---
_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
gn knockouts. The functional GN mutant variant GNfewerroots,
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. eLife. 2024;13. doi:10.7554/elife.68993
apa: Adamowski, M., Matijevic, I., & Friml, J. (2024). Developmental patterning
function of GNOM ARF-GEF mediated from the cell periphery. ELife. eLife
Sciences Publications. https://doi.org/10.7554/elife.68993
chicago: Adamowski, Maciek, Ivana Matijevic, and Jiří Friml. “Developmental Patterning
Function of GNOM ARF-GEF Mediated from the Cell Periphery.” ELife. eLife
Sciences Publications, 2024. https://doi.org/10.7554/elife.68993.
ieee: M. Adamowski, I. Matijevic, and J. Friml, “Developmental patterning function
of GNOM ARF-GEF mediated from the cell periphery,” eLife, 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.” ELife, vol. 13, eLife Sciences Publications,
2024, doi:10.7554/elife.68993.
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: '14683'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables the generation
of genetic mosaic tissue in mice and high-resolution phenotyping at the individual
cell level. Here, we present a protocol for isolating MADM-labeled cells with
high yield for downstream molecular analyses using fluorescence-activated cell
sorting (FACS). We describe steps for generating MADM-labeled mice, perfusion,
single-cell suspension, and debris removal. We then detail procedures for cell
sorting by FACS and downstream analysis. This protocol is suitable for embryonic
to adult mice.\r\nFor complete details on the use and execution of this protocol,
please refer to Contreras et al. (2021).1"
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: This research was supported by the Scientific Service Units (SSU)
at IST Austria through resources provided by the Imaging & Optics Facility (IOF)
and Preclinical Facilities (PCF). N.A. received support from FWF Firnberg-Programme
(T 1031). G.C. received support from the European Union’s Horizon 2020 research
and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411
as an ISTplus postdoctoral fellow. This work was also supported by IST Austria institutional
funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European
Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780
LinPro) to S.H.
article_number: '102771'
article_processing_charge: No
article_type: review
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains
labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols.
2023;5(1). doi:10.1016/j.xpro.2023.102771
apa: Amberg, N., Cheung, G. T., & Hippenmeyer, S. (2023). Protocol for sorting
cells from mouse brains labeled with mosaic analysis with double markers by flow
cytometry. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102771
chicago: Amberg, Nicole, Giselle T Cheung, and Simon Hippenmeyer. “Protocol for
Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers
by Flow Cytometry.” STAR Protocols. Elsevier, 2023. https://doi.org/10.1016/j.xpro.2023.102771.
ieee: N. Amberg, G. T. Cheung, and S. Hippenmeyer, “Protocol for sorting cells from
mouse brains labeled with mosaic analysis with double markers by flow cytometry,”
STAR Protocols, vol. 5, no. 1. Elsevier, 2023.
ista: Amberg N, Cheung GT, Hippenmeyer S. 2023. Protocol for sorting cells from
mouse brains labeled with mosaic analysis with double markers by flow cytometry.
STAR Protocols. 5(1), 102771.
mla: Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled
with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols,
vol. 5, no. 1, 102771, Elsevier, 2023, doi:10.1016/j.xpro.2023.102771.
short: N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2023).
date_created: 2023-12-13T11:48:05Z
date_published: 2023-12-08T00:00:00Z
date_updated: 2023-12-18T08:06:14Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2023.102771
ec_funded: 1
external_id:
pmid:
- '38070137'
intvolume: ' 5'
issue: '1'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.xpro.2023.102771
month: '12'
oa: 1
oa_version: Submitted Version
pmid: 1
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: STAR Protocols
publication_identifier:
issn:
- 2666-1667
publication_status: epub_ahead
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Protocol for sorting cells from mouse brains labeled with mosaic analysis with
double markers by flow cytometry
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: 5
year: '2023'
...
