---
OA_place: publisher
_id: '9962'
abstract:
- lang: eng
text: The brain is one of the largest and most complex organs and it is composed
of billions of neurons that communicate together enabling e.g. consciousness.
The cerebral cortex is the largest site of neural integration in the central nervous
system. Concerted radial migration of newly born cortical projection neurons,
from their birthplace to their final position, is a key step in the assembly of
the cerebral cortex. The cellular and molecular mechanisms regulating radial neuronal
migration in vivo are however still unclear. Recent evidence suggests that distinct
signaling cues act cell-autonomously but differentially at certain steps during
the overall migration process. Moreover, functional analysis of genetic mosaics
(mutant neurons present in wild-type/heterozygote environment) using the MADM
(Mosaic Analysis with Double Markers) analyses in comparison to global knockout
also indicate a significant degree of non-cell-autonomous and/or community effects
in the control of cortical neuron migration. The interactions of cell-intrinsic
(cell-autonomous) and cell-extrinsic (non-cell-autonomous) components are largely
unknown. In part of this thesis work we established a MADM-based experimental
strategy for the quantitative analysis of cell-autonomous gene function versus
non-cell-autonomous and/or community effects. The direct comparison of mutant
neurons from the genetic mosaic (cell-autonomous) to mutant neurons in the conditional
and/or global knockout (cell-autonomous + non-cell-autonomous) allows to quantitatively
analyze non-cell-autonomous effects. Such analysis enable the high-resolution
analysis of projection neuron migration dynamics in distinct environments with
concomitant isolation of genomic and proteomic profiles. Using these experimental
paradigms and in combination with computational modeling we show and characterize
the nature of non-cell-autonomous effects to coordinate radial neuron migration.
Furthermore, this thesis discusses recent developments in neurodevelopment with
focus on neuronal polarization and non-cell-autonomous mechanisms in neuronal
migration.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
citation:
ama: Hansen AH. Cell-autonomous gene function and non-cell-autonomous effects in
radial projection neuron migration. 2021. doi:10.15479/at:ista:9962
apa: Hansen, A. H. (2021). Cell-autonomous gene function and non-cell-autonomous
effects in radial projection neuron migration. Institute of Science and Technology
Austria. https://doi.org/10.15479/at:ista:9962
chicago: Hansen, Andi H. “Cell-Autonomous Gene Function and Non-Cell-Autonomous
Effects in Radial Projection Neuron Migration.” Institute of Science and Technology
Austria, 2021. https://doi.org/10.15479/at:ista:9962.
ieee: A. H. Hansen, “Cell-autonomous gene function and non-cell-autonomous effects
in radial projection neuron migration,” Institute of Science and Technology Austria,
2021.
ista: Hansen AH. 2021. Cell-autonomous gene function and non-cell-autonomous effects
in radial projection neuron migration. Institute of Science and Technology Austria.
mla: Hansen, Andi H. Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects
in Radial Projection Neuron Migration. Institute of Science and Technology
Austria, 2021, doi:10.15479/at:ista:9962.
short: A.H. Hansen, Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects
in Radial Projection Neuron Migration, Institute of Science and Technology Austria,
2021.
