---
_id: '14788'
abstract:
- lang: eng
text: "Eukaryotic cells use clathrin-mediated endocytosis to take up a large range
of extracellular cargo. During endocytosis, a clathrin coat forms on the plasma
membrane, but it remains controversial when and how it is remodeled into a spherical
vesicle.\r\nHere, we use 3D superresolution microscopy to determine the precise
geometry of the clathrin coat at large numbers of endocytic sites. Through pseudo-temporal
sorting, we determine the average trajectory of clathrin remodeling during endocytosis.
We find that clathrin coats assemble first on flat membranes to 50% of the coat
area before they become rapidly and continuously bent, and this mechanism is confirmed
in three cell lines. We introduce the cooperative curvature model, which is based
on positive feedback for curvature generation. It accurately describes the measured
shapes and dynamics of the clathrin coat and could represent a general mechanism
for clathrin coat remodeling on the plasma membrane."
acknowledgement: We thank the entire Ries and Kaksonen labs for fruitful discussions
and support. This work was supported by the European Research Council (ERC CoG-724489
to J. Ries), the National Institutes of Health Common Fund 4D Nucleome Program (Grant
U01 to J. Ries), the Human Frontier Science Program (RGY0065/2017 to J. Ries), the
EMBL Interdisciplinary Postdoc Programme (EIPOD) under Marie Curie Actions COFUND
(Grant 229597 to O. Avinoam), the European Molecular Biology Laboratory (M. Mund,
A. Tschanz, Y.-L. Wu and J. Ries), and the Swiss National Science Foundation (grant
310030B_182825 and NCCR Chemical Biology to M. Kaksonen). O. Avinoam is an incumbent
of the Miriam Berman Presidential Development Chair.
article_number: e202206038
article_processing_charge: No
article_type: original
author:
- first_name: Markus
full_name: Mund, Markus
last_name: Mund
- first_name: Aline
full_name: Tschanz, Aline
last_name: Tschanz
- first_name: Yu-Le
full_name: Wu, Yu-Le
last_name: Wu
- first_name: Felix F
full_name: Frey, Felix F
id: a0270b37-8f1a-11ec-95c7-8e710c59a4f3
last_name: Frey
orcid: 0000-0001-8501-6017
- first_name: Johanna L.
full_name: Mehl, Johanna L.
last_name: Mehl
- first_name: Marko
full_name: Kaksonen, Marko
last_name: Kaksonen
- first_name: Ori
full_name: Avinoam, Ori
last_name: Avinoam
- first_name: Ulrich S.
full_name: Schwarz, Ulrich S.
last_name: Schwarz
- first_name: Jonas
full_name: Ries, Jonas
last_name: Ries
citation:
ama: Mund M, Tschanz A, Wu Y-L, et al. Clathrin coats partially preassemble and
subsequently bend during endocytosis. Journal of Cell Biology. 2023;222(3).
doi:10.1083/jcb.202206038
apa: Mund, M., Tschanz, A., Wu, Y.-L., Frey, F. F., Mehl, J. L., Kaksonen, M., …
Ries, J. (2023). Clathrin coats partially preassemble and subsequently bend during
endocytosis. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202206038
chicago: Mund, Markus, Aline Tschanz, Yu-Le Wu, Felix F Frey, Johanna L. Mehl, Marko
Kaksonen, Ori Avinoam, Ulrich S. Schwarz, and Jonas Ries. “Clathrin Coats Partially
Preassemble and Subsequently Bend during Endocytosis.” Journal of Cell Biology.
Rockefeller University Press, 2023. https://doi.org/10.1083/jcb.202206038.
ieee: M. Mund et al., “Clathrin coats partially preassemble and subsequently
bend during endocytosis,” Journal of Cell Biology, vol. 222, no. 3. Rockefeller
University Press, 2023.
ista: Mund M, Tschanz A, Wu Y-L, Frey FF, Mehl JL, Kaksonen M, Avinoam O, Schwarz
US, Ries J. 2023. Clathrin coats partially preassemble and subsequently bend during
endocytosis. Journal of Cell Biology. 222(3), e202206038.
mla: Mund, Markus, et al. “Clathrin Coats Partially Preassemble and Subsequently
Bend during Endocytosis.” Journal of Cell Biology, vol. 222, no. 3, e202206038,
Rockefeller University Press, 2023, doi:10.1083/jcb.202206038.
short: M. Mund, A. Tschanz, Y.-L. Wu, F.F. Frey, J.L. Mehl, M. Kaksonen, O. Avinoam,
U.S. Schwarz, J. Ries, Journal of Cell Biology 222 (2023).
date_created: 2024-01-10T10:45:55Z
date_published: 2023-02-03T00:00:00Z
date_updated: 2024-01-16T10:17:05Z
day: '03'
ddc:
- '570'
department:
- _id: AnSa
doi: 10.1083/jcb.202206038
external_id:
isi:
- '000978065000001'
pmid:
- '36734980'
file:
- access_level: open_access
checksum: 505d5cac36c14b073b68c7fed1a92bd3
content_type: application/pdf
creator: dernst
date_created: 2024-01-16T10:15:09Z
date_updated: 2024-01-16T10:15:09Z
file_id: '14811'
file_name: 2023_JCB_Mund.pdf
file_size: 5678069
relation: main_file
success: 1
file_date_updated: 2024-01-16T10:15:09Z
has_accepted_license: '1'
intvolume: ' 222'
isi: 1
issue: '3'
keyword:
- Cell Biology
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
status: public
title: Clathrin coats partially preassemble and subsequently bend during endocytosis
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: 222
year: '2023'
...
---
_id: '12080'
abstract:
- lang: eng
text: 'Endocytosis is a multistep process involving the sequential recruitment and
action of numerous proteins. This process can be divided into two phases: an early
phase, in which sites of endocytosis are formed, and a late phase in which clathrin-coated
vesicles are formed and internalized into the cytosol, but how these phases link
to each other remains unclear. In this study, we demonstrate that anchoring the
yeast Eps15-like protein Pan1p to the peroxisome triggers most of the events occurring
during the late phase at the peroxisome. At this ectopic location, Pan1p recruits
most proteins that function in the late phases—including actin nucleation promoting
factors—and then initiates actin polymerization. Pan1p also recruited Prk1 kinase
and actin depolymerizing factors, thereby triggering disassembly immediately after
actin assembly and inducing dissociation of endocytic proteins from the peroxisome.
These observations suggest that Pan1p is a key regulator for initiating, processing,
and completing the late phase of endocytosis.'
acknowledgement: 'This work was supported by JSPS KAKENHI GRANT #18K062291, and the
Takeda Science Foundation to J.Y. Toshima, as well as JSPS KAKENHI GRANT #19K065710,
the Uehara Memorial Foundation, and Life Science Foundation of JAPAN to J. Toshima.'
article_number: e202112138
article_processing_charge: No
article_type: original
author:
- first_name: Mariko
full_name: Enshoji, Mariko
last_name: Enshoji
- first_name: Yoshiko
full_name: Miyano, Yoshiko
last_name: Miyano
- first_name: Nao
full_name: Yoshida, Nao
last_name: Yoshida
- first_name: Makoto
full_name: Nagano, Makoto
last_name: Nagano
- first_name: Minami
full_name: Watanabe, Minami
last_name: Watanabe
- first_name: Mayumi
full_name: Kunihiro, Mayumi
last_name: Kunihiro
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Junko Y.
full_name: Toshima, Junko Y.
last_name: Toshima
- first_name: Jiro
full_name: Toshima, Jiro
last_name: Toshima
citation:
ama: Enshoji M, Miyano Y, Yoshida N, et al. Eps15/Pan1p is a master regulator of
the late stages of the endocytic pathway. Journal of Cell Biology. 2022;221(10).
doi:10.1083/jcb.202112138
apa: Enshoji, M., Miyano, Y., Yoshida, N., Nagano, M., Watanabe, M., Kunihiro, M.,
… Toshima, J. (2022). Eps15/Pan1p is a master regulator of the late stages of
the endocytic pathway. Journal of Cell Biology. Rockefeller University
Press. https://doi.org/10.1083/jcb.202112138
chicago: Enshoji, Mariko, Yoshiko Miyano, Nao Yoshida, Makoto Nagano, Minami Watanabe,
Mayumi Kunihiro, Daria E Siekhaus, Junko Y. Toshima, and Jiro Toshima. “Eps15/Pan1p
Is a Master Regulator of the Late Stages of the Endocytic Pathway.” Journal
of Cell Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202112138.
ieee: M. Enshoji et al., “Eps15/Pan1p is a master regulator of the late stages
of the endocytic pathway,” Journal of Cell Biology, vol. 221, no. 10. Rockefeller
University Press, 2022.
ista: Enshoji M, Miyano Y, Yoshida N, Nagano M, Watanabe M, Kunihiro M, Siekhaus
DE, Toshima JY, Toshima J. 2022. Eps15/Pan1p is a master regulator of the late
stages of the endocytic pathway. Journal of Cell Biology. 221(10), e202112138.
mla: Enshoji, Mariko, et al. “Eps15/Pan1p Is a Master Regulator of the Late Stages
of the Endocytic Pathway.” Journal of Cell Biology, vol. 221, no. 10, e202112138,
Rockefeller University Press, 2022, doi:10.1083/jcb.202112138.
short: M. Enshoji, Y. Miyano, N. Yoshida, M. Nagano, M. Watanabe, M. Kunihiro, D.E.
Siekhaus, J.Y. Toshima, J. Toshima, Journal of Cell Biology 221 (2022).
date_created: 2022-09-11T22:01:54Z
date_published: 2022-08-19T00:00:00Z
date_updated: 2023-08-03T13:49:07Z
day: '19'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1083/jcb.202112138
external_id:
isi:
- '000932770500001'
pmid:
- '35984332'
file:
- access_level: open_access
checksum: f2e581e66b5cdab9df81b56e850b3eaa
content_type: application/pdf
creator: dernst
date_created: 2023-01-20T09:32:53Z
date_updated: 2023-02-21T23:30:39Z
embargo: 2023-02-20
file_id: '12321'
file_name: 2022_JCB_Enshoji.pdf
file_size: 7816875
relation: main_file
file_date_updated: 2023-02-21T23:30:39Z
has_accepted_license: '1'
intvolume: ' 221'
isi: 1
issue: '10'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Eps15/Pan1p is a master regulator of the late stages of the endocytic pathway
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 221
year: '2022'
...