---
_id: '10812'
abstract:
- lang: eng
text: Several promising strategies based on combining or cycling different antibiotics
have been proposed to increase efficacy and counteract resistance evolution, but
we still lack a deep understanding of the physiological responses and genetic
mechanisms that underlie antibiotic interactions and the clinical applicability
of these strategies. In antibiotic-exposed bacteria, the combined effects of physiological
stress responses and emerging resistance mutations (occurring at different time
scales) generate complex and often unpredictable dynamics. In this Review, we
present our current understanding of bacterial cell physiology and genetics of
responses to antibiotics. We emphasize recently discovered mechanisms of synergistic
and antagonistic drug interactions, hysteresis in temporal interactions between
antibiotics that arise from microbial physiology and interactions between antibiotics
and resistance mutations that can cause collateral sensitivity or cross-resistance.
We discuss possible connections between the different phenomena and indicate relevant
research directions. A better and more unified understanding of drug and genetic
interactions is likely to advance antibiotic therapy.
acknowledgement: The authors thank B. Kavčič and H. Schulenburg for constructive feedback
on the manuscript.
article_processing_charge: No
article_type: review
author:
- first_name: Roderich
full_name: Römhild, Roderich
id: 68E56E44-62B0-11EA-B963-444F3DDC885E
last_name: Römhild
orcid: 0000-0001-9480-5261
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Dan I.
full_name: Andersson, Dan I.
last_name: Andersson
citation:
ama: Römhild R, Bollenbach MT, Andersson DI. The physiology and genetics of bacterial
responses to antibiotic combinations. Nature Reviews Microbiology. 2022;20:478-490.
doi:10.1038/s41579-022-00700-5
apa: Römhild, R., Bollenbach, M. T., & Andersson, D. I. (2022). The physiology
and genetics of bacterial responses to antibiotic combinations. Nature Reviews
Microbiology. Springer Nature. https://doi.org/10.1038/s41579-022-00700-5
chicago: Römhild, Roderich, Mark Tobias Bollenbach, and Dan I. Andersson. “The Physiology
and Genetics of Bacterial Responses to Antibiotic Combinations.” Nature Reviews
Microbiology. Springer Nature, 2022. https://doi.org/10.1038/s41579-022-00700-5.
ieee: R. Römhild, M. T. Bollenbach, and D. I. Andersson, “The physiology and genetics
of bacterial responses to antibiotic combinations,” Nature Reviews Microbiology,
vol. 20. Springer Nature, pp. 478–490, 2022.
ista: Römhild R, Bollenbach MT, Andersson DI. 2022. The physiology and genetics
of bacterial responses to antibiotic combinations. Nature Reviews Microbiology.
20, 478–490.
mla: Römhild, Roderich, et al. “The Physiology and Genetics of Bacterial Responses
to Antibiotic Combinations.” Nature Reviews Microbiology, vol. 20, Springer
Nature, 2022, pp. 478–90, doi:10.1038/s41579-022-00700-5.
short: R. Römhild, M.T. Bollenbach, D.I. Andersson, Nature Reviews Microbiology
20 (2022) 478–490.
date_created: 2022-03-04T04:33:49Z
date_published: 2022-08-01T00:00:00Z
date_updated: 2023-08-02T14:41:44Z
day: '01'
department:
- _id: CaGu
doi: 10.1038/s41579-022-00700-5
external_id:
isi:
- '000763891900001'
pmid:
- '35241807'
intvolume: ' 20'
isi: 1
keyword:
- General Immunology and Microbiology
- Microbiology
- Infectious Diseases
language:
- iso: eng
month: '08'
oa_version: None
page: 478-490
pmid: 1
publication: Nature Reviews Microbiology
publication_identifier:
eissn:
- 1740-1534
issn:
- 1740-1526
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: The physiology and genetics of bacterial responses to antibiotic combinations
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2022'
...
---
_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. eLife. 2022;11. doi:10.7554/elife.75842
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. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.75842
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.” ELife. eLife Sciences Publications, 2022.
https://doi.org/10.7554/elife.75842.
ieee: L. Gonzalez Somermeyer et al., “Heterogeneity of the GFP fitness landscape
and data-driven protein design,” eLife, 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.” ELife, vol. 11, 75842, eLife Sciences
Publications, 2022, doi:10.7554/elife.75842.
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: '12117'
abstract:
- lang: eng
text: "To understand how potential gene manipulations affect in vitro microglia,
we provide a set of short protocols to evaluate microglia identity and function.
