that exit the stem cell domain acquire transit amplifying
    cell identity before they are incorporated into organs and differentiate. In this
    study, we used an integrated approach to elucidate the role of HECATE (HEC) genes
    in regulating developmental trajectories of shoot stem cells in Arabidopsis thaliana.
    Our work reveals that HEC function stabilizes cell fate in distinct zones of the
    shoot meristem thereby controlling the spatio-temporal dynamics of stem cell differentiation.
    Importantly, this activity is concomitant with the local modulation of cellular
    responses to cytokinin and auxin, two key phytohormones regulating cell behaviour.
    Mechanistically, we show that HEC factors transcriptionally control and physically
    interact with MONOPTEROS (MP), a key regulator of auxin signalling, and modulate
    the autocatalytic stabilization of auxin signalling output.</jats:p>
article_number: e30135
article_processing_charge: No
article_type: original
author:
- first_name: Christophe
  full_name: Gaillochet, Christophe
  last_name: Gaillochet
- first_name: Thomas
  full_name: Stiehl, Thomas
  last_name: Stiehl
- first_name: Christian
  full_name: Wenzl, Christian
  last_name: Wenzl
- first_name: Juan-José
  full_name: Ripoll, Juan-José
  last_name: Ripoll
- first_name: Lindsay J
  full_name: Bailey-Steinitz, Lindsay J
  last_name: Bailey-Steinitz
- first_name: Lanxin
  full_name: Li, Lanxin
  id: 367EF8FA-F248-11E8-B48F-1D18A9856A87
  last_name: Li
  orcid: 0000-0002-5607-272X
- first_name: Anne
  full_name: Pfeiffer, Anne
  last_name: Pfeiffer
- first_name: Andrej
  full_name: Miotk, Andrej
  last_name: Miotk
- first_name: Jana P
  full_name: Hakenjos, Jana P
  last_name: Hakenjos
- first_name: Joachim
  full_name: Forner, Joachim
  last_name: Forner
- first_name: Martin F
  full_name: Yanofsky, Martin F
  last_name: Yanofsky
- first_name: Anna
  full_name: Marciniak-Czochra, Anna
  last_name: Marciniak-Czochra
- first_name: Jan U
  full_name: Lohmann, Jan U
  last_name: Lohmann
citation:
  ama: Gaillochet C, Stiehl T, Wenzl C, et al. Control of plant cell fate transitions
    by transcriptional and hormonal signals. <i>eLife</i>. 2017;6. doi:<a href="https://doi.org/10.7554/elife.30135">10.7554/elife.30135</a>
  apa: Gaillochet, C., Stiehl, T., Wenzl, C., Ripoll, J.-J., Bailey-Steinitz, L. J.,
    Li, L., … Lohmann, J. U. (2017). Control of plant cell fate transitions by transcriptional
    and hormonal signals. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.30135">https://doi.org/10.7554/elife.30135</a>
  chicago: Gaillochet, Christophe, Thomas Stiehl, Christian Wenzl, Juan-José Ripoll,
    Lindsay J Bailey-Steinitz, Lanxin Li, Anne Pfeiffer, et al. “Control of Plant
    Cell Fate Transitions by Transcriptional and Hormonal Signals.” <i>ELife</i>.
    eLife Sciences Publications, 2017. <a href="https://doi.org/10.7554/elife.30135">https://doi.org/10.7554/elife.30135</a>.
  ieee: C. Gaillochet <i>et al.</i>, “Control of plant cell fate transitions by transcriptional
    and hormonal signals,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017.
  ista: Gaillochet C, Stiehl T, Wenzl C, Ripoll J-J, Bailey-Steinitz LJ, Li L, Pfeiffer
    A, Miotk A, Hakenjos JP, Forner J, Yanofsky MF, Marciniak-Czochra A, Lohmann JU.
    2017. Control of plant cell fate transitions by transcriptional and hormonal signals.
    eLife. 6, e30135.
  mla: Gaillochet, Christophe, et al. “Control of Plant Cell Fate Transitions by Transcriptional
    and Hormonal Signals.” <i>ELife</i>, vol. 6, e30135, eLife Sciences Publications,
    2017, doi:<a href="https://doi.org/10.7554/elife.30135">10.7554/elife.30135</a>.
  short: C. Gaillochet, T. Stiehl, C. Wenzl, J.-J. Ripoll, L.J. Bailey-Steinitz, L.