---
_id: '12121'
abstract:
- lang: eng
text: Autophagosomes are double-membraned vesicles that traffic harmful or unwanted
cellular macromolecules to the vacuole for recycling. Although autophagosome biogenesis
has been extensively studied, autophagosome maturation, i.e., delivery and fusion
with the vacuole, remains largely unknown in plants. Here, we have identified
an autophagy adaptor, CFS1, that directly interacts with the autophagosome marker
ATG8 and localizes on both membranes of the autophagosome. Autophagosomes form
normally in Arabidopsis thaliana cfs1 mutants, but their delivery to the vacuole
is disrupted. CFS1’s function is evolutionarily conserved in plants, as it also
localizes to the autophagosomes and plays a role in autophagic flux in the liverwort
Marchantia polymorpha. CFS1 regulates autophagic flux by bridging autophagosomes
with the multivesicular body-localized ESCRT-I component VPS23A, leading to the
formation of amphisomes. Similar to CFS1-ATG8 interaction, disrupting the CFS1-VPS23A
interaction blocks autophagic flux and renders plants sensitive to nitrogen starvation.
Altogether, our results reveal a conserved vacuolar sorting hub that regulates
autophagic flux in plants.
acknowledgement: "We thank Suayip Ustün, Karin Schumacher, Erika Isono, Gerd Juergens,
Takashi Ueda, Daniel Hofius, and Liwen Jiang for sharing published materials.\r\nWe
acknowledge funding from Austrian Academy of Sciences, Austrian Science Fund (FWF,
P 32355, P 34944), Austrian Science Fund (FWF-SFB F79), Vienna Science and Technology\r\nFund
(WWTF, LS17-047) to Y. Dagdas; Austrian Academy of Sciences DOC Fellowship to J.
Zhao, Marie Curie VIP2 Fellowship to J.C. De La Concepcion and M. Clavel; Hong Kong
Research Grant Council (GRF14121019, 14113921, AoE/M-05/12, C4002-17G) to B.-H.
Kang. We thank Vienna Biocenter Core Facilities (VBCF) Protein Chemistry, Biooptics,
Plant Sciences, Molecular Biology, and Protein Technologies. We thank J. Matthew
Watson\r\nand members of the Dagdas lab for the critical reading and editing of
the manuscript."
article_number: e202203139
article_processing_charge: No
article_type: original
author:
- first_name: Jierui
full_name: Zhao, Jierui
last_name: Zhao
- first_name: Mai Thu
full_name: Bui, Mai Thu
last_name: Bui
- first_name: Juncai
full_name: Ma, Juncai
last_name: Ma
- first_name: Fabian
full_name: Künzl, Fabian
last_name: Künzl
- first_name: Lorenzo
full_name: Picchianti, Lorenzo
last_name: Picchianti
- first_name: Juan Carlos
full_name: De La Concepcion, Juan Carlos
last_name: De La Concepcion
- first_name: Yixuan
full_name: Chen, Yixuan
last_name: Chen
- first_name: Sofia
full_name: Petsangouraki, Sofia
last_name: Petsangouraki
- first_name: Azadeh
full_name: Mohseni, Azadeh
last_name: Mohseni
- first_name: Marta
full_name: García-Leon, Marta
last_name: García-Leon
- first_name: Marta Salas
full_name: Gomez, Marta Salas
last_name: Gomez
- first_name: Caterina
full_name: Giannini, Caterina
id: e3fdddd5-f6e0-11ea-865d-ca99ee6367f4
last_name: Giannini
- first_name: Dubois
full_name: Gwennogan, Dubois
last_name: Gwennogan
- first_name: Roksolana
full_name: Kobylinska, Roksolana
last_name: Kobylinska
- first_name: Marion
full_name: Clavel, Marion
last_name: Clavel
- first_name: Swen
full_name: Schellmann, Swen
last_name: Schellmann
- first_name: Yvon
full_name: Jaillais, Yvon
last_name: Jaillais
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Byung-Ho
full_name: Kang, Byung-Ho
last_name: Kang
- first_name: Yasin
full_name: Dagdas, Yasin
last_name: Dagdas
citation:
ama: Zhao J, Bui MT, Ma J, et al. Plant autophagosomes mature into amphisomes prior
to their delivery to the central vacuole. Journal of Cell Biology. 2022;221(12).
doi:10.1083/jcb.202203139
apa: Zhao, J., Bui, M. T., Ma, J., Künzl, F., Picchianti, L., De La Concepcion,
J. C., … Dagdas, Y. (2022). Plant autophagosomes mature into amphisomes prior
to their delivery to the central vacuole. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.202203139
chicago: Zhao, Jierui, Mai Thu Bui, Juncai Ma, Fabian Künzl, Lorenzo Picchianti,
Juan Carlos De La Concepcion, Yixuan Chen, et al. “Plant Autophagosomes Mature
into Amphisomes Prior to Their Delivery to the Central Vacuole.” Journal of
Cell Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202203139.
ieee: J. Zhao et al., “Plant autophagosomes mature into amphisomes prior
to their delivery to the central vacuole,” Journal of Cell Biology, vol.
221, no. 12. Rockefeller University Press, 2022.
ista: Zhao J, Bui MT, Ma J, Künzl F, Picchianti L, De La Concepcion JC, Chen Y,
Petsangouraki S, Mohseni A, García-Leon M, Gomez MS, Giannini C, Gwennogan D,
Kobylinska R, Clavel M, Schellmann S, Jaillais Y, Friml J, Kang B-H, Dagdas Y.
2022. Plant autophagosomes mature into amphisomes prior to their delivery to the
central vacuole. Journal of Cell Biology. 221(12), e202203139.
mla: Zhao, Jierui, et al. “Plant Autophagosomes Mature into Amphisomes Prior to
Their Delivery to the Central Vacuole.” Journal of Cell Biology, vol. 221,
no. 12, e202203139, Rockefeller University Press, 2022, doi:10.1083/jcb.202203139.
short: J. Zhao, M.T. Bui, J. Ma, F. Künzl, L. Picchianti, J.C. De La Concepcion,
Y. Chen, S. Petsangouraki, A. Mohseni, M. García-Leon, M.S. Gomez, C. Giannini,
D. Gwennogan, R. Kobylinska, M. Clavel, S. Schellmann, Y. Jaillais, J. Friml,
B.-H. Kang, Y. Dagdas, Journal of Cell Biology 221 (2022).
date_created: 2023-01-12T11:57:10Z
date_published: 2022-12-01T00:00:00Z
date_updated: 2023-08-03T14:20:15Z
day: '01'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1083/jcb.202203139
external_id:
isi:
- '000932958800001'
pmid:
- '36260289'
file:
- access_level: open_access
checksum: 050b5cc4b25e6b94fe3e3cbfe0f5c06b
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T10:30:11Z
date_updated: 2023-01-23T10:30:11Z
file_id: '12342'
file_name: 2022_JCB_Zhao.pdf
file_size: 10365777
relation: main_file
success: 1
file_date_updated: 2023-01-23T10:30:11Z
has_accepted_license: '1'
intvolume: ' 221'
isi: 1
issue: '12'
keyword:
- Cell Biology
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Plant autophagosomes mature into amphisomes prior to their delivery to the
central vacuole
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: 221
year: '2022'
...
---
_id: '12122'
abstract:
- lang: eng
text: Centrosomes play a crucial role during immune cell interactions and initiation
of the immune response. In proliferating cells, centrosome numbers are tightly
controlled and generally limited to one in G1 and two prior to mitosis. Defects
in regulating centrosome numbers have been associated with cell transformation
and tumorigenesis. Here, we report the emergence of extra centrosomes in leukocytes
during immune activation. Upon antigen encounter, dendritic cells pass through
incomplete mitosis and arrest in the subsequent G1 phase leading to tetraploid
cells with accumulated centrosomes. In addition, cell stimulation increases expression
of polo-like kinase 2, resulting in diploid cells with two centrosomes in G1-arrested
cells. During cell migration, centrosomes tightly cluster and act as functional
microtubule-organizing centers allowing for increased persistent locomotion along
gradients of chemotactic cues. Moreover, dendritic cells with extra centrosomes
display enhanced secretion of inflammatory cytokines and optimized T cell responses.
Together, these results demonstrate a previously unappreciated role of extra centrosomes
for regular cell and tissue homeostasis.
acknowledgement: "We thank Markéta Dalecká and Irena Krejzová for their support with
FIB-SEM imaging, the Imaging Methods Core Facility at BIOCEV supported by the Ministry
of Education, Youth and Sports Czech Republic (Large RI Project LM2018129 Czech-BioImaging),
and European Regional Development Fund (project No. CZ.02.1.01/0.0/0.0/18_046/0016045)
for their support with obtaining imaging data presented in this paper. The authors
further thank Andreas Villunger, Florian Gärtner, Frank Bradke, and Sarah Förster
for helpful discussions; Andy Zielinski for help with statistics; and Björn Weiershausen
for assisting with figure illustration.\r\n\r\nThis work was funded by a fellowship
of the Ministry of Innovation, Science and Research of North-Rhine-Westphalia (AZ:
421-8.03.03.02-137069) to E. Kiermaier and the Deutsche Forschungsgemeinschaft (German
Research Foundation) under Germany’s Excellence Strategy – EXC 2151 – 390873048.
R. Hauschild was funded by grant number 2020-225401 from the Chan Zuckerberg Initiative
Donor-Advised Fund, an advised fund of Silicon Valley Community Foundation. M. Hons
is supported by Czech Science Foundation GACR 20-24603Y and Charles University PRIMUS/20/MED/013."
article_number: e202107134
article_processing_charge: No
article_type: original
author:
- first_name: Ann-Kathrin
full_name: Weier, Ann-Kathrin
last_name: Weier
- first_name: Mirka
full_name: Homrich, Mirka
last_name: Homrich
- first_name: Stephanie
full_name: Ebbinghaus, Stephanie
last_name: Ebbinghaus
- first_name: Pavel
full_name: Juda, Pavel
last_name: Juda
- first_name: Eliška
full_name: Miková, Eliška
last_name: Miková
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Lili
full_name: Zhang, Lili
last_name: Zhang
- first_name: Thomas
full_name: Quast, Thomas
last_name: Quast
- first_name: Elvira
full_name: Mass, Elvira
last_name: Mass
- first_name: Andreas
full_name: Schlitzer, Andreas
last_name: Schlitzer
- first_name: Waldemar
full_name: Kolanus, Waldemar
last_name: Kolanus
- first_name: Sven
full_name: Burgdorf, Sven
last_name: Burgdorf
- first_name: Oliver J.
full_name: Gruß, Oliver J.
last_name: Gruß
- first_name: Miroslav
full_name: Hons, Miroslav
last_name: Hons
- first_name: Stefan
full_name: Wieser, Stefan
last_name: Wieser
- first_name: Eva
full_name: Kiermaier, Eva
last_name: Kiermaier
citation:
ama: Weier A-K, Homrich M, Ebbinghaus S, et al. Multiple centrosomes enhance migration
and immune cell effector functions of mature dendritic cells. Journal of Cell
Biology. 2022;221(12). doi:10.1083/jcb.202107134
apa: Weier, A.-K., Homrich, M., Ebbinghaus, S., Juda, P., Miková, E., Hauschild,
R., … Kiermaier, E. (2022). Multiple centrosomes enhance migration and immune
cell effector functions of mature dendritic cells. Journal of Cell Biology.