We detail steps for immunostaining to determine microglia identity. We describe
three functional assays for microglia: phagocytosis, calcium response following
ATP stimulation, and cytokine expression upon inflammatory stimuli. We apply these
protocols to human induced-pluripotent-stem-cell (hiPSC)-derived microglia, but
they can be also applied to other in vitro microglial models including primary
mouse microglia.\r\nFor complete details on the use and execution of this protocol,
please refer to Bartalska et al. (2022).1"
acknowledged_ssus:
- _id: Bio
acknowledgement: This project has received funding from the European Research Council
(ERC) under the European Union’s Horizon 2020 research and innovation program (grant
No. 715571 to S.S.) and from the Gesellschaft für Forschungsförderung Niederösterreich
(grant No. Sc19-017 to V.H.). We thank Rouven Schulz and Alessandro Venturino for
their insights into functional assays and data analysis, Verena Seiboth for insights
into necessary institutional permission, and ISTA imaging & optics facility (IOF)
especially Bernhard Hochreiter for their support.
article_number: '101866'
article_processing_charge: No
article_type: letter_note
author:
- first_name: Verena
full_name: Hübschmann, Verena
id: 32B7C918-F248-11E8-B48F-1D18A9856A87
last_name: Hübschmann
- first_name: Medina
full_name: Korkut, Medina
id: 4B51CE74-F248-11E8-B48F-1D18A9856A87
last_name: Korkut
orcid: 0000-0003-4309-2251
- first_name: Sandra
full_name: Siegert, Sandra
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
citation:
ama: Hübschmann V, Korkut M, Siegert S. Assessing human iPSC-derived microglia identity
and function by immunostaining, phagocytosis, calcium activity, and inflammation
assay. STAR Protocols. 2022;3(4). doi:10.1016/j.xpro.2022.101866
apa: Hübschmann, V., Korkut, M., & Siegert, S. (2022). Assessing human iPSC-derived
microglia identity and function by immunostaining, phagocytosis, calcium activity,
and inflammation assay. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2022.101866
chicago: Hübschmann, Verena, Medina Korkut, and Sandra Siegert. “Assessing Human
IPSC-Derived Microglia Identity and Function by Immunostaining, Phagocytosis,
Calcium Activity, and Inflammation Assay.” STAR Protocols. Elsevier, 2022.
https://doi.org/10.1016/j.xpro.2022.101866.
ieee: V. Hübschmann, M. Korkut, and S. Siegert, “Assessing human iPSC-derived microglia
identity and function by immunostaining, phagocytosis, calcium activity, and inflammation
assay,” STAR Protocols, vol. 3, no. 4. Elsevier, 2022.
ista: Hübschmann V, Korkut M, Siegert S. 2022. Assessing human iPSC-derived microglia
identity and function by immunostaining, phagocytosis, calcium activity, and inflammation
assay. STAR Protocols. 3(4), 101866.
mla: Hübschmann, Verena, et al. “Assessing Human IPSC-Derived Microglia Identity
and Function by Immunostaining, Phagocytosis, Calcium Activity, and Inflammation
Assay.” STAR Protocols, vol. 3, no. 4, 101866, Elsevier, 2022, doi:10.1016/j.xpro.2022.101866.
short: V. Hübschmann, M. Korkut, S. Siegert, STAR Protocols 3 (2022).
date_created: 2023-01-12T11:56:38Z
date_published: 2022-12-16T00:00:00Z
date_updated: 2023-11-02T12:21:32Z
day: '16'
ddc:
- '570'
department:
- _id: SaSi
- _id: GradSch
doi: 10.1016/j.xpro.2022.101866
ec_funded: 1
file:
- access_level: open_access
checksum: 3c71b8a60633d42c2f77c49025d5559b
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T09:50:51Z
date_updated: 2023-01-23T09:50:51Z
file_id: '12340'
file_name: 2022_STARProtocols_Huebschmann.pdf
file_size: 6251945
relation: main_file
success: 1
file_date_updated: 2023-01-23T09:50:51Z
has_accepted_license: '1'
intvolume: ' 3'
issue: '4'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25D4A630-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715571'
name: Microglia action towards neuronal circuit formation and function in health
and disease
- _id: 9B99D380-BA93-11EA-9121-9846C619BF3A
grant_number: SC19-017
name: How human microglia shape developing neurons during health and inflammation
publication: STAR Protocols
publication_identifier:
issn:
- 2666-1667
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '11478'
relation: other
status: public
scopus_import: '1'
status: public
title: Assessing human iPSC-derived microglia identity and function by immunostaining,
phagocytosis, calcium activity, and inflammation assay
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 3
year: '2022'
...