corr_author: '1'
date_created: 2021-08-29T12:36:50Z
date_published: 2021-09-02T00:00:00Z
date_updated: 2026-04-08T07:19:09Z
day: '02'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: SiHi
doi: 10.15479/at:ista:9962
file:
- access_level: closed
checksum: 66b56f5b988b233dc66a4f4b4fb2cdfe
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: ahansen
date_created: 2021-08-30T09:17:39Z
date_updated: 2022-09-03T22:30:04Z
embargo_to: open_access
file_id: '9971'
file_name: Thesis_Hansen.docx
file_size: 10629190
relation: source_file
- access_level: open_access
checksum: 204fa40321a1c6289b68c473634c4bf3
content_type: application/pdf
creator: ahansen
date_created: 2021-08-30T09:29:44Z
date_updated: 2022-09-03T22:30:04Z
embargo: 2022-09-02
file_id: '9972'
file_name: Thesis_Hansen_PDFA-1a.pdf
file_size: 13457469
relation: main_file
file_date_updated: 2022-09-03T22:30:04Z
has_accepted_license: '1'
keyword:
- Neuronal migration
- Non-cell-autonomous
- Cell-autonomous
- Neurodevelopmental disease
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '09'
oa: 1
oa_version: Published Version
page: '182'
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular mechanisms of radial neuronal migration
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '8569'
relation: part_of_dissertation
status: public
- id: '960'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
title: Cell-autonomous gene function and non-cell-autonomous effects in radial projection
neuron migration
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: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2021'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '8402'
abstract:
- lang: eng
text: "Background: The mitochondrial pyruvate carrier (MPC) plays a central role
in energy metabolism by transporting pyruvate across the inner mitochondrial membrane.
Its heterodimeric composition and homology to SWEET and semiSWEET transporters
set the MPC apart from the canonical mitochondrial carrier family (named MCF or
SLC25). The import of the canonical carriers is mediated by the carrier translocase
of the inner membrane (TIM22) pathway and is dependent on their structure, which
features an even number of transmembrane segments and both termini in the intermembrane
space. The import pathway of MPC proteins has not been elucidated. The odd number
of transmembrane segments and positioning of the N-terminus in the matrix argues
against an import via the TIM22 carrier pathway but favors an import via the flexible
presequence pathway.\r\nResults: Here, we systematically analyzed the import pathways
of Mpc2 and Mpc3 and report that, contrary to an expected import via the flexible
presequence pathway, yeast MPC proteins with an odd number of transmembrane segments
and matrix-exposed N-terminus are imported by the carrier pathway, using the receptor
Tom70, small TIM chaperones, and the TIM22 complex. The TIM9·10 complex chaperones
MPC proteins through the mitochondrial intermembrane space using conserved hydrophobic
motifs that are also required for the interaction with canonical carrier proteins.\r\nConclusions:
The carrier pathway can import paired and non-paired transmembrane helices and
translocate N-termini to either side of the mitochondrial inner membrane, revealing
an unexpected versatility of the mitochondrial import pathway for non-cleavable
inner membrane proteins."
article_number: '2'
article_processing_charge: No
article_type: original
author:
- first_name: Heike
full_name: Rampelt, Heike
last_name: Rampelt
- first_name: Iva
full_name: Sucec, Iva
last_name: Sucec
- first_name: Beate
full_name: Bersch, Beate
last_name: Bersch
- first_name: Patrick
full_name: Horten, Patrick
last_name: Horten
- first_name: Inge
full_name: Perschil, Inge
last_name: Perschil
- first_name: Jean-Claude
full_name: Martinou, Jean-Claude
last_name: Martinou
- first_name: Martin
full_name: van der Laan, Martin
last_name: van der Laan
- first_name: Nils
full_name: Wiedemann, Nils
last_name: Wiedemann
- first_name: Paul
full_name: Schanda, Paul
id: 7B541462-FAF6-11E9-A490-E8DFE5697425
last_name: Schanda
orcid: 0000-0002-9350-7606
- first_name: Nikolaus
full_name: Pfanner, Nikolaus
last_name: Pfanner
citation:
ama: Rampelt H, Sucec I, Bersch B, et al. The mitochondrial carrier pathway transports
non-canonical substrates with an odd number of transmembrane segments. BMC
Biology. 2020;18. doi:10.1186/s12915-019-0733-6
apa: Rampelt, H., Sucec, I., Bersch, B., Horten, P., Perschil, I., Martinou, J.-C.,
… Pfanner, N. (2020). The mitochondrial carrier pathway transports non-canonical
substrates with an odd number of transmembrane segments. BMC Biology. Springer
Nature. https://doi.org/10.1186/s12915-019-0733-6
chicago: Rampelt, Heike, Iva Sucec, Beate Bersch, Patrick Horten, Inge Perschil,
Jean-Claude Martinou, Martin van der Laan, Nils Wiedemann, Paul Schanda, and Nikolaus
Pfanner. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates
with an Odd Number of Transmembrane Segments.” BMC Biology. Springer Nature,
2020. https://doi.org/10.1186/s12915-019-0733-6.