    Li, A. Pfeiffer, A. Miotk, J.P. Hakenjos, J. Forner, M.F. Yanofsky, A. Marciniak-Czochra,
    J.U. Lohmann, ELife 6 (2017).
date_created: 2021-02-24T17:06:13Z
date_published: 2017-10-23T00:00:00Z
date_updated: 2021-03-02T09:33:54Z
day: '23'
ddc:
- '580'
doi: 10.7554/elife.30135
extern: '1'
external_id:
  pmid:
  - '29058667'
file:
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  creator: dernst
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  file_size: 11669407
  relation: main_file
  success: 1
file_date_updated: 2021-03-02T09:29:56Z
has_accepted_license: '1'
intvolume: '         6'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Control of plant cell fate transitions by transcriptional and hormonal signals
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '10370'
abstract:
- lang: eng
  text: Eukaryotic cells are densely packed with macromolecular complexes and intertwining
    organelles, continually transported and reshaped. Intriguingly, organelles avoid
    clashing and entangling with each other in such limited space. Mitochondria form
    extensive networks constantly remodeled by fission and fusion. Here, we show that
    mitochondrial fission is triggered by mechanical forces. Mechano-stimulation of
    mitochondria – via encounter with motile intracellular pathogens, via external
    pressure applied by an atomic force microscope, or via cell migration across uneven
    microsurfaces – results in the recruitment of the mitochondrial fission machinery,
    and subsequent division. We propose that MFF, owing to affinity for narrow mitochondria,
    acts as a membrane-bound force sensor to recruit the fission machinery to mechanically
    strained sites. Thus, mitochondria adapt to the environment by sensing and responding
    to biomechanical cues. Our findings that mechanical triggers can be coupled to
    biochemical responses in membrane dynamics may explain how organelles orderly
    cohabit in the crowded cytoplasm.
article_number: e30292
article_processing_charge: No
article_type: original
author:
- first_name: Sebastian Carsten Johannes
  full_name: Helle, Sebastian Carsten Johannes
  last_name: Helle
- first_name: Qian
  full_name: Feng, Qian
  last_name: Feng
- first_name: Mathias J
  full_name: Aebersold, Mathias J
  last_name: Aebersold
- first_name: Luca
  full_name: Hirt, Luca
  last_name: Hirt
- first_name: Raphael R
  full_name: Grüter, Raphael R
  last_name: Grüter
- first_name: Afshin
  full_name: Vahid, Afshin
  last_name: Vahid
- first_name: Andrea
  full_name: Sirianni, Andrea
  last_name: Sirianni
- first_name: Serge
  full_name: Mostowy, Serge
  last_name: Mostowy
- first_name: Jess G
  full_name: Snedeker, Jess G
  last_name: Snedeker
- first_name: Anđela
  full_name: Šarić, Anđela
  id: bf63d406-f056-11eb-b41d-f263a6566d8b
  last_name: Šarić
  orcid: 0000-0002-7854-2139
- first_name: Timon
  full_name: Idema, Timon
  last_name: Idema
- first_name: Tomaso
  full_name: Zambelli, Tomaso
  last_name: Zambelli
- first_name: Benoît
  full_name: Kornmann, Benoît
  last_name: Kornmann
citation:
  ama: Helle SCJ, Feng Q, Aebersold MJ, et al. Mechanical force induces mitochondrial
    fission. <i>eLife</i>. 2017;6. doi:<a href="https://doi.org/10.7554/elife.30292">10.7554/elife.30292</a>
  apa: Helle, S. C. J., Feng, Q., Aebersold, M. J., Hirt, L., Grüter, R. R., Vahid,
    A., … Kornmann, B. (2017). Mechanical force induces mitochondrial fission. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.30292">https://doi.org/10.7554/elife.30292</a>
  chicago: Helle, Sebastian Carsten Johannes, Qian Feng, Mathias J Aebersold, Luca
    Hirt, Raphael R Grüter, Afshin Vahid, Andrea Sirianni, et al. “Mechanical Force
    Induces Mitochondrial Fission.” <i>ELife</i>. eLife Sciences Publications, 2017.
    <a href="https://doi.org/10.7554/elife.30292">https://doi.org/10.7554/elife.30292</a>.
  ieee: S. C. J. Helle <i>et al.</i>, “Mechanical force induces mitochondrial fission,”
    <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017.
  ista: Helle SCJ, Feng Q, Aebersold MJ, Hirt L, Grüter RR, Vahid A, Sirianni A, Mostowy
    S, Snedeker JG, Šarić A, Idema T, Zambelli T, Kornmann B. 2017. Mechanical force
    induces mitochondrial fission. eLife. 6, e30292.
  mla: Helle, Sebastian Carsten Johannes, et al. “Mechanical Force Induces Mitochondrial
    Fission.” <i>ELife</i>, vol. 6, e30292, eLife Sciences Publications, 2017, doi:<a
    href="https://doi.org/10.7554/elife.30292">10.7554/elife.30292</a>.
  short: S.C.J. Helle, Q. Feng, M.J. Aebersold, L. Hirt, R.R. Grüter, A. Vahid, A.
    Sirianni, S. Mostowy, J.G. Snedeker, A. Šarić, T. Idema, T. Zambelli, B. Kornmann,
    ELife 6 (2017).
date_created: 2021-11-29T08:51:38Z
date_published: 2017-11-09T00:00:00Z
date_updated: 2021-11-29T09:28:14Z
day: '09'
ddc:
- '572'
doi: 10.7554/elife.30292
extern: '1'
external_id:
  pmid:
  - '29119945'
file:
- access_level: open_access
  checksum: c35f42dcfb007f6d6c761a27e24c26d3
  content_type: application/pdf
  creator: cchlebak
  date_created: 2021-11-29T09:07:41Z
  date_updated: 2021-11-29T09:07:41Z
  file_id: '10372'
  file_name: 2017_eLife_Helle.pdf
  file_size: 6120157
  relation: main_file
  success: 1
file_date_updated: 2021-11-29T09:07:41Z
has_accepted_license: '1'
intvolume: '         6'
keyword:
- general immunology and microbiology
- general biochemistry
- genetics and molecular biology
- general medicine
- general neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://elifesciences.org/articles/30292
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanical force induces mitochondrial fission
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: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 6
year: '2017'
...