---
_id: '12157'
abstract:
- lang: eng
text: 'Polygenic adaptation is thought to be ubiquitous, yet remains poorly understood.
Here, we model this process analytically, in the plausible setting of a highly
polygenic, quantitative trait that experiences a sudden shift in the fitness optimum.
We show how the mean phenotype changes over time, depending on the effect sizes
of loci that contribute to variance in the trait, and characterize the allele
dynamics at these loci. Notably, we describe the two phases of the allele dynamics:
The first is a rapid phase, in which directional selection introduces small frequency
differences between alleles whose effects are aligned with or opposed to the shift,
ultimately leading to small differences in their probability of fixation during
a second, longer phase, governed by stabilizing selection. As we discuss, key
results should hold in more general settings and have important implications for
efforts to identify the genetic basis of adaptation in humans and other species.'
acknowledgement: "We thank Guy Amster, Jeremy Berg, Nick Barton, Yuval Simons and
Molly Przeworski for many helpful discussions, and Jeremy Berg, Graham Coop, Joachim
Hermisson, Guillaume Martin, Will Milligan, Peter Ralph, Yuval Simons, Leo Speidel
and Molly Przeworski for comments on the manuscript.\r\nNational Institutes of Health
GM115889 Laura Katharine Hayward Guy Sella \r\nNational Institutes of Health GM121372
Laura Katharine Hayward"
article_number: '66697'
article_processing_charge: No
article_type: original
author:
- first_name: Laura
full_name: Hayward, Laura
id: fc885ee5-24bf-11eb-ad7b-bcc5104c0c1b
last_name: Hayward
- first_name: Guy
full_name: Sella, Guy
last_name: Sella
citation:
ama: Hayward L, Sella G. Polygenic adaptation after a sudden change in environment.
eLife. 2022;11. doi:10.7554/elife.66697
apa: Hayward, L., & Sella, G. (2022). Polygenic adaptation after a sudden change
in environment. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.66697
chicago: Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change
in Environment.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/elife.66697.
ieee: L. Hayward and G. Sella, “Polygenic adaptation after a sudden change in environment,”
eLife, vol. 11. eLife Sciences Publications, 2022.
ista: Hayward L, Sella G. 2022. Polygenic adaptation after a sudden change in environment.
eLife. 11, 66697.
mla: Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change
in Environment.” ELife, vol. 11, 66697, eLife Sciences Publications, 2022,
doi:10.7554/elife.66697.
short: L. Hayward, G. Sella, ELife 11 (2022).
date_created: 2023-01-12T12:09:00Z
date_published: 2022-09-26T00:00:00Z
date_updated: 2023-08-04T09:04:58Z
day: '26'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.7554/elife.66697
external_id:
isi:
- '000890735600001'
file:
- access_level: open_access
checksum: 28de155b231ac1c8d4501c98b2fb359a
content_type: application/pdf
creator: dernst
date_created: 2023-01-24T12:21:32Z
date_updated: 2023-01-24T12:21:32Z
file_id: '12363'
file_name: 2022_eLife_Hayward.pdf
file_size: 18935612
relation: main_file
success: 1
file_date_updated: 2023-01-24T12:21:32Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Polygenic adaptation after a sudden change in environment
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '12261'
abstract:
- lang: eng
text: 'Dose–response relationships are a general concept for quantitatively describing
biological systems across multiple scales, from the molecular to the whole-cell
level. A clinically relevant example is the bacterial growth response to antibiotics,
which is routinely characterized by dose–response curves. The shape of the dose–response
curve varies drastically between antibiotics and plays a key role in treatment,
drug interactions, and resistance evolution. However, the mechanisms shaping the
dose–response curve remain largely unclear. Here, we show in Escherichia coli
that the distinctively shallow dose–response curve of the antibiotic trimethoprim
is caused by a negative growth-mediated feedback loop: Trimethoprim slows growth,
which in turn weakens the effect of this antibiotic. At the molecular level, this
feedback is caused by the upregulation of the drug target dihydrofolate reductase
(FolA/DHFR). We show that this upregulation is not a specific response to trimethoprim
but follows a universal trend line that depends primarily on the growth rate,
irrespective of its cause. Rewiring the feedback loop alters the dose–response
curve in a predictable manner, which we corroborate using a mathematical model
of cellular resource allocation and growth. Our results indicate that growth-mediated
feedback loops may shape drug responses more generally and could be exploited
to design evolutionary traps that enable selection against drug resistance.'