Rockefeller University Press. https://doi.org/10.1083/jcb.202107134
chicago: Weier, Ann-Kathrin, Mirka Homrich, Stephanie Ebbinghaus, Pavel Juda, Eliška
Miková, Robert Hauschild, Lili Zhang, et al. “Multiple Centrosomes Enhance Migration
and Immune Cell Effector Functions of Mature Dendritic Cells.” Journal of Cell
Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202107134.
ieee: A.-K. Weier et al., “Multiple centrosomes enhance migration and immune
cell effector functions of mature dendritic cells,” Journal of Cell Biology,
vol. 221, no. 12. Rockefeller University Press, 2022.
ista: Weier A-K, Homrich M, Ebbinghaus S, Juda P, Miková E, Hauschild R, Zhang L,
Quast T, Mass E, Schlitzer A, Kolanus W, Burgdorf S, Gruß OJ, Hons M, Wieser S,
Kiermaier E. 2022. Multiple centrosomes enhance migration and immune cell effector
functions of mature dendritic cells. Journal of Cell Biology. 221(12), e202107134.
mla: Weier, Ann-Kathrin, et al. “Multiple Centrosomes Enhance Migration and Immune
Cell Effector Functions of Mature Dendritic Cells.” Journal of Cell Biology,
vol. 221, no. 12, e202107134, Rockefeller University Press, 2022, doi:10.1083/jcb.202107134.
short: A.-K. Weier, M. Homrich, S. Ebbinghaus, P. Juda, E. Miková, R. Hauschild,
L. Zhang, T. Quast, E. Mass, A. Schlitzer, W. Kolanus, S. Burgdorf, O.J. Gruß,
M. Hons, S. Wieser, E. Kiermaier, Journal of Cell Biology 221 (2022).
date_created: 2023-01-12T12:01:09Z
date_published: 2022-12-05T00:00:00Z
date_updated: 2023-08-16T11:29:12Z
day: '05'
ddc:
- '570'
department:
- _id: Bio
doi: 10.1083/jcb.202107134
external_id:
isi:
- '000932941400001'
pmid:
- '36214847 '
file:
- access_level: open_access
checksum: 0c9af38f82af30c6ce528f2caece4246
content_type: application/pdf
creator: dernst
date_created: 2023-08-16T11:24:53Z
date_updated: 2023-08-16T11:24:53Z
file_id: '14065'
file_name: 2023_JCB_Weier.pdf
file_size: 11090179
relation: main_file
success: 1
file_date_updated: 2023-08-16T11:24:53Z
has_accepted_license: '1'
intvolume: ' 221'
isi: 1
issue: '12'
keyword:
- Cell Biology
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: c08e9ad1-5a5b-11eb-8a69-9d1cf3b07473
grant_number: CZI01
name: Tools for automation and feedback microscopy
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multiple centrosomes enhance migration and immune cell effector functions of
mature dendritic cells
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 221
year: '2022'
...
---
_id: '12272'
abstract:
- lang: eng
text: Reading, interpreting and crawling along gradients of chemotactic cues is
one of the most complex questions in cell biology. In this issue, Georgantzoglou
et al. (2022. J. Cell. Biol.https://doi.org/10.1083/jcb.202103207) use in vivo
models to map the temporal sequence of how neutrophils respond to an acutely arising
gradient of chemoattractant.
article_number: e202206127
article_processing_charge: No
article_type: original
author:
- first_name: Julian A
full_name: Stopp, Julian A
id: 489E3F00-F248-11E8-B48F-1D18A9856A87
last_name: Stopp
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Stopp JA, Sixt MK. Plan your trip before you leave: The neutrophils’ search-and-run
journey. Journal of Cell Biology. 2022;221(8). doi:10.1083/jcb.202206127'
apa: 'Stopp, J. A., & Sixt, M. K. (2022). Plan your trip before you leave: The
neutrophils’ search-and-run journey. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.202206127'
chicago: 'Stopp, Julian A, and Michael K Sixt. “Plan Your Trip before You Leave:
The Neutrophils’ Search-and-Run Journey.” Journal of Cell Biology. Rockefeller
University Press, 2022. https://doi.org/10.1083/jcb.202206127.'
ieee: 'J. A. Stopp and M. K. Sixt, “Plan your trip before you leave: The neutrophils’
search-and-run journey,” Journal of Cell Biology, vol. 221, no. 8. Rockefeller
University Press, 2022.'
ista: 'Stopp JA, Sixt MK. 2022. Plan your trip before you leave: The neutrophils’
search-and-run journey. Journal of Cell Biology. 221(8), e202206127.'
mla: 'Stopp, Julian A., and Michael K. Sixt. “Plan Your Trip before You Leave: The
Neutrophils’ Search-and-Run Journey.” Journal of Cell Biology, vol. 221,
no. 8, e202206127, Rockefeller University Press, 2022, doi:10.1083/jcb.202206127.'
short: J.A. Stopp, M.K. Sixt, Journal of Cell Biology 221 (2022).
date_created: 2023-01-16T10:01:08Z
date_published: 2022-07-20T00:00:00Z
date_updated: 2023-12-21T14:30:01Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1083/jcb.202206127
external_id:
isi:
- '000874717200001'
pmid:
- '35856919'
file:
- access_level: open_access
checksum: 6b1620743669679b48b9389bb40f5a11
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T10:39:34Z
date_updated: 2023-01-30T10:39:34Z
file_id: '12451'
file_name: 2022_JourCellBiology_Stopp.pdf
file_size: 969969
relation: main_file
success: 1
file_date_updated: 2023-01-30T10:39:34Z
has_accepted_license: '1'
intvolume: ' 221'
isi: 1
issue: '8'
keyword:
- Cell Biology
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
related_material:
record:
- id: '14697'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: 'Plan your trip before you leave: The neutrophils’ search-and-run journey'
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 221
year: '2022'
...
---
_id: '9094'
abstract:
- lang: eng
text: Dendritic cells (DCs) are crucial for the priming of naive T cells and the
initiation of adaptive immunity. Priming is initiated at a heterologous cell–cell
contact, the immunological synapse (IS). While it is established that F-actin
dynamics regulates signaling at the T cell side of the contact, little is known
about the cytoskeletal contribution on the DC side. Here, we show that the DC
actin cytoskeleton is decisive for the formation of a multifocal synaptic structure,
which correlates with T cell priming efficiency. DC actin at the IS appears in
transient foci that are dynamized by the WAVE regulatory complex (WRC). The absence
of the WRC in DCs leads to stabilized contacts with T cells, caused by an increase
in ICAM1-integrin–mediated cell–cell adhesion. This results in lower numbers of
activated and proliferating T cells, demonstrating an important role for DC actin
in the regulation of immune synapse functionality.
article_number: e202006081
article_processing_charge: No
article_type: original
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: LM
full_name: Altenburger, LM
last_name: Altenburger
- first_name: R
full_name: Hauschild, R
last_name: Hauschild
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: K
full_name: Rottner, K
last_name: Rottner
- first_name: Stradal
full_name: TEB, Stradal
last_name: TEB
- first_name: A
full_name: Diz-Muñoz, A
last_name: Diz-Muñoz
- first_name: JV
full_name: Stein, JV
last_name: Stein
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Altenburger L, Hauschild R, et al. Dendritic cell actin dynamics
control contact duration and priming efficiency at the immunological synapse.
Journal of Cell Biology. 2021;220(4). doi:10.1083/jcb.202006081
apa: Leithner, A. F., Altenburger, L., Hauschild, R., Assen, F. P., Rottner, K.,
TEB, S., … Sixt, M. K. (2021). Dendritic cell actin dynamics control contact duration
and priming efficiency at the immunological synapse. Journal of Cell Biology.
Rockefeller University Press. https://doi.org/10.1083/jcb.202006081
chicago: Leithner, Alexander F, LM Altenburger, R Hauschild, Frank P Assen, K Rottner,
Stradal TEB, A Diz-Muñoz, JV Stein, and Michael K Sixt. “Dendritic Cell Actin
Dynamics Control Contact Duration and Priming Efficiency at the Immunological
Synapse.” Journal of Cell Biology. Rockefeller University Press, 2021.
https://doi.org/10.1083/jcb.202006081.
ieee: A. F. Leithner et al., “Dendritic cell actin dynamics control contact
duration and priming efficiency at the immunological synapse,” Journal of Cell
Biology, vol. 220, no. 4. Rockefeller University Press, 2021.
ista: Leithner AF, Altenburger L, Hauschild R, Assen FP, Rottner K, TEB S, Diz-Muñoz
A, Stein J, Sixt MK. 2021. Dendritic cell actin dynamics control contact duration
and priming efficiency at the immunological synapse. Journal of Cell Biology.
220(4), e202006081.
mla: Leithner, Alexander F., et al. “Dendritic Cell Actin Dynamics Control Contact
Duration and Priming Efficiency at the Immunological Synapse.” Journal of Cell
Biology, vol. 220, no. 4, e202006081, Rockefeller University Press, 2021,
doi:10.1083/jcb.202006081.
short: A.F. Leithner, L. Altenburger, R. Hauschild, F.P. Assen, K. Rottner, S. TEB,
A. Diz-Muñoz, J. Stein, M.K. Sixt, Journal of Cell Biology 220 (2021).
date_created: 2021-02-05T10:08:04Z
date_published: 2021-04-05T00:00:00Z
date_updated: 2023-09-05T13:57:53Z
day: '05'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1083/jcb.202006081
external_id:
isi:
- '000626365700001'
pmid:
- '33533935'
file:
- access_level: open_access
checksum: 843ebc153847c8626e13c9c5ce71d533
content_type: application/pdf
creator: dernst
date_created: 2022-05-12T14:16:21Z
date_updated: 2022-05-12T14:16:21Z
file_id: '11367'
file_name: 2021_JournCellBiology_Leithner.pdf
file_size: 5102328
relation: main_file
success: 1
file_date_updated: 2022-05-12T14:16:21Z
has_accepted_license: '1'
intvolume: ' 220'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dendritic cell actin dynamics control contact duration and priming efficiency
at the immunological synapse
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 220
year: '2021'
...