ieee: H. Rampelt et al., “The mitochondrial carrier pathway transports non-canonical
substrates with an odd number of transmembrane segments,” BMC Biology,
vol. 18. Springer Nature, 2020.
ista: Rampelt H, Sucec I, Bersch B, Horten P, Perschil I, Martinou J-C, van der
Laan M, Wiedemann N, Schanda P, Pfanner N. 2020. The mitochondrial carrier pathway
transports non-canonical substrates with an odd number of transmembrane segments.
BMC Biology. 18, 2.
mla: Rampelt, Heike, et al. “The Mitochondrial Carrier Pathway Transports Non-Canonical
Substrates with an Odd Number of Transmembrane Segments.” BMC Biology,
vol. 18, 2, Springer Nature, 2020, doi:10.1186/s12915-019-0733-6.
short: H. Rampelt, I. Sucec, B. Bersch, P. Horten, I. Perschil, J.-C. Martinou,
M. van der Laan, N. Wiedemann, P. Schanda, N. Pfanner, BMC Biology 18 (2020).
date_created: 2020-09-17T10:26:53Z
date_published: 2020-01-06T00:00:00Z
date_updated: 2024-10-15T13:23:11Z
day: '06'
doi: 10.1186/s12915-019-0733-6
extern: '1'
external_id:
pmid:
- '31907035'
intvolume: ' 18'
keyword:
- Biotechnology
- Plant Science
- General Biochemistry
- Genetics and Molecular Biology
- Developmental Biology
- Cell Biology
- Physiology
- Ecology
- Evolution
- Behavior and Systematics
- Structural Biology
- General Agricultural and Biological Sciences
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1186/s12915-019-0733-6
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
publication: BMC Biology
publication_identifier:
issn:
- 1741-7007
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: The mitochondrial carrier pathway transports non-canonical substrates with
an odd number of transmembrane segments
type: journal_article
user_id: 0043cee0-e5fc-11ee-9736-f83bc23afbf0
volume: 18
year: '2020'
...
---
_id: '8586'
abstract:
- lang: eng
text: Cryo-electron microscopy (cryo-EM) of cellular specimens provides insights
into biological processes and structures within a native context. However, a major
challenge still lies in the efficient and reproducible preparation of adherent
cells for subsequent cryo-EM analysis. This is due to the sensitivity of many
cellular specimens to the varying seeding and culturing conditions required for
EM experiments, the often limited amount of cellular material and also the fragility
of EM grids and their substrate. Here, we present low-cost and reusable 3D printed
grid holders, designed to improve specimen preparation when culturing challenging
cellular samples directly on grids. The described grid holders increase cell culture
reproducibility and throughput, and reduce the resources required for cell culturing.
We show that grid holders can be integrated into various cryo-EM workflows, including
micro-patterning approaches to control cell seeding on grids, and for generating
samples for cryo-focused ion beam milling and cryo-electron tomography experiments.
Their adaptable design allows for the generation of specialized grid holders customized
to a large variety of applications.