acknowledged_ssus:
- _id: M-Shop
acknowledgement: This work was in part supported by Human Frontier Science Program
GrantRGP0042/2013, Marie Curie Career Integration Grant303507, AustrianScience Fund
(FWF) Grant P27201-B22, and German Research Foundation(DFG) Collaborative Research
Center (SFB)1310to TB. SAA was supportedby the European Union’s Horizon2020Research
and Innovation Programunder the Marie Skłodowska-Curie Grant agreement No707352.
We wouldlike to thank the Bollenbach group for regular fruitful discussions. We
areparticularly thankful for the technical assistance of Booshini Fernando andfor
discussions of the theoretical aspects with Gerrit Ansmann. We areindebted to Bor
Kavˇciˇc for invaluable advice, help with setting up theluciferase-based growth
monitoring system, and for sharing plasmids. Weacknowledge the IST Austria Miba
Machine Shop for their support inbuilding a housing for the stacker of the plate
reader, which enabled thehigh-throughput luciferase-based experiments. We are grateful
to RosalindAllen, Bor Kavˇciˇc and Dor Russ for feedback on the manuscript. Open
Accessfunding enabled and organized by Projekt DEAL.
article_number: e10490
article_processing_charge: No
article_type: original
author:
- first_name: Andreas
full_name: Angermayr, Andreas
id: 4677C796-F248-11E8-B48F-1D18A9856A87
last_name: Angermayr
orcid: 0000-0001-8619-2223
- first_name: Tin Yau
full_name: Pang, Tin Yau
last_name: Pang
- first_name: Guillaume
full_name: Chevereau, Guillaume
last_name: Chevereau
- first_name: Karin
full_name: Mitosch, Karin
id: 39B66846-F248-11E8-B48F-1D18A9856A87
last_name: Mitosch
- first_name: Martin J
full_name: Lercher, Martin J
last_name: Lercher
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. Growth‐mediated
negative feedback shapes quantitative antibiotic response. Molecular Systems
Biology. 2022;18(9). doi:10.15252/msb.202110490
apa: Angermayr, A., Pang, T. Y., Chevereau, G., Mitosch, K., Lercher, M. J., &
Bollenbach, M. T. (2022). Growth‐mediated negative feedback shapes quantitative
antibiotic response. Molecular Systems Biology. Embo Press. https://doi.org/10.15252/msb.202110490
chicago: Angermayr, Andreas, Tin Yau Pang, Guillaume Chevereau, Karin Mitosch, Martin
J Lercher, and Mark Tobias Bollenbach. “Growth‐mediated Negative Feedback Shapes
Quantitative Antibiotic Response.” Molecular Systems Biology. Embo Press,
2022. https://doi.org/10.15252/msb.202110490.
ieee: A. Angermayr, T. Y. Pang, G. Chevereau, K. Mitosch, M. J. Lercher, and M.
T. Bollenbach, “Growth‐mediated negative feedback shapes quantitative antibiotic
response,” Molecular Systems Biology, vol. 18, no. 9. Embo Press, 2022.
ista: Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. 2022.