---
_id: '10337'
abstract:
- lang: eng
text: The T cell receptor (TCR) pathway receives, processes, and amplifies the signal
from pathogenic antigens to the activation of T cells. Although major components
in this pathway have been identified, the knowledge on how individual components
cooperate to effectively transduce signals remains limited. Phase separation emerges
as a biophysical principle in organizing signaling molecules into liquid-like
condensates. Here, we report that phospholipase Cγ1 (PLCγ1) promotes phase separation
of LAT, a key adaptor protein in the TCR pathway. PLCγ1 directly cross-links LAT
through its two SH2 domains. PLCγ1 also protects LAT from dephosphorylation by
the phosphatase CD45 and promotes LAT-dependent ERK activation and SLP76 phosphorylation.
Intriguingly, a nonmonotonic effect of PLCγ1 on LAT clustering was discovered.
Computer simulations, based on patchy particles, revealed how the cluster size
is regulated by protein compositions. Together, these results define a critical
function of PLCγ1 in promoting phase separation of the LAT complex and TCR signal
transduction.
acknowledgement: Charles H. Hood Foundation (NO AWARD) ; Rally Foundation (NO AWARD)
article_number: e202009154
article_processing_charge: No
article_type: original
author:
- first_name: Longhui
full_name: Zeng, Longhui
last_name: Zeng
- first_name: Ivan
full_name: Palaia, Ivan
last_name: Palaia
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
- first_name: Xiaolei
full_name: Su, Xiaolei
last_name: Su
citation:
ama: Zeng L, Palaia I, Šarić A, Su X. PLCγ1 promotes phase separation of T cell
signaling components. Journal of Cell Biology. 2021;220(6). doi:10.1083/jcb.202009154
apa: Zeng, L., Palaia, I., Šarić, A., & Su, X. (2021). PLCγ1 promotes phase
separation of T cell signaling components. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.202009154
chicago: Zeng, Longhui, Ivan Palaia, Anđela Šarić, and Xiaolei Su. “PLCγ1 Promotes
Phase Separation of T Cell Signaling Components.” Journal of Cell Biology.
Rockefeller University Press, 2021. https://doi.org/10.1083/jcb.202009154.
ieee: L. Zeng, I. Palaia, A. Šarić, and X. Su, “PLCγ1 promotes phase separation
of T cell signaling components,” Journal of Cell Biology, vol. 220, no.
6. Rockefeller University Press, 2021.
ista: Zeng L, Palaia I, Šarić A, Su X. 2021. PLCγ1 promotes phase separation of
T cell signaling components. Journal of Cell Biology. 220(6), e202009154.
mla: Zeng, Longhui, et al. “PLCγ1 Promotes Phase Separation of T Cell Signaling
Components.” Journal of Cell Biology, vol. 220, no. 6, e202009154, Rockefeller
University Press, 2021, doi:10.1083/jcb.202009154.
short: L. Zeng, I. Palaia, A. Šarić, X. Su, Journal of Cell Biology 220 (2021).
date_created: 2021-11-25T15:21:30Z
date_published: 2021-04-30T00:00:00Z
date_updated: 2021-11-25T15:33:08Z
day: '30'
doi: 10.1083/jcb.202009154
extern: '1'
external_id:
pmid:
- '33929486'
intvolume: ' 220'
issue: '6'
keyword:
- cell biology
language:
- iso: eng
month: '04'
oa_version: None
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: PLCγ1 promotes phase separation of T cell signaling components
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 220
year: '2021'
...
---
_id: '11061'
abstract:
- lang: eng
text: Many adult tissues contain postmitotic cells as old as the host organism.
The only organelle that does not turn over in these cells is the nucleus, and
its maintenance represents a formidable challenge, as it harbors regulatory proteins
that persist throughout adulthood. Here we developed strategies to visualize two
classes of such long-lived proteins, histones and nucleoporins, to understand
the function of protein longevity in nuclear maintenance. Genome-wide mapping
of histones revealed specific enrichment of long-lived variants at silent gene
loci. Interestingly, nuclear pores are maintained by piecemeal replacement of
subunits, resulting in mosaic complexes composed of polypeptides with vastly different
ages. In contrast, nondividing quiescent cells remove old nuclear pores in an
ESCRT-dependent manner. Our findings reveal distinct molecular strategies of nuclear
maintenance, linking lifelong protein persistence to gene regulation and nuclear
integrity.
article_processing_charge: No
article_type: original
author:
- first_name: Brandon H.
full_name: Toyama, Brandon H.
last_name: Toyama
- first_name: Rafael
full_name: Arrojo e Drigo, Rafael
last_name: Arrojo e Drigo
- first_name: Varda
full_name: Lev-Ram, Varda
last_name: Lev-Ram
- first_name: Ranjan
full_name: Ramachandra, Ranjan
last_name: Ramachandra
- first_name: Thomas J.
full_name: Deerinck, Thomas J.
last_name: Deerinck
- first_name: Claude
full_name: Lechene, Claude
last_name: Lechene
- first_name: Mark H.
full_name: Ellisman, Mark H.
last_name: Ellisman
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Toyama BH, Arrojo e Drigo R, Lev-Ram V, et al. Visualization of long-lived
proteins reveals age mosaicism within nuclei of postmitotic cells. Journal
of Cell Biology. 2019;218(2):433-444. doi:10.1083/jcb.201809123
apa: Toyama, B. H., Arrojo e Drigo, R., Lev-Ram, V., Ramachandra, R., Deerinck,
T. J., Lechene, C., … Hetzer, M. (2019). Visualization of long-lived proteins
reveals age mosaicism within nuclei of postmitotic cells. Journal of Cell Biology.
Rockefeller University Press. https://doi.org/10.1083/jcb.201809123
chicago: Toyama, Brandon H., Rafael Arrojo e Drigo, Varda Lev-Ram, Ranjan Ramachandra,
Thomas J. Deerinck, Claude Lechene, Mark H. Ellisman, and Martin Hetzer. “Visualization
of Long-Lived Proteins Reveals Age Mosaicism within Nuclei of Postmitotic Cells.”
Journal of Cell Biology. Rockefeller University Press, 2019. https://doi.org/10.1083/jcb.201809123.
ieee: B. H. Toyama et al., “Visualization of long-lived proteins reveals
age mosaicism within nuclei of postmitotic cells,” Journal of Cell Biology,
vol. 218, no. 2. Rockefeller University Press, pp. 433–444, 2019.
ista: Toyama BH, Arrojo e Drigo R, Lev-Ram V, Ramachandra R, Deerinck TJ, Lechene
C, Ellisman MH, Hetzer M. 2019. Visualization of long-lived proteins reveals age
mosaicism within nuclei of postmitotic cells. Journal of Cell Biology. 218(2),
433–444.
mla: Toyama, Brandon H., et al. “Visualization of Long-Lived Proteins Reveals Age
Mosaicism within Nuclei of Postmitotic Cells.” Journal of Cell Biology,
vol. 218, no. 2, Rockefeller University Press, 2019, pp. 433–44, doi:10.1083/jcb.201809123.
short: B.H. Toyama, R. Arrojo e Drigo, V. Lev-Ram, R. Ramachandra, T.J. Deerinck,
C. Lechene, M.H. Ellisman, M. Hetzer, Journal of Cell Biology 218 (2019) 433–444.
date_created: 2022-04-07T07:45:11Z
date_published: 2019-02-04T00:00:00Z
date_updated: 2022-07-18T08:31:52Z
day: '04'
ddc:
- '570'
doi: 10.1083/jcb.201809123
extern: '1'
external_id:
pmid:
- '30552100'
file:
- access_level: open_access
checksum: 7964ebbf833b0b35f9fba840eea9531d
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T08:26:32Z
date_updated: 2022-04-08T08:26:32Z
file_id: '11139'
file_name: 2019_JCB_Toyama.pdf
file_size: 2503838
relation: main_file
success: 1
file_date_updated: 2022-04-08T08:26:32Z
has_accepted_license: '1'
intvolume: ' 218'
issue: '2'
keyword:
- Cell Biology
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 433-444
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Visualization of long-lived proteins reveals age mosaicism within nuclei of
postmitotic cells
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 218
year: '2019'
...
---
_id: '11069'
abstract:
- lang: eng
text: Repeated rounds of nuclear envelope (NE) rupture and repair have been observed
in laminopathy and cancer cells and result in intermittent loss of nucleus compartmentalization.
Currently, the causes of NE rupture are unclear. Here, we show that NE rupture
in cancer cells relies on the assembly of contractile actin bundles that interact
with the nucleus via the linker of nucleoskeleton and cytoskeleton (LINC) complex.
We found that the loss of actin bundles or the LINC complex did not rescue nuclear
lamina defects, a previously identified determinant of nuclear membrane stability,
but did decrease the number and size of chromatin hernias. Finally, NE rupture
inhibition could be rescued in cells treated with actin-depolymerizing drugs by
mechanically constraining nucleus height. These data suggest a model of NE rupture
where weak membrane areas, caused by defects in lamina organization, rupture because
of an increase in intranuclear pressure from actin-based nucleus confinement.
article_processing_charge: No
article_type: original
author:
- first_name: Emily M.
full_name: Hatch, Emily M.
last_name: Hatch
- 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: Hatch EM, Hetzer M. Nuclear envelope rupture is induced by actin-based nucleus
confinement. Journal of Cell Biology. 2016;215(1):27-36. doi:10.1083/jcb.201603053
apa: Hatch, E. M., & Hetzer, M. (2016). Nuclear envelope rupture is induced
by actin-based nucleus confinement. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.201603053
chicago: Hatch, Emily M., and Martin Hetzer. “Nuclear Envelope Rupture Is Induced
by Actin-Based Nucleus Confinement.” Journal of Cell Biology. Rockefeller
University Press, 2016. https://doi.org/10.1083/jcb.201603053.
ieee: E. M. Hatch and M. Hetzer, “Nuclear envelope rupture is induced by actin-based
nucleus confinement,” Journal of Cell Biology, vol. 215, no. 1. Rockefeller
University Press, pp. 27–36, 2016.
ista: Hatch EM, Hetzer M. 2016. Nuclear envelope rupture is induced by actin-based
nucleus confinement. Journal of Cell Biology. 215(1), 27–36.
mla: Hatch, Emily M., and Martin Hetzer. “Nuclear Envelope Rupture Is Induced by
Actin-Based Nucleus Confinement.” Journal of Cell Biology, vol. 215, no.