acknowledged_ssus:
- _id: ScienComp
- _id: LifeSc
- _id: Bio
- _id: EM-Fac
acknowledgement: This work was supported by the Austrian Science Fund (FWF, P33367)
to FKMS. BZ acknowledges support by the Niederösterreich Fond. This research was
also supported by the Scientific Service Units (SSU) of IST Austria through resources
provided by Scientific Computing (SciComp), the Life Science Facility (LSF), the
BioImaging Facility (BIF) and the Electron Microscopy Facility (EMF). We thank Georgi
Dimchev (IST Austria) and Sonja Jacob (Vienna Biocenter Core Facilities) for testing
our grid holders in different experimental setups and Daniel Gütl and the Kondrashov
group (IST Austria) for granting us repeated access to their 3D printers. We also
thank Jonna Alanko and the Sixt lab (IST Austria) for providing us HeLa cells, primary
BL6 mouse tail fibroblasts, NIH 3T3 fibroblasts and human telomerase immortalised
foreskin fibroblasts for our experiments. We are thankful to Ori Avinoam and William
Wan for helpful comments on the manuscript and also thank Dorotea Fracchiolla (Art&Science)
for illustrating the graphical abstract.
article_number: '107633'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Florian
full_name: Fäßler, Florian
id: 404F5528-F248-11E8-B48F-1D18A9856A87
last_name: Fäßler
orcid: 0000-0001-7149-769X
- first_name: Bettina
full_name: Zens, Bettina
id: 45FD126C-F248-11E8-B48F-1D18A9856A87
last_name: Zens
orcid: 0000-0002-9561-1239
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
citation:
ama: Fäßler F, Zens B, Hauschild R, Schur FK. 3D printed cell culture grid holders
for improved cellular specimen preparation in cryo-electron microscopy. Journal
of Structural Biology. 2020;212(3). doi:10.1016/j.jsb.2020.107633
apa: Fäßler, F., Zens, B., Hauschild, R., & Schur, F. K. (2020). 3D printed
cell culture grid holders for improved cellular specimen preparation in cryo-electron
microscopy. Journal of Structural Biology. Elsevier. https://doi.org/10.1016/j.jsb.2020.107633
chicago: Fäßler, Florian, Bettina Zens, Robert Hauschild, and Florian KM Schur.
“3D Printed Cell Culture Grid Holders for Improved Cellular Specimen Preparation
in Cryo-Electron Microscopy.” Journal of Structural Biology. Elsevier,
2020. https://doi.org/10.1016/j.jsb.2020.107633.
ieee: F. Fäßler, B. Zens, R. Hauschild, and F. K. Schur, “3D printed cell culture
grid holders for improved cellular specimen preparation in cryo-electron microscopy,”
Journal of Structural Biology, vol. 212, no. 3. Elsevier, 2020.
ista: Fäßler F, Zens B, Hauschild R, Schur FK. 2020. 3D printed cell culture grid
holders for improved cellular specimen preparation in cryo-electron microscopy.
Journal of Structural Biology. 212(3), 107633.
mla: Fäßler, Florian, et al. “3D Printed Cell Culture Grid Holders for Improved
Cellular Specimen Preparation in Cryo-Electron Microscopy.” Journal of Structural
Biology, vol. 212, no. 3, 107633, Elsevier, 2020, doi:10.1016/j.jsb.2020.107633.
short: F. Fäßler, B. Zens, R. Hauschild, F.K. Schur, Journal of Structural Biology
212 (2020).
corr_author: '1'
date_created: 2020-09-29T13:24:06Z
date_published: 2020-12-01T00:00:00Z
date_updated: 2026-08-28T22:30:02Z
day: '01'
ddc:
- '570'
department:
- _id: FlSc
doi: 10.1016/j.jsb.2020.107633
external_id:
isi:
- '000600997800008'
pmid:
- '32987119'
file:
- access_level: open_access
checksum: c48cbf594e84fc2f91966ffaafc0918c
content_type: application/pdf
creator: dernst
date_created: 2020-12-10T14:01:10Z
date_updated: 2020-12-10T14:01:10Z
file_id: '8937'
file_name: 2020_JourStrucBiology_Faessler.pdf
file_size: 7076870
relation: main_file
success: 1
file_date_updated: 2020-12-10T14:01:10Z
has_accepted_license: '1'
intvolume: ' 212'
isi: 1
issue: '3'
keyword:
- electron microscopy
- cryo-EM
- EM sample preparation
- 3D printing
- cell culture
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 9B954C5C-BA93-11EA-9121-9846C619BF3A
grant_number: P33367
name: Structure and isoform diversity of the Arp2/3 complex
- _id: 059B463C-7A3F-11EA-A408-12923DDC885E
name: NÖ-Fonds Preis für die Jungforscherin des Jahres am IST Austria
publication: Journal of Structural Biology
publication_identifier:
issn:
- 1047-8477
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '14592'
relation: used_in_publication
status: public
- id: '12491'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: 3D printed cell culture grid holders for improved cellular specimen preparation
in cryo-electron microscopy
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: 212
year: '2020'
...