---
_id: '6120'
abstract:
- lang: eng
  text: Brains organize behavior and physiology to optimize the response to threats
    or opportunities. We dissect how 21% O2, an indicator of surface exposure, reprograms
    C. elegans' global state, inducing sustained locomotory arousal and altering expression
    of neuropeptides, metabolic enzymes, and other non-neural genes. The URX O2-sensing
    neurons drive arousal at 21% O2 by tonically activating the RMG interneurons.
    Stimulating RMG is sufficient to switch behavioral state. Ablating the ASH, ADL,
    or ASK sensory neurons connected to RMG by gap junctions does not disrupt arousal.
    However, disrupting cation currents in these neurons curtails RMG neurosecretion
    and arousal. RMG signals high O2 by peptidergic secretion. Neuropeptide reporters
    reveal neural circuit state, as neurosecretion stimulates neuropeptide expression.
    Neural imaging in unrestrained animals shows that URX and RMG encode O2 concentration
    rather than behavior, while the activity of downstream interneurons such as AVB
    and AIY reflect both O2 levels and the behavior being executed.
article_number: e04241
author:
- first_name: Patrick
  full_name: Laurent, Patrick
  last_name: Laurent
- first_name: Zoltan
  full_name: Soltesz, Zoltan
  last_name: Soltesz
- first_name: Geoffrey M
  full_name: Nelson, Geoffrey M
  last_name: Nelson
- first_name: Changchun
  full_name: Chen, Changchun
  last_name: Chen
- first_name: Fausto
  full_name: Arellano-Carbajal, Fausto
  last_name: Arellano-Carbajal
- first_name: Emmanuel
  full_name: Levy, Emmanuel
  last_name: Levy
- first_name: Mario
  full_name: de Bono, Mario
  id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
  last_name: de Bono
  orcid: 0000-0001-8347-0443
citation:
  ama: Laurent P, Soltesz Z, Nelson GM, et al. Decoding a neural circuit controlling
    global animal state in C. elegans. <i>eLife</i>. 2015;4. doi:<a href="https://doi.org/10.7554/elife.04241">10.7554/elife.04241</a>
  apa: Laurent, P., Soltesz, Z., Nelson, G. M., Chen, C., Arellano-Carbajal, F., Levy,
    E., &#38; de Bono, M. (2015). Decoding a neural circuit controlling global animal
    state in C. elegans. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/elife.04241">https://doi.org/10.7554/elife.04241</a>
  chicago: Laurent, Patrick, Zoltan Soltesz, Geoffrey M Nelson, Changchun Chen, Fausto
    Arellano-Carbajal, Emmanuel Levy, and Mario de Bono. “Decoding a Neural Circuit
    Controlling Global Animal State in C. Elegans.” <i>ELife</i>. eLife Sciences Publications,
    2015. <a href="https://doi.org/10.7554/elife.04241">https://doi.org/10.7554/elife.04241</a>.
  ieee: P. Laurent <i>et al.</i>, “Decoding a neural circuit controlling global animal
    state in C. elegans,” <i>eLife</i>, vol. 4. eLife Sciences Publications, 2015.
  ista: Laurent P, Soltesz Z, Nelson GM, Chen C, Arellano-Carbajal F, Levy E, de Bono
    M. 2015. Decoding a neural circuit controlling global animal state in C. elegans.
    eLife. 4, e04241.
  mla: Laurent, Patrick, et al. “Decoding a Neural Circuit Controlling Global Animal
    State in C. Elegans.” <i>ELife</i>, vol. 4, e04241, eLife Sciences Publications,
    2015, doi:<a href="https://doi.org/10.7554/elife.04241">10.7554/elife.04241</a>.
  short: P. Laurent, Z. Soltesz, G.M. Nelson, C. Chen, F. Arellano-Carbajal, E. Levy,
    M. de Bono, ELife 4 (2015).
date_created: 2019-03-19T14:23:51Z
date_published: 2015-03-11T00:00:00Z
date_updated: 2021-01-12T08:06:13Z
day: '11'
ddc:
- '570'
doi: 10.7554/elife.04241
extern: '1'
external_id:
  pmid:
  - '25760081'
file:
- access_level: open_access
  checksum: cf641b7a363aecd0a101755d23dee7e0
  content_type: application/pdf
  creator: kschuh
  date_created: 2019-03-19T14:29:43Z
  date_updated: 2020-07-14T12:47:20Z
  file_id: '6121'
  file_name: 2015_elife_Laurent.pdf
  file_size: 6723528
  relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: '         4'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
  issn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Decoding a neural circuit controlling global animal state in C. elegans
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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 4
year: '2015'
...