Growth‐mediated negative feedback shapes quantitative antibiotic response. Molecular
Systems Biology. 18(9), e10490.
mla: Angermayr, Andreas, et al. “Growth‐mediated Negative Feedback Shapes Quantitative
Antibiotic Response.” Molecular Systems Biology, vol. 18, no. 9, e10490,
Embo Press, 2022, doi:10.15252/msb.202110490.
short: A. Angermayr, T.Y. Pang, G. Chevereau, K. Mitosch, M.J. Lercher, M.T. Bollenbach,
Molecular Systems Biology 18 (2022).
date_created: 2023-01-16T09:58:34Z
date_published: 2022-09-01T00:00:00Z
date_updated: 2023-08-04T09:51:49Z
day: '01'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.15252/msb.202110490
external_id:
isi:
- '000856482800001'
file:
- access_level: open_access
checksum: 8b1d8f5ea20c8408acf466435fb6ae01
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T09:49:55Z
date_updated: 2023-01-30T09:49:55Z
file_id: '12446'
file_name: 2022_MolecularSystemsBio_Angermayr.pdf
file_size: 1098812
relation: main_file
success: 1
file_date_updated: 2023-01-30T09:49:55Z
has_accepted_license: '1'
intvolume: ' 18'
isi: 1
issue: '9'
keyword:
- Applied Mathematics
- Computational Theory and Mathematics
- General Agricultural and Biological Sciences
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- Information Systems
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: Molecular Systems Biology
publication_identifier:
eissn:
- 1744-4292
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Growth‐mediated negative feedback shapes quantitative antibiotic response
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 18
year: '2022'
...
---
_id: '12288'
abstract:
- lang: eng
text: To understand the function of neuronal circuits, it is crucial to disentangle
the connectivity patterns within the network. However, most tools currently used
to explore connectivity have low throughput, low selectivity, or limited accessibility.
Here, we report the development of an improved packaging system for the production
of the highly neurotropic RVdGenvA-CVS-N2c rabies viral vectors, yielding titers
orders of magnitude higher with no background contamination, at a fraction of
the production time, while preserving the efficiency of transsynaptic labeling.
Along with the production pipeline, we developed suites of ‘starter’ AAV and bicistronic
RVdG-CVS-N2c vectors, enabling retrograde labeling from a wide range of neuronal
populations, tailored for diverse experimental requirements. We demonstrate the
power and flexibility of the new system by uncovering hidden local and distal
inhibitory connections in the mouse hippocampal formation and by imaging the functional
properties of a cortical microcircuit across weeks. Our novel production pipeline
provides a convenient approach to generate new rabies vectors, while our toolkit
flexibly and efficiently expands the current capacity to label, manipulate and
image the neuronal activity of interconnected neuronal circuits in vitro and in
vivo.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We thank F Marr for technical assistance, A Murray for RVdG-CVS-N2c
viruses and Neuro2A packaging cell-lines and J Watson for reading the manuscript.
This research was supported by the Scientific Service Units (SSU) of IST-Austria
through resources provided by the Imaging and Optics Facility (IOF) and the Preclinical
Facility (PCF). This project was funded by the European Research Council (ERC) under
the European Union’s Horizon 2020 research and innovation programme (ERC advanced
grant No 692692, PJ, ERC starting grant No 756502, MJ), the Fond zur Förderung der
Wissenschaftlichen Forschung (Z 312-B27, Wittgenstein award, PJ), the Human Frontier
Science Program (LT000256/2018-L, AS) and EMBO (ALTF 1098-2017, AS).
article_number: '79848'
article_processing_charge: No
article_type: original
author:
- first_name: Anton L
full_name: Sumser, Anton L
id: 3320A096-F248-11E8-B48F-1D18A9856A87
last_name: Sumser
orcid: 0000-0002-4792-1881
- first_name: Maximilian A
full_name: Jösch, Maximilian A
id: 2BD278E6-F248-11E8-B48F-1D18A9856A87
last_name: Jösch
orcid: 0000-0002-3937-1330
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Yoav
full_name: Ben Simon, Yoav
id: 43DF3136-F248-11E8-B48F-1D18A9856A87
last_name: Ben Simon
citation:
ama: Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. Fast, high-throughput production
of improved rabies viral vectors for specific, efficient and versatile transsynaptic
retrograde labeling. eLife. 2022;11. doi:10.7554/elife.79848
apa: Sumser, A. L., Jösch, M. A., Jonas, P. M., & Ben Simon, Y. (2022). Fast,
high-throughput production of improved rabies viral vectors for specific, efficient
and versatile transsynaptic retrograde labeling. ELife. eLife Sciences
Publications. https://doi.org/10.7554/elife.79848
chicago: Sumser, Anton L, Maximilian A Jösch, Peter M Jonas, and Yoav Ben Simon.