---
_id: '8434'
abstract:
- lang: eng
text: 'Efficient migration on adhesive surfaces involves the protrusion of lamellipodial
actin networks and their subsequent stabilization by nascent adhesions. The actin-binding
protein lamellipodin (Lpd) is thought to play a critical role in lamellipodium
protrusion, by delivering Ena/VASP proteins onto the growing plus ends of actin
filaments and by interacting with the WAVE regulatory complex, an activator of
the Arp2/3 complex, at the leading edge. Using B16-F1 melanoma cell lines, we
demonstrate that genetic ablation of Lpd compromises protrusion efficiency and
coincident cell migration without altering essential parameters of lamellipodia,
including their maximal rate of forward advancement and actin polymerization.
We also confirmed lamellipodia and migration phenotypes with CRISPR/Cas9-mediated
Lpd knockout Rat2 fibroblasts, excluding cell type-specific effects. Moreover,
computer-aided analysis of cell-edge morphodynamics on B16-F1 cell lamellipodia
revealed that loss of Lpd correlates with reduced temporal protrusion maintenance
as a prerequisite of nascent adhesion formation. We conclude that Lpd optimizes
protrusion and nascent adhesion formation by counteracting frequent, chaotic retraction
and membrane ruffling.This article has an associated First Person interview with
the first author of the paper. '
acknowledgement: This work was supported in part by Deutsche Forschungsgemeinschaft
(DFG)[GRK2223/1, RO2414/5-1 (to K.R.), FA350/11-1 (to M.F.) and FA330/11-1 (to J.F.)],as
well as by intramural funding from the Helmholtz Association (to T.E.B.S. andK.R.).
G.D. was additionally funded by the Austrian Science Fund (FWF) LiseMeitner Program
[M-2495]. A.C.H. and M.W. are supported by the Francis CrickInstitute, which receives
its core funding from Cancer Research UK [FC001209], theMedical Research Council
[FC001209] and the Wellcome Trust [FC001209]. M.K. issupported by the Biotechnology
and Biological Sciences Research Council [BB/F011431/1, BB/J000590/1, BB/N000226/1].
Deposited in PMC for release after 6months.
article_number: jcs239020
article_processing_charge: No
article_type: original
author:
- first_name: Georgi A
full_name: Dimchev, Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- first_name: Behnam
full_name: Amiri, Behnam
last_name: Amiri
- first_name: Ashley C.
full_name: Humphries, Ashley C.
last_name: Humphries
- first_name: Matthias
full_name: Schaks, Matthias
last_name: Schaks
- first_name: Vanessa
full_name: Dimchev, Vanessa
last_name: Dimchev
- first_name: Theresia E. B.
full_name: Stradal, Theresia E. B.
last_name: Stradal
- first_name: Jan
full_name: Faix, Jan
last_name: Faix
- first_name: Matthias
full_name: Krause, Matthias
last_name: Krause
- first_name: Michael
full_name: Way, Michael
last_name: Way
- first_name: Martin
full_name: Falcke, Martin
last_name: Falcke
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
citation:
ama: Dimchev GA, Amiri B, Humphries AC, et al. Lamellipodin tunes cell migration
by stabilizing protrusions and promoting adhesion formation. Journal of Cell
Science. 2020;133(7). doi:10.1242/jcs.239020
apa: Dimchev, G. A., Amiri, B., Humphries, A. C., Schaks, M., Dimchev, V., Stradal,
T. E. B., … Rottner, K. (2020). Lamellipodin tunes cell migration by stabilizing
protrusions and promoting adhesion formation. Journal of Cell Science.