1, Rockefeller University Press, 2016, pp. 27–36, doi:10.1083/jcb.201603053.
short: E.M. Hatch, M. Hetzer, Journal of Cell Biology 215 (2016) 27–36.
date_created: 2022-04-07T07:47:42Z
date_published: 2016-10-03T00:00:00Z
date_updated: 2022-07-18T08:33:47Z
day: '03'
doi: 10.1083/jcb.201603053
extern: '1'
external_id:
pmid:
- '27697922'
intvolume: ' 215'
issue: '1'
keyword:
- Cell Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1083/jcb.201603053
month: '10'
oa: 1
oa_version: Published Version
page: 27-36
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
issn:
- 0021-9525
- 1540-8140
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nuclear envelope rupture is induced by actin-based nucleus confinement
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 215
year: '2016'
...
---
_id: '11075'
abstract:
- lang: eng
text: Previously, we identified the nucleoporin gp210/Nup210 as a critical regulator
of muscle and neuronal differentiation, but how this nucleoporin exerts its function
and whether it modulates nuclear pore complex (NPC) activity remain unknown. Here,
we show that gp210/Nup210 mediates muscle cell differentiation in vitro via its
conserved N-terminal domain that extends into the perinuclear space. Removal of
the C-terminal domain, which partially mislocalizes gp210/Nup210 away from NPCs,
efficiently rescues the differentiation defect caused by the knockdown of endogenous
gp210/Nup210. Unexpectedly, a gp210/Nup210 mutant lacking the NPC-targeting transmembrane
and C-terminal domains is sufficient for C2C12 myoblast differentiation. We demonstrate
that the endoplasmic reticulum (ER) stress-specific caspase cascade is exacerbated
during Nup210 depletion and that blocking ER stress-mediated apoptosis rescues
differentiation of Nup210-deficient cells. Our results suggest that the role of
gp210/Nup210 in cell differentiation is mediated by its large luminal domain,
which can act independently of NPC association and appears to play a pivotal role
in the maintenance of nuclear envelope/ER homeostasis.
article_processing_charge: No
article_type: original
author:
- first_name: J. Sebastian
full_name: Gomez-Cavazos, J. Sebastian
last_name: Gomez-Cavazos
- 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: Gomez-Cavazos JS, Hetzer M. The nucleoporin gp210/Nup210 controls muscle differentiation
by regulating nuclear envelope/ER homeostasis. Journal of Cell Biology.
2015;208(6):671-681. doi:10.1083/jcb.201410047
apa: Gomez-Cavazos, J. S., & Hetzer, M. (2015). The nucleoporin gp210/Nup210
controls muscle differentiation by regulating nuclear envelope/ER homeostasis.
Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201410047
chicago: Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210
Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.”
Journal of Cell Biology. Rockefeller University Press, 2015. https://doi.org/10.1083/jcb.201410047.
ieee: J. S. Gomez-Cavazos and M. Hetzer, “The nucleoporin gp210/Nup210 controls
muscle differentiation by regulating nuclear envelope/ER homeostasis,” Journal
of Cell Biology, vol. 208, no. 6. Rockefeller University Press, pp. 671–681,
2015.
ista: Gomez-Cavazos JS, Hetzer M. 2015. The nucleoporin gp210/Nup210 controls muscle
differentiation by regulating nuclear envelope/ER homeostasis. Journal of Cell
Biology. 208(6), 671–681.
mla: Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210
Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.”
Journal of Cell Biology, vol. 208, no. 6, Rockefeller University Press,
2015, pp. 671–81, doi:10.1083/jcb.201410047.
short: J.S. Gomez-Cavazos, M. Hetzer, Journal of Cell Biology 208 (2015) 671–681.
date_created: 2022-04-07T07:49:10Z
date_published: 2015-03-16T00:00:00Z
date_updated: 2022-07-18T08:43:00Z
day: '16'
doi: 10.1083/jcb.201410047
extern: '1'
external_id:
pmid:
- '25778917'
intvolume: ' 208'
issue: '6'
keyword:
- Cell Biology
language:
- iso: eng
month: '03'
oa_version: Published Version
page: 671-681
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: The nucleoporin gp210/Nup210 controls muscle differentiation by regulating
nuclear envelope/ER homeostasis
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 208
year: '2015'
...
---
_id: '11081'
abstract:
- lang: eng
text: In eukaryotic cells the nuclear genome is enclosed by the nuclear envelope
(NE). In metazoans, the NE breaks down in mitosis and it has been assumed that
the physical barrier separating nucleoplasm and cytoplasm remains intact during
the rest of the cell cycle and cell differentiation. However, recent studies suggest
that nonmitotic NE remodeling plays a critical role in development, virus infection,
laminopathies, and cancer. Although the mechanisms underlying these NE restructuring
events are currently being defined, one common theme is activation of protein
kinase C family members in the interphase nucleus to disrupt the nuclear lamina,
demonstrating the importance of the lamina in maintaining nuclear integrity.
article_processing_charge: No
article_type: review
author:
- first_name: Emily
full_name: Hatch, Emily
last_name: Hatch
- 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: Hatch E, Hetzer M. Breaching the nuclear envelope in development and disease.
Journal of Cell Biology. 2014;205(2):133-141. doi:10.1083/jcb.201402003
apa: Hatch, E., & Hetzer, M. (2014). Breaching the nuclear envelope in development
and disease. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201402003
chicago: Hatch, Emily, and Martin Hetzer. “Breaching the Nuclear Envelope in Development
and Disease.” Journal of Cell Biology. Rockefeller University Press, 2014.
https://doi.org/10.1083/jcb.201402003.
ieee: E. Hatch and M. Hetzer, “Breaching the nuclear envelope in development and
disease,” Journal of Cell Biology, vol. 205, no. 2. Rockefeller University
Press, pp. 133–141, 2014.
ista: Hatch E, Hetzer M. 2014. Breaching the nuclear envelope in development and
disease. Journal of Cell Biology. 205(2), 133–141.
mla: Hatch, Emily, and Martin Hetzer. “Breaching the Nuclear Envelope in Development
and Disease.” Journal of Cell Biology, vol. 205, no. 2, Rockefeller University
Press, 2014, pp. 133–41, doi:10.1083/jcb.201402003.
short: E. Hatch, M. Hetzer, Journal of Cell Biology 205 (2014) 133–141.
date_created: 2022-04-07T07:50:13Z
date_published: 2014-04-21T00:00:00Z
date_updated: 2022-07-18T08:45:09Z
day: '21'
doi: 10.1083/jcb.201402003
extern: '1'
external_id:
pmid:
- '24751535'
intvolume: ' 205'
issue: '2'
keyword:
- Cell Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1083/jcb.201402003
month: '04'
oa: 1
oa_version: Published Version
page: 133-141
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
issn:
- 1540-8140
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Breaching the nuclear envelope in development and disease
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 205
year: '2014'
...
---
_id: '11094'
abstract:
- lang: eng
text: Nuclear pore complexes (NPCs) assemble at the end of mitosis during nuclear
envelope (NE) reformation and into an intact NE as cells progress through interphase.
Although recent studies have shown that NPC formation occurs by two different
molecular mechanisms at two distinct cell cycle stages, little is known about
the molecular players that mediate the fusion of the outer and inner nuclear membranes
to form pores. In this paper, we provide evidence that the transmembrane nucleoporin
(Nup), POM121, but not the Nup107–160 complex, is present at new pore assembly
sites at a time that coincides with inner nuclear membrane (INM) and outer nuclear
membrane (ONM) fusion. Overexpression of POM121 resulted in juxtaposition of the
INM and ONM. Additionally, Sun1, an INM protein that is known to interact with
the cytoskeleton, was specifically required for interphase assembly and localized
with POM121 at forming pores. We propose a model in which POM121 and Sun1 interact
transiently to promote early steps of interphase NPC assembly.
article_processing_charge: No
article_type: original
author:
- first_name: Jessica A.
full_name: Talamas, Jessica A.
last_name: Talamas
- 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: Talamas JA, Hetzer M. POM121 and Sun1 play a role in early steps of interphase
NPC assembly. Journal of Cell Biology. 2011;194(1):27-37. doi:10.1083/jcb.201012154
apa: Talamas, J. A., & Hetzer, M. (2011). POM121 and Sun1 play a role in early
steps of interphase NPC assembly. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.201012154
chicago: Talamas, Jessica A., and Martin Hetzer. “POM121 and Sun1 Play a Role in
Early Steps of Interphase NPC Assembly.” Journal of Cell Biology. Rockefeller
University Press, 2011. https://doi.org/10.1083/jcb.201012154.
ieee: J. A. Talamas and M. Hetzer, “POM121 and Sun1 play a role in early steps of
interphase NPC assembly,” Journal of Cell Biology, vol. 194, no. 1. Rockefeller
University Press, pp. 27–37, 2011.
ista: Talamas JA, Hetzer M. 2011. POM121 and Sun1 play a role in early steps of
interphase NPC assembly. Journal of Cell Biology. 194(1), 27–37.
mla: Talamas, Jessica A., and Martin Hetzer. “POM121 and Sun1 Play a Role in Early
Steps of Interphase NPC Assembly.” Journal of Cell Biology, vol. 194, no.
1, Rockefeller University Press, 2011, pp. 27–37, doi:10.1083/jcb.201012154.
short: J.A. Talamas, M. Hetzer, Journal of Cell Biology 194 (2011) 27–37.
date_created: 2022-04-07T07:52:18Z
date_published: 2011-07-04T00:00:00Z
date_updated: 2022-07-18T08:53:46Z
day: '04'
doi: 10.1083/jcb.201012154
extern: '1'
external_id:
pmid:
- '21727197'
intvolume: ' 194'
issue: '1'
keyword:
- Cell Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1083/jcb.201012154
month: '07'
oa: 1
oa_version: Published Version
page: 27-37
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: POM121 and Sun1 play a role in early steps of interphase NPC assembly
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 194
year: '2011'
...