“Fast, High-Throughput Production of Improved Rabies Viral Vectors for Specific,
Efficient and Versatile Transsynaptic Retrograde Labeling.” ELife. eLife
Sciences Publications, 2022. https://doi.org/10.7554/elife.79848.
ieee: A. L. Sumser, M. A. Jösch, P. M. Jonas, and Y. Ben Simon, “Fast, high-throughput
production of improved rabies viral vectors for specific, efficient and versatile
transsynaptic retrograde labeling,” eLife, vol. 11. eLife Sciences Publications,
2022.
ista: Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. 2022. Fast, high-throughput production
of improved rabies viral vectors for specific, efficient and versatile transsynaptic
retrograde labeling. eLife. 11, 79848.
mla: Sumser, Anton L., et al. “Fast, High-Throughput Production of Improved Rabies
Viral Vectors for Specific, Efficient and Versatile Transsynaptic Retrograde Labeling.”
ELife, vol. 11, 79848, eLife Sciences Publications, 2022, doi:10.7554/elife.79848.
short: A.L. Sumser, M.A. Jösch, P.M. Jonas, Y. Ben Simon, ELife 11 (2022).
date_created: 2023-01-16T10:04:15Z
date_published: 2022-09-15T00:00:00Z
date_updated: 2023-08-04T10:29:48Z
day: '15'
ddc:
- '570'
department:
- _id: MaJö
- _id: PeJo
doi: 10.7554/elife.79848
ec_funded: 1
external_id:
isi:
- '000892204300001'
pmid:
- '36040301'
file:
- access_level: open_access
checksum: 5a2a65e3e7225090c3d8199f3bbd7b7b
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T11:50:53Z
date_updated: 2023-01-30T11:50:53Z
file_id: '12463'
file_name: 2022_eLife_Sumser.pdf
file_size: 8506811
relation: main_file
success: 1
file_date_updated: 2023-01-30T11:50:53Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glumatergic synapse
- _id: 2634E9D2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '756502'
name: Circuits of Visual Attention
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z00312
name: The Wittgenstein Prize
- _id: 266D407A-B435-11E9-9278-68D0E5697425
grant_number: LT000256
name: Neuronal networks of salience and spatial detection in the murine superior
colliculus
- _id: 264FEA02-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1098-2017
name: Connecting sensory with motor processing in the superior colliculus
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Fast, high-throughput production of improved rabies viral vectors for specific,
efficient and versatile transsynaptic retrograde labeling
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '9387'
abstract:
- lang: eng
text: We report the complete analysis of a deterministic model of deleterious mutations
and negative selection against them at two haploid loci without recombination.
As long as mutation is a weaker force than selection, mutant alleles remain rare
at the only stable equilibrium, and otherwise, a variety of dynamics are possible.
If the mutation-free genotype is absent, generally the only stable equilibrium
is the one that corresponds to fixation of the mutant allele at the locus where
it is less deleterious. This result suggests that fixation of a deleterious allele
that follows a click of the Muller’s ratchet is governed by natural selection,
instead of random drift.
acknowledgement: This work was supported by the Russian Science Foundation grant N
16-14-10173.
article_number: '110729'
article_processing_charge: No
article_type: original
author:
- first_name: Kseniia
full_name: Khudiakova, Kseniia
id: 4E6DC800-AE37-11E9-AC72-31CAE5697425
last_name: Khudiakova
orcid: 0000-0002-6246-1465
- first_name: Tatiana Yu.
full_name: Neretina, Tatiana Yu.
last_name: Neretina
- first_name: Alexey S.
full_name: Kondrashov, Alexey S.