The Company of Biologists. https://doi.org/10.1242/jcs.239020
chicago: Dimchev, Georgi A, Behnam Amiri, Ashley C. Humphries, Matthias Schaks,
Vanessa Dimchev, Theresia E. B. Stradal, Jan Faix, et al. “Lamellipodin Tunes
Cell Migration by Stabilizing Protrusions and Promoting Adhesion Formation.” Journal
of Cell Science. The Company of Biologists, 2020. https://doi.org/10.1242/jcs.239020.
ieee: G. A. Dimchev et al., “Lamellipodin tunes cell migration by stabilizing
protrusions and promoting adhesion formation,” Journal of Cell Science,
vol. 133, no. 7. The Company of Biologists, 2020.
ista: Dimchev GA, Amiri B, Humphries AC, Schaks M, Dimchev V, Stradal TEB, Faix
J, Krause M, Way M, Falcke M, Rottner K. 2020. Lamellipodin tunes cell migration
by stabilizing protrusions and promoting adhesion formation. Journal of Cell Science.
133(7), jcs239020.
mla: Dimchev, Georgi A., et al. “Lamellipodin Tunes Cell Migration by Stabilizing
Protrusions and Promoting Adhesion Formation.” Journal of Cell Science,
vol. 133, no. 7, jcs239020, The Company of Biologists, 2020, doi:10.1242/jcs.239020.
short: G.A. Dimchev, B. Amiri, A.C. Humphries, M. Schaks, V. Dimchev, T.E.B. Stradal,
J. Faix, M. Krause, M. Way, M. Falcke, K. Rottner, Journal of Cell Science 133
(2020).
date_created: 2020-09-17T14:00:33Z
date_published: 2020-04-09T00:00:00Z
date_updated: 2025-04-15T07:52:13Z
day: '09'
ddc:
- '570'
department:
- _id: FlSc
doi: 10.1242/jcs.239020
external_id:
isi:
- '000534387800005'
pmid:
- ' 32094266'
file:
- access_level: open_access
checksum: ba917e551acc4ece2884b751434df9ae
content_type: application/pdf
creator: dernst
date_created: 2020-09-17T14:07:51Z
date_updated: 2020-10-11T22:30:02Z
embargo: 2020-10-10
file_id: '8435'
file_name: 2020_JournalCellScience_Dimchev.pdf
file_size: 13493302
relation: main_file
file_date_updated: 2020-10-11T22:30:02Z
has_accepted_license: '1'
intvolume: ' 133'
isi: 1
issue: '7'
keyword:
- Cell Biology
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2674F658-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02495
name: Protein structure and function in filopodia across scales
publication: Journal of Cell Science
publication_identifier:
eissn:
- 1477-9137
issn:
- 0021-9533
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lamellipodin tunes cell migration by stabilizing protrusions and promoting
adhesion formation
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 133
year: '2020'
...
---
_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: 2024-10-14T11:19:21Z
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
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 218
year: '2019'
...
---
_id: '11062'
abstract:
- lang: eng
text: Most neurons are not replaced during an animal’s lifetime. This nondividing
state is characterized by extreme longevity and age-dependent decline of key regulatory
proteins. To study the lifespans of cells and proteins in adult tissues, we combined
isotope labeling of mice with a hybrid imaging method (MIMS-EM). Using 15N mapping,
we show that liver and pancreas are composed of cells with vastly different ages,
many as old as the animal. Strikingly, we also found that a subset of fibroblasts
and endothelial cells, both known for their replicative potential, are characterized
by the absence of cell division during adulthood. In addition, we show that the
primary cilia of beta cells and neurons contains different structural regions
with vastly different lifespans. Based on these results, we propose that age mosaicism
across multiple scales is a fundamental principle of adult tissue, cell, and protein
complex organization.