---
_id: '11106'
abstract:
- lang: eng
text: Formation of the nuclear envelope (NE) around segregated chromosomes occurs
by the reshaping of the endoplasmic reticulum (ER), a reservoir for disassembled
nuclear membrane components during mitosis. In this study, we show that inner
nuclear membrane proteins such as lamin B receptor (LBR), MAN1, Lap2β, and the
trans-membrane nucleoporins Ndc1 and POM121 drive the spreading of ER membranes
into the emerging NE via their capacity to bind chromatin in a collaborative manner.
Despite their redundant functions, decreasing the levels of any of these trans-membrane
proteins by RNAi-mediated knockdown delayed NE formation, whereas increasing the
levels of any of them had the opposite effect. Furthermore, acceleration of NE
formation interferes with chromosome separation during mitosis, indicating that
the time frame over which chromatin becomes membrane enclosed is physiologically
relevant and regulated. These data suggest that functionally distinct classes
of chromatin-interacting membrane proteins, which are present at nonsaturating
levels, collaborate to rapidly reestablish the nuclear compartment at the end
of mitosis.
article_processing_charge: No
article_type: original
author:
- first_name: Daniel J.
full_name: Anderson, Daniel J.
last_name: Anderson
- first_name: Jesse D.
full_name: Vargas, Jesse D.
last_name: Vargas
- first_name: Joshua P.
full_name: Hsiao, Joshua P.
last_name: Hsiao
- 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: Anderson DJ, Vargas JD, Hsiao JP, Hetzer M. Recruitment of functionally distinct
membrane proteins to chromatin mediates nuclear envelope formation in vivo. Journal
of Cell Biology. 2009;186(2):183-191. doi:10.1083/jcb.200901106
apa: Anderson, D. J., Vargas, J. D., Hsiao, J. P., & Hetzer, M. (2009). Recruitment
of functionally distinct membrane proteins to chromatin mediates nuclear envelope
formation in vivo. Journal of Cell Biology. Rockefeller University Press.
https://doi.org/10.1083/jcb.200901106
chicago: Anderson, Daniel J., Jesse D. Vargas, Joshua P. Hsiao, and Martin Hetzer.
“Recruitment of Functionally Distinct Membrane Proteins to Chromatin Mediates
Nuclear Envelope Formation in Vivo.” Journal of Cell Biology. Rockefeller
University Press, 2009. https://doi.org/10.1083/jcb.200901106.
ieee: D. J. Anderson, J. D. Vargas, J. P. Hsiao, and M. Hetzer, “Recruitment of
functionally distinct membrane proteins to chromatin mediates nuclear envelope
formation in vivo,” Journal of Cell Biology, vol. 186, no. 2. Rockefeller
University Press, pp. 183–191, 2009.
ista: Anderson DJ, Vargas JD, Hsiao JP, Hetzer M. 2009. Recruitment of functionally
distinct membrane proteins to chromatin mediates nuclear envelope formation in
vivo. Journal of Cell Biology. 186(2), 183–191.
mla: Anderson, Daniel J., et al. “Recruitment of Functionally Distinct Membrane
Proteins to Chromatin Mediates Nuclear Envelope Formation in Vivo.” Journal
of Cell Biology, vol. 186, no. 2, Rockefeller University Press, 2009, pp.
183–91, doi:10.1083/jcb.200901106.
short: D.J. Anderson, J.D. Vargas, J.P. Hsiao, M. Hetzer, Journal of Cell Biology
186 (2009) 183–191.
date_created: 2022-04-07T07:54:18Z
date_published: 2009-07-20T00:00:00Z
date_updated: 2022-07-18T08:58:35Z
day: '20'
doi: 10.1083/jcb.200901106
extern: '1'
external_id:
pmid:
- '19620630'
intvolume: ' 186'
issue: '2'
keyword:
- Cell Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1083/jcb.200901106
month: '07'
oa: 1
oa_version: Published Version
page: 183-191
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1083/jcb.20090110620090903c
scopus_import: '1'
status: public
title: Recruitment of functionally distinct membrane proteins to chromatin mediates
nuclear envelope formation in vivo
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 186
year: '2009'
...
---
_id: '11107'
abstract:
- lang: eng
text: Nucleocytoplasmic transport occurs exclusively through nuclear pore complexes
(NPCs) embedded in pores formed by inner and outer nuclear membrane fusion. The
mechanism for de novo pore and NPC biogenesis remains unclear. Reticulons (RTNs)
and Yop1/DP1 are conserved membrane protein families required to form and maintain
the tubular endoplasmic reticulum (ER) and the postmitotic nuclear envelope. In
this study, we report that members of the RTN and Yop1/DP1 families are required
for nuclear pore formation. Analysis of Saccharomyces cerevisiae prp20-G282S and
nup133Δ NPC assembly mutants revealed perturbations in Rtn1–green fluorescent
protein (GFP) and Yop1-GFP ER distribution and colocalization to NPC clusters.
Combined deletion of RTN1 and YOP1 resulted in NPC clustering, nuclear import
defects, and synthetic lethality with the additional absence of Pom34, Pom152,
and Nup84 subcomplex members. We tested for a direct role in NPC biogenesis using
Xenopus laevis in vitro assays and found that anti-Rtn4a antibodies specifically
inhibited de novo nuclear pore formation. We hypothesize that these ER membrane–bending
proteins mediate early NPC assembly steps.
article_processing_charge: No
article_type: original
author:
- first_name: T. Renee
full_name: Dawson, T. Renee
last_name: Dawson
- first_name: Michelle D.
full_name: Lazarus, Michelle D.
last_name: Lazarus
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
- first_name: Susan R.
full_name: Wente, Susan R.
last_name: Wente
citation:
ama: Dawson TR, Lazarus MD, Hetzer M, Wente SR. ER membrane–bending proteins are
necessary for de novo nuclear pore formation. Journal of Cell Biology.
2009;184(5):659-675. doi:10.1083/jcb.200806174
apa: Dawson, T. R., Lazarus, M. D., Hetzer, M., & Wente, S. R. (2009). ER membrane–bending
proteins are necessary for de novo nuclear pore formation. Journal of Cell
Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.200806174
chicago: Dawson, T. Renee, Michelle D. Lazarus, Martin Hetzer, and Susan R. Wente.
“ER Membrane–Bending Proteins Are Necessary for de Novo Nuclear Pore Formation.”
Journal of Cell Biology. Rockefeller University Press, 2009. https://doi.org/10.1083/jcb.200806174.
ieee: T. R. Dawson, M. D. Lazarus, M. Hetzer, and S. R. Wente, “ER membrane–bending
proteins are necessary for de novo nuclear pore formation,” Journal of Cell
Biology, vol. 184, no. 5. Rockefeller University Press, pp. 659–675, 2009.
ista: Dawson TR, Lazarus MD, Hetzer M, Wente SR. 2009. ER membrane–bending proteins
are necessary for de novo nuclear pore formation. Journal of Cell Biology. 184(5),
659–675.
mla: Dawson, T. Renee, et al. “ER Membrane–Bending Proteins Are Necessary for de
Novo Nuclear Pore Formation.” Journal of Cell Biology, vol. 184, no. 5,
Rockefeller University Press, 2009, pp. 659–75, doi:10.1083/jcb.200806174.
short: T.R. Dawson, M.D. Lazarus, M. Hetzer, S.R. Wente, Journal of Cell Biology
184 (2009) 659–675.
date_created: 2022-04-07T07:54:44Z
date_published: 2009-03-09T00:00:00Z
date_updated: 2022-07-18T08:55:05Z
day: '09'
doi: 10.1083/jcb.200806174
extern: '1'
external_id:
pmid:
- '19273614'
intvolume: ' 184'
issue: '5'
keyword:
- Cell Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1083/jcb.200806174
month: '03'
oa: 1
oa_version: Published Version
page: 659-675
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: ER membrane–bending proteins are necessary for de novo nuclear pore formation
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 184
year: '2009'
...
---
_id: '11111'
abstract:
- lang: eng
text: During mitosis in metazoans, segregated chromosomes become enclosed by the
nuclear envelope (NE), a double membrane that is continuous with the endoplasmic
reticulum (ER). Recent in vitro data suggest that NE formation occurs by chromatin-mediated
reorganization of the tubular ER; however, the basic principles of such a membrane-reshaping
process remain uncharacterized. Here, we present a quantitative analysis of nuclear
membrane assembly in mammalian cells using time-lapse microscopy. From the initial
recruitment of ER tubules to chromatin, the formation of a membrane-enclosed,
transport-competent nucleus occurs within ∼12 min. Overexpression of the ER tubule-forming
proteins reticulon 3, reticulon 4, and DP1 inhibits NE formation and nuclear expansion,
whereas their knockdown accelerates nuclear assembly. This suggests that the transition
from membrane tubules to sheets is rate-limiting for nuclear assembly. Our results
provide evidence that ER-shaping proteins are directly involved in the reconstruction
of the nuclear compartment and that morphological restructuring of the ER is the
principal mechanism of NE formation in vivo.
article_processing_charge: No
article_type: original
author:
- first_name: Daniel J.
full_name: Anderson, Daniel J.
last_name: Anderson
- 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: Anderson DJ, Hetzer M. Reshaping of the endoplasmic reticulum limits the rate
for nuclear envelope formation. Journal of Cell Biology. 2008;182(5):911-924.
doi:10.1083/jcb.200805140
apa: Anderson, D. J., & Hetzer, M. (2008). Reshaping of the endoplasmic reticulum
limits the rate for nuclear envelope formation. Journal of Cell Biology.
Rockefeller University Press. https://doi.org/10.1083/jcb.200805140
chicago: Anderson, Daniel J., and Martin Hetzer. “Reshaping of the Endoplasmic Reticulum
Limits the Rate for Nuclear Envelope Formation.” Journal of Cell Biology.
Rockefeller University Press, 2008. https://doi.org/10.1083/jcb.200805140.
ieee: D. J. Anderson and M. Hetzer, “Reshaping of the endoplasmic reticulum limits
the rate for nuclear envelope formation,” Journal of Cell Biology, vol.