last_name: Kondrashov
citation:
ama: Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection
balance and Muller’s ratchet. Journal of Theoretical Biology. 2021;524.
doi:10.1016/j.jtbi.2021.110729
apa: Khudiakova, K., Neretina, T. Y., & Kondrashov, A. S. (2021). Two linked
loci under mutation-selection balance and Muller’s ratchet. Journal of Theoretical
Biology. Elsevier . https://doi.org/10.1016/j.jtbi.2021.110729
chicago: Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two
Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” Journal
of Theoretical Biology. Elsevier , 2021. https://doi.org/10.1016/j.jtbi.2021.110729.
ieee: K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under
mutation-selection balance and Muller’s ratchet,” Journal of Theoretical Biology,
vol. 524. Elsevier , 2021.
ista: Khudiakova K, Neretina TY, Kondrashov AS. 2021. Two linked loci under mutation-selection
balance and Muller’s ratchet. Journal of Theoretical Biology. 524, 110729.
mla: Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance
and Muller’s Ratchet.” Journal of Theoretical Biology, vol. 524, 110729,
Elsevier , 2021, doi:10.1016/j.jtbi.2021.110729.
short: K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology
524 (2021).
date_created: 2021-05-12T05:58:42Z
date_published: 2021-04-24T00:00:00Z
date_updated: 2023-08-08T13:32:40Z
day: '24'
department:
- _id: GradSch
doi: 10.1016/j.jtbi.2021.110729
external_id:
isi:
- '000659161500002'
intvolume: ' 524'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- Modelling and Simulation
- Statistics and Probability
- General Immunology and Microbiology
- Applied Mathematics
- General Agricultural and Biological Sciences
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/477489v1
month: '04'
oa: 1
oa_version: Preprint
publication: Journal of Theoretical Biology
publication_identifier:
issn:
- 0022-5193
publication_status: published
publisher: 'Elsevier '
quality_controlled: '1'
status: public
title: Two linked loci under mutation-selection balance and Muller’s ratchet
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 524
year: '2021'
...
---
_id: '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.
eLife. 2021;10. doi:10.7554/elife.71575
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.
ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.71575
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.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.71575.
ieee: M. J. Conde-Dusman et al., “Control of protein synthesis and memory
by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” eLife,
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.” ELife,
vol. 10, e71575, eLife Sciences Publications, 2021, doi:10.7554/elife.71575.
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: '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. eLife. 2020;9. doi:10.7554/elife.54383
apa: 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.
eLife Sciences Publications. https://doi.org/10.7554/elife.54383
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.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/elife.54383.
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,” eLife, 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.” ELife, vol. 9, e54383, eLife Sciences Publications,
2020, doi:10.7554/elife.54383.
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: '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. eLife. 2019;8. doi:10.7554/elife.49796
apa: 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. eLife Sciences Publications. https://doi.org/10.7554/elife.49796
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.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/elife.49796.
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,” eLife, 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.” ELife, vol. 8,
e49796, eLife Sciences Publications, 2019, doi:10.7554/elife.49796.
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: '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.
eLife. 2019;8. doi:10.7554/elife.42530
apa: 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. eLife Sciences Publications, Ltd. https://doi.org/10.7554/elife.42530
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.” ELife. eLife Sciences Publications, Ltd, 2019.
https://doi.org/10.7554/elife.42530.
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,” eLife, 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.” ELife,
vol. 8, 42530, eLife Sciences Publications, Ltd, 2019, doi:10.7554/elife.42530.
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: '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. eLife. 2017;6. doi:10.7554/elife.30292
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. ELife.
eLife Sciences Publications. https://doi.org/10.7554/elife.30292
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.” ELife. eLife Sciences Publications, 2017.
https://doi.org/10.7554/elife.30292.
ieee: S. C. J. Helle et al., “Mechanical force induces mitochondrial fission,”
eLife, 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.” ELife, vol. 6, e30292, eLife Sciences Publications, 2017, doi:10.7554/elife.30292.
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:
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doi: 10.7554/elife.30292
extern: '1'
external_id:
pmid:
- '29119945'
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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
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publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
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status: public
title: Mechanical force induces mitochondrial fission
tmp:
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