article_processing_charge: No
article_type: original
author:
- 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: Swati
full_name: Tyagi, Swati
last_name: Tyagi
- first_name: Ranjan
full_name: Ramachandra, Ranjan
last_name: Ramachandra
- first_name: Thomas
full_name: Deerinck, Thomas
last_name: Deerinck
- first_name: Eric
full_name: Bushong, Eric
last_name: Bushong
- first_name: Sebastien
full_name: Phan, Sebastien
last_name: Phan
- first_name: Victoria
full_name: Orphan, Victoria
last_name: Orphan
- 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: Arrojo e Drigo R, Lev-Ram V, Tyagi S, et al. Age mosaicism across multiple
scales in adult tissues. Cell Metabolism. 2019;30(2):343-351.e3. doi:10.1016/j.cmet.2019.05.010
apa: Arrojo e Drigo, R., Lev-Ram, V., Tyagi, S., Ramachandra, R., Deerinck, T.,
Bushong, E., … Hetzer, M. (2019). Age mosaicism across multiple scales in adult
tissues. Cell Metabolism. Elsevier. https://doi.org/10.1016/j.cmet.2019.05.010
chicago: Arrojo e Drigo, Rafael, Varda Lev-Ram, Swati Tyagi, Ranjan Ramachandra,
Thomas Deerinck, Eric Bushong, Sebastien Phan, et al. “Age Mosaicism across Multiple
Scales in Adult Tissues.” Cell Metabolism. Elsevier, 2019. https://doi.org/10.1016/j.cmet.2019.05.010.
ieee: R. Arrojo e Drigo et al., “Age mosaicism across multiple scales in
adult tissues,” Cell Metabolism, vol. 30, no. 2. Elsevier, p. 343–351.e3,
2019.
ista: Arrojo e Drigo R, Lev-Ram V, Tyagi S, Ramachandra R, Deerinck T, Bushong E,
Phan S, Orphan V, Lechene C, Ellisman MH, Hetzer M. 2019. Age mosaicism across
multiple scales in adult tissues. Cell Metabolism. 30(2), 343–351.e3.
mla: Arrojo e Drigo, Rafael, et al. “Age Mosaicism across Multiple Scales in Adult
Tissues.” Cell Metabolism, vol. 30, no. 2, Elsevier, 2019, p. 343–351.e3,
doi:10.1016/j.cmet.2019.05.010.
short: R. Arrojo e Drigo, V. Lev-Ram, S. Tyagi, R. Ramachandra, T. Deerinck, E.
Bushong, S. Phan, V. Orphan, C. Lechene, M.H. Ellisman, M. Hetzer, Cell Metabolism
30 (2019) 343–351.e3.
date_created: 2022-04-07T07:45:21Z
date_published: 2019-08-06T00:00:00Z
date_updated: 2025-12-15T10:02:11Z
day: '06'
department:
- _id: MaHe
doi: 10.1016/j.cmet.2019.05.010
extern: '1'
external_id:
pmid:
- '31178361'
intvolume: ' 30'
issue: '2'
keyword:
- Cell Biology
- Molecular Biology
- Physiology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cmet.2019.05.010
month: '08'
oa: 1
oa_version: Published Version
page: 343-351.e3
pmid: 1
publication: Cell Metabolism
publication_identifier:
issn:
- 1550-4131
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Age mosaicism across multiple scales in adult tissues
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 30
year: '2019'
...
---
_id: '10354'
abstract:
- lang: eng
text: "Background\r\nESCRT-III is a membrane remodelling filament with the unique
ability to cut membranes from the inside of the membrane neck. It is essential
for the final stage of cell division, the formation of vesicles, the release of
viruses, and membrane repair. Distinct from other cytoskeletal filaments, ESCRT-III
filaments do not consume energy themselves, but work in conjunction with another
ATP-consuming complex. Despite rapid progress in describing the cell biology of
ESCRT-III, we lack an understanding of the physical mechanisms behind its force
production and membrane remodelling.\r\nResults\r\nHere we present a minimal coarse-grained
model that captures all the experimentally reported cases of ESCRT-III driven
membrane sculpting, including the formation of downward and upward cones and tubules.