182, no. 5. Rockefeller University Press, pp. 911–924, 2008.
ista: Anderson DJ, Hetzer M. 2008. Reshaping of the endoplasmic reticulum limits
the rate for nuclear envelope formation. Journal of Cell Biology. 182(5), 911–924.
mla: Anderson, Daniel J., and Martin Hetzer. “Reshaping of the Endoplasmic Reticulum
Limits the Rate for Nuclear Envelope Formation.” Journal of Cell Biology,
vol. 182, no. 5, Rockefeller University Press, 2008, pp. 911–24, doi:10.1083/jcb.200805140.
short: D.J. Anderson, M. Hetzer, Journal of Cell Biology 182 (2008) 911–924.
date_created: 2022-04-07T07:55:23Z
date_published: 2008-09-08T00:00:00Z
date_updated: 2022-07-18T08:56:02Z
day: '08'
doi: 10.1083/jcb.200805140
extern: '1'
external_id:
pmid:
- '18779370'
intvolume: ' 182'
issue: '5'
keyword:
- Cell Biology
language:
- iso: eng
month: '09'
oa_version: None
page: 911-924
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Reshaping of the endoplasmic reticulum limits the rate for nuclear envelope
formation
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 182
year: '2008'
...
---
_id: '3930'
abstract:
- lang: eng
text: 'An active involvement of blood-brain barrier endothelial cell basement membranes
in development of inflammatory lesions in the central nervous system (CNS) has
not been considered to date. Here we investigated the molecular composition and
possible function of the extracellular matrix encountered by extravasating T lymphocytes
during experimental autoimmune encephalomyelitis (EAE). Endothelial basement membranes
contained laminin 8 (alpha4beta1gamma1) and/or 10 (alpha5beta1gamma1) and their
expression was influenced by proinflammatory cytokines or angiostatic agents.
T cells emigrating into the CNS during EAE encountered two biochemically distinct
basement membranes, the endothelial (containing laminins 8 and 10) and the parenchymal
(containing laminins 1 and 2) basement membranes. However, inflammatory cuffs
occurred exclusively around endothelial basement membranes containing laminin
8, whereas in the presence of laminin 10 no infiltration was detectable. In vitro
assays using encephalitogenic T cell lines revealed adhesion to laminins 8 and
10, whereas binding to laminins 1 and 2 could not be induced. Downregulation of
integrin alpha6 on cerebral endothelium at sites of T cell infiltration, plus
a high turnover of laminin 8 at these sites, suggested two possible roles for
laminin 8 in the endothelial basement membrane: one at the level of the endothelial
cells resulting in reduced adhesion and, thereby, increased penetrability of the
monolayer; and secondly at the level of the T cells providing direct signals to
the transmigrating cells.'
acknowledgement: The authors thank Stefanie Karosi for careful and critical reading
of the manuscript and Monika Bruckner for expert technical assistance. We are particularly
grateful to Winfried Neuhuber for help with confocal microscopy and interpretation
of the data. This work was supported by Deutsche Forschungsgemeinschaft grants So285/1-3
and So285/1-4 to L.M. Sorokin.
article_processing_charge: No
article_type: original
author:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Britta
full_name: Engelhardt, Britta
last_name: Engelhardt
- first_name: Friederike
full_name: Pausch, Friederike
last_name: Pausch
- first_name: Rupert
full_name: Hallmann, Rupert
last_name: Hallmann
- first_name: Olaf
full_name: Wendler, Olaf
last_name: Wendler
- first_name: Lydia
full_name: Sorokin, Lydia
last_name: Sorokin
citation:
ama: Sixt MK, Engelhardt B, Pausch F, Hallmann R, Wendler O, Sorokin L. Endothelial
cell laminin isoforms, laminins 8 and 10, play decisive roles in T cell recruitment
across the blood-brain barrier in experimental autoimmune encephalomyelitis. Journal
of Cell Biology. 2001;153(5):933-946. doi:10.1083/jcb.153.5.933
apa: Sixt, M. K., Engelhardt, B., Pausch, F., Hallmann, R., Wendler, O., & Sorokin,
L. (2001). Endothelial cell laminin isoforms, laminins 8 and 10, play decisive
roles in T cell recruitment across the blood-brain barrier in experimental autoimmune
encephalomyelitis. Journal of Cell Biology. Rockefeller University Press.
https://doi.org/10.1083/jcb.153.5.933
chicago: Sixt, Michael K, Britta Engelhardt, Friederike Pausch, Rupert Hallmann,
Olaf Wendler, and Lydia Sorokin. “Endothelial Cell Laminin Isoforms, Laminins
8 and 10, Play Decisive Roles in T Cell Recruitment across the Blood-Brain Barrier
in Experimental Autoimmune Encephalomyelitis.” Journal of Cell Biology.
Rockefeller University Press, 2001. https://doi.org/10.1083/jcb.153.5.933 .
ieee: M. K. Sixt, B. Engelhardt, F. Pausch, R. Hallmann, O. Wendler, and L. Sorokin,
“Endothelial cell laminin isoforms, laminins 8 and 10, play decisive roles in
T cell recruitment across the blood-brain barrier in experimental autoimmune encephalomyelitis,”
Journal of Cell Biology, vol. 153, no. 5. Rockefeller University Press,
pp. 933–946, 2001.
ista: Sixt MK, Engelhardt B, Pausch F, Hallmann R, Wendler O, Sorokin L. 2001. Endothelial
cell laminin isoforms, laminins 8 and 10, play decisive roles in T cell recruitment
across the blood-brain barrier in experimental autoimmune encephalomyelitis. Journal
of Cell Biology. 153(5), 933–946.
mla: Sixt, Michael K., et al. “Endothelial Cell Laminin Isoforms, Laminins 8 and
10, Play Decisive Roles in T Cell Recruitment across the Blood-Brain Barrier in
Experimental Autoimmune Encephalomyelitis.” Journal of Cell Biology, vol.
153, no. 5, Rockefeller University Press, 2001, pp. 933–46, doi:10.1083/jcb.153.5.933 .
short: M.K. Sixt, B. Engelhardt, F. Pausch, R. Hallmann, O. Wendler, L. Sorokin,
Journal of Cell Biology 153 (2001) 933–946.
date_created: 2018-12-11T12:05:57Z
date_published: 2001-05-21T00:00:00Z
date_updated: 2023-05-11T12:19:36Z
day: '21'
doi: '10.1083/jcb.153.5.933 '
extern: '1'
external_id:
pmid:
- '11381080'
intvolume: ' 153'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174323/
month: '05'
oa: 1
oa_version: Published Version
page: 933 - 946
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
publist_id: '2198'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Endothelial cell laminin isoforms, laminins 8 and 10, play decisive roles in
T cell recruitment across the blood-brain barrier in experimental autoimmune encephalomyelitis
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 153
year: '2001'
...
---
_id: '11126'
abstract:
- lang: eng
text: Nuclear import of the two uracil-rich small nuclear ribonucleoprotein (U snRNP)
components U1A and U2B′′ is mediated by unusually long and complex nuclear localization
signals (NLSs). Here we investigate nuclear import of U1A and U2B′′ in vitro and
demonstrate that it occurs by an active, saturable process. Several lines of evidence
suggest that import of the two proteins occurs by an import mechanism different
to those characterized previously. No cross competition is seen with a variety
of previously studied NLSs. In contrast to import mediated by members of the importin-β
family of nucleocytoplasmic transport receptors, U1A/U2B′′ import is not inhibited
by either nonhydrolyzable guanosine triphosphate (GTP) analogues or by a mutant
of the GTPase Ran that is incapable of GTP hydrolysis. Adenosine triphosphate
is capable of supporting U1A and U2B′′ import, whereas neither nonhydrolyzable
adenosine triphosphate analogues nor GTP can do so. U1A and U2B′′ import in vitro
does not require the addition of soluble cytosolic proteins, but a factor or factors
required for U1A and U2B′′ import remains tightly associated with the nuclear
fraction of conventionally permeabilized cells. This activity can be solubilized
in the presence of elevated MgCl2. These data suggest that U1A and U2B′′ import
into the nucleus occurs by a hitherto uncharacterized mechanism.
article_processing_charge: No
article_type: original
author:
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
- first_name: Iain W.
full_name: Mattaj, Iain W.
last_name: Mattaj
citation:
ama: Hetzer M, Mattaj IW. An Atp-dependent, Ran-independent mechanism for nuclear
import of the U1a and U2b′′ spliceosome proteins. Journal of Cell Biology.
2000;148(2):293-304. doi:10.1083/jcb.148.2.293
apa: Hetzer, M., & Mattaj, I. W. (2000). An Atp-dependent, Ran-independent mechanism
for nuclear import of the U1a and U2b′′ spliceosome proteins. Journal of Cell
Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.148.2.293
chicago: Hetzer, Martin, and Iain W. Mattaj. “An Atp-Dependent, Ran-Independent
Mechanism for Nuclear Import of the U1a and U2b′′ Spliceosome Proteins.” Journal
of Cell Biology. Rockefeller University Press, 2000. https://doi.org/10.1083/jcb.148.2.293.
ieee: M. Hetzer and I. W. Mattaj, “An Atp-dependent, Ran-independent mechanism for
nuclear import of the U1a and U2b′′ spliceosome proteins,” Journal of Cell
Biology, vol. 148, no. 2. Rockefeller University Press, pp. 293–304, 2000.
ista: Hetzer M, Mattaj IW. 2000. An Atp-dependent, Ran-independent mechanism for
nuclear import of the U1a and U2b′′ spliceosome proteins. Journal of Cell Biology.
148(2), 293–304.
mla: Hetzer, Martin, and Iain W. Mattaj. “An Atp-Dependent, Ran-Independent Mechanism
for Nuclear Import of the U1a and U2b′′ Spliceosome Proteins.” Journal of Cell
Biology, vol. 148, no. 2, Rockefeller University Press, 2000, pp. 293–304,
doi:10.1083/jcb.148.2.293.
short: M. Hetzer, I.W. Mattaj, Journal of Cell Biology 148 (2000) 293–304.
date_created: 2022-04-07T07:57:49Z
date_published: 2000-01-24T00:00:00Z
date_updated: 2022-07-18T08:58:29Z
day: '24'
doi: 10.1083/jcb.148.2.293
extern: '1'
external_id:
pmid:
- '10648562'
intvolume: ' 148'
issue: '2'
keyword:
- Cell Biology
language:
- iso: eng
month: '01'
oa_version: None
page: 293-304
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: An Atp-dependent, Ran-independent mechanism for nuclear import of the U1a and
U2b′′ spliceosome proteins
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 148
year: '2000'
...