This model suggests that a change in the geometry of membrane bound ESCRT-III
filaments—from a flat spiral to a 3D helix—drives membrane deformation. We then
show that such repetitive filament geometry transitions can induce the fission
of cargo-containing vesicles.\r\nConclusions\r\nOur model provides a general physical
mechanism that explains the full range of ESCRT-III-dependent membrane remodelling
and scission events observed in cells. This mechanism for filament force production
is distinct from the mechanisms described for other cytoskeletal elements discovered
so far. The mechanistic principles revealed here suggest new ways of manipulating
ESCRT-III-driven processes in cells and could be used to guide the engineering
of synthetic membrane-sculpting systems."
acknowledgement: We thank Jeremy Carlton, Mike Staddon, Geraint Harker, and the Wellcome
Trust Consortium “Archaeal Origins of Eukaryotic Cell Organisation” for fruitful
conversations. We thank Peter Wirnsberger and Tine Curk for discussions about the
membrane model implementation.
article_number: '82'
article_processing_charge: No
article_type: original
author:
- first_name: Lena
full_name: Harker-Kirschneck, Lena
last_name: Harker-Kirschneck
- first_name: Buzz
full_name: Baum, Buzz
last_name: Baum
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
citation:
ama: Harker-Kirschneck L, Baum B, Šarić A. Changes in ESCRT-III filament geometry
drive membrane remodelling and fission in silico. BMC Biology. 2019;17(1).
doi:10.1186/s12915-019-0700-2
apa: Harker-Kirschneck, L., Baum, B., & Šarić, A. (2019). Changes in ESCRT-III
filament geometry drive membrane remodelling and fission in silico. BMC Biology.
Springer Nature. https://doi.org/10.1186/s12915-019-0700-2
chicago: Harker-Kirschneck, Lena, Buzz Baum, and Anđela Šarić. “Changes in ESCRT-III
Filament Geometry Drive Membrane Remodelling and Fission in Silico.” BMC Biology.
Springer Nature, 2019. https://doi.org/10.1186/s12915-019-0700-2.
ieee: L. Harker-Kirschneck, B. Baum, and A. Šarić, “Changes in ESCRT-III filament
geometry drive membrane remodelling and fission in silico,” BMC Biology,
vol. 17, no. 1. Springer Nature, 2019.
ista: Harker-Kirschneck L, Baum B, Šarić A. 2019. Changes in ESCRT-III filament
geometry drive membrane remodelling and fission in silico. BMC Biology. 17(1),
82.
mla: Harker-Kirschneck, Lena, et al. “Changes in ESCRT-III Filament Geometry Drive
Membrane Remodelling and Fission in Silico.” BMC Biology, vol. 17, no.
1, 82, Springer Nature, 2019, doi:10.1186/s12915-019-0700-2.
short: L. Harker-Kirschneck, B. Baum, A. Šarić, BMC Biology 17 (2019).
date_created: 2021-11-26T11:25:03Z
date_published: 2019-10-22T00:00:00Z
date_updated: 2021-11-26T11:54:29Z
day: '22'
ddc:
- '570'
doi: 10.1186/s12915-019-0700-2
extern: '1'
external_id:
pmid:
- '31640700'
file:
- access_level: open_access
checksum: 31d8bae55a376d30925f53f7e1a02396
content_type: application/pdf
creator: cchlebak
date_created: 2021-11-26T11:37:54Z
date_updated: 2021-11-26T11:37:54Z
file_id: '10356'
file_name: 2019_BMCBio_Harker_Kirschneck.pdf
file_size: 1648926
relation: main_file
success: 1
file_date_updated: 2021-11-26T11:37:54Z
has_accepted