---
_id: '3756'
abstract:
- lang: eng
text: 'In many eukaryotic cells going through M-phase, a bipolar spindle is formed
by microtubules nucleated from centrosomes. These microtubules, in addition to
being `''captured” by kinetochores, may be stabilized by chromatin in two different
ways: short-range stabilization effects may affect microtubules in close contact
with the chromatin, while long-range stabilization effects may `''guide” microtubule
growth towards the chromatin (e.g., by introducing a diffusive gradient of an
enzymatic activity that affects microtubule assembly). Here, we use both meiotic
and mitotic extracts from Xenopus laevis eggs to study microtubule aster formation
and microtubule dynamics in the presence of chromatin. In `''low-speed” meiotic
extracts, in the presence of salmon sperm chromatin, we find that short-range
stabilization effects lead to a strong anisotropy of the microtubule asters. Analysis
of the dynamic parameters of microtubule growth shows that this anisotropy arises
from a decrease in the catastrophe frequency, an increase in the rescue frequency
and a decrease in the growth velocity. In this system we also find evidence for
long-range `''guidance” effects, which lead to a weak anisotropy of the asters.
Statistically relevant results on these long-range effects are obtained in `''high-speed”
mitotic extracts in the presence of artificially constructed chromatin stripes.
We find that aster anisotropy is biased in the direction of the chromatin and
that the catastrophe frequency is reduced in its vicinity. In this system we also
find a surprising dependence of the catastrophe and the rescue frequencies on
the length of microtubules nucleated from centrosomes: the catastrophe frequency
increases and the rescue frequency decreases with microtubule length.'
acknowledgement: "We would like to thank T. Holy and T. Mitchison for providing us
with centrosomes; M. Glotzer and T. Mitchison for giving us the plasmid for A90
cyclin B; J. Stock and members of his laboratory for help with biochemical preparations;
R. Zimmerman for help with the biotinylation of DNA; J. Shepard for help with the
patterning of surfaces; D. Tsui for use\r\nof his clean room facility, and D. Fygenson,
T. Holy, E. Karsenti, E. Kennedy, A. Levine, T. Mitchison, and G. Waters for valuable
discussions, constant encouragement and technical help. This work was partially
supported by the National Institutes of Health (Grant No. GM-50712) and the Human
Frontier Science Program."
article_processing_charge: No
article_type: original
author:
- first_name: Marileen
full_name: Dogterom, Marileen
last_name: Dogterom
- first_name: M.
full_name: Felix, M.
last_name: Felix
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
- first_name: Stanislas
full_name: Leibler, Stanislas
last_name: Leibler
citation:
ama: 'Dogterom M, Felix M, Guet CC, Leibler S. Influence of M-phase chromatin on
the anisotropy of microtubule asters. Journal of Cell Biology. 1996;133(1):125-140.
doi:doi: 10.1083/jcb.133.1.125
'
apa: 'Dogterom, M., Felix, M., Guet, C. C., & Leibler, S. (1996). Influence
of M-phase chromatin on the anisotropy of microtubule asters. Journal of Cell
Biology. Rockefeller University Press. https://doi.org/doi: 10.1083/jcb.133.1.125 '
chicago: 'Dogterom, Marileen, M. Felix, Calin C Guet, and Stanislas Leibler. “Influence
of M-Phase Chromatin on the Anisotropy of Microtubule Asters.” Journal of Cell
Biology. Rockefeller University Press, 1996. https://doi.org/doi: 10.1083/jcb.133.1.125 .'
ieee: M. Dogterom, M. Felix, C. C. Guet, and S. Leibler, “Influence of M-phase chromatin
on the anisotropy of microtubule asters,” Journal of Cell Biology, vol.
133, no. 1. Rockefeller University Press, pp. 125–140, 1996.
ista: Dogterom M, Felix M, Guet CC, Leibler S. 1996. Influence of M-phase chromatin
on the anisotropy of microtubule asters. Journal of Cell Biology. 133(1), 125–140.
mla: 'Dogterom, Marileen, et al. “Influence of M-Phase Chromatin on the Anisotropy
of Microtubule Asters.” Journal of Cell Biology, vol. 133, no. 1, Rockefeller
University Press, 1996, pp. 125–40, doi:doi: 10.1083/jcb.133.1.125 .'
short: M. Dogterom, M. Felix, C.C. Guet, S. Leibler, Journal of Cell Biology 133
(1996) 125–140.
date_created: 2018-12-11T12:05:00Z
date_published: 1996-01-01T00:00:00Z
date_updated: 2022-08-09T14:20:13Z
day: '01'
doi: 'doi: 10.1083/jcb.133.1.125 '
extern: '1'
external_id:
pmid:
- '8601601'
intvolume: ' 133'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2120784/
month: '01'
oa: 1
oa_version: Published Version
page: 125 - 140
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
publist_id: '2473'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Influence of M-phase chromatin on the anisotropy of microtubule asters
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 133
year: '1996'
...
---
_id: '4177'
abstract:
- lang: eng
text: Thyroid hormones play an important role in brain development, but the mechanism(s)
by which triiodothyronine (T3) mediates neuronal differentiation is poorly understood.
Here we demonstrate that T3 regulates the neurotrophic factor, neurotrophin-3
(NT-3), in developing rat cerebellar granule cells both in cell culture and in
vivo. In situ hybridization experiments showed that developing Purkinje cells
do not express NT-3 mRNA but do express trkC, the putative neuronal receptor for
NT-3. Addition of recombinant NT-3 to cerebellar cultures from embryonic rat brain
induces hypertrophy and neurite sprouting of Purkinje cells, and upregulates the
mRNA encoding the calcium-binding protein, calbindin-28 kD. The present study
demonstrates a novel interaction between cerebellar granule neurons and developing
Purkinje cells in which NT-3 induced by T3 in the granule cells promotes Purkinje
cell differentiation.
acknowledgement: "E. Castrtn is an Alexander von Humboldt fellow. M. Berzaghi is supported
by a scholarship from CNPQ, Brasil. L. F. Parada, P. Tsoulfas, and L. Tesarollo
were supported by a National Institutes of Health grant. We thank D. Stratmann and
K. Angermeyer for skillful technical assistance; I. Hajjar for secretarial work
and Dr. R. G~rtner for help with\r\ninducing hypothyroidism; Dr. W. Hunzieker for
the calbindin-28 kD eDNA; Dr. M. Fishman for the GAP-43 eDNA; and Dr. Y.-A. Barde
for critical comments."
article_processing_charge: No
article_type: original
author:
- first_name: Dan
full_name: Lindholm, Dan
last_name: Lindholm
- first_name: Eero
full_name: Castrén, Eero
last_name: Castrén
- first_name: Pantelis
full_name: Tsoulfas, Pantelis
last_name: Tsoulfas
- first_name: Roland
full_name: Kolbeck, Roland
last_name: Kolbeck
- first_name: Maria
full_name: Berzaghi, Maria
last_name: Berzaghi
- first_name: Axel
full_name: Leingärtner, Axel
last_name: Leingärtner
- 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
- first_name: Lino
full_name: Tesarollo, Lino
last_name: Tesarollo
- first_name: Luis
full_name: Parada, Luis
last_name: Parada
- first_name: Hans
full_name: Thoenen, Hans
last_name: Thoenen
citation:
ama: Lindholm D, Castrén E, Tsoulfas P, et al. Neurotrophin-3 induced by tri-iodothyronine
in cerebellar granule cells promotes Purkinje cell differentiation. Journal
of Cell Biology. 1993;122(2):443-450. doi:10.1083/jcb.122.2.443
apa: Lindholm, D., Castrén, E., Tsoulfas, P., Kolbeck, R., Berzaghi, M., Leingärtner,
A., … Thoenen, H. (1993). Neurotrophin-3 induced by tri-iodothyronine in cerebellar
granule cells promotes Purkinje cell differentiation. Journal of Cell Biology.
Rockefeller University Press. https://doi.org/10.1083/jcb.122.2.443
chicago: Lindholm, Dan, Eero Castrén, Pantelis Tsoulfas, Roland Kolbeck, Maria Berzaghi,
Axel Leingärtner, Carl-Philipp J Heisenberg, Lino Tesarollo, Luis Parada, and
Hans Thoenen. “Neurotrophin-3 Induced by Tri-Iodothyronine in Cerebellar Granule
Cells Promotes Purkinje Cell Differentiation.” Journal of Cell Biology.
Rockefeller University Press, 1993. https://doi.org/10.1083/jcb.122.2.443.
ieee: D. Lindholm et al., “Neurotrophin-3 induced by tri-iodothyronine in
cerebellar granule cells promotes Purkinje cell differentiation,” Journal of
Cell Biology, vol. 122, no. 2. Rockefeller University Press, pp. 443–450,
1993.
ista: Lindholm D, Castrén E, Tsoulfas P, Kolbeck R, Berzaghi M, Leingärtner A, Heisenberg
C-PJ, Tesarollo L, Parada L, Thoenen H. 1993. Neurotrophin-3 induced by tri-iodothyronine
in cerebellar granule cells promotes Purkinje cell differentiation. Journal of
Cell Biology. 122(2), 443–450.
mla: Lindholm, Dan, et al. “Neurotrophin-3 Induced by Tri-Iodothyronine in Cerebellar
Granule Cells Promotes Purkinje Cell Differentiation.” Journal of Cell Biology,
vol. 122, no. 2, Rockefeller University Press, 1993, pp. 443–50, doi:10.1083/jcb.122.2.443.
short: D. Lindholm, E. Castrén, P. Tsoulfas, R. Kolbeck, M. Berzaghi, A. Leingärtner,
C.-P.J. Heisenberg, L. Tesarollo, L. Parada, H. Thoenen, Journal of Cell Biology
122 (1993) 443–450.
date_created: 2018-12-11T12:07:25Z
date_published: 1993-07-15T00:00:00Z
date_updated: 2022-03-24T12:59:20Z
day: '15'
doi: 10.1083/jcb.122.2.443
extern: '1'
external_id:
pmid:
- '8320266'
intvolume: ' 122'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119654/
month: '07'
oa: 1
oa_version: None
page: 443 - 450
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
publist_id: '1942'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neurotrophin-3 induced by tri-iodothyronine in cerebellar granule cells promotes
Purkinje cell differentiation
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 122
year: '1993'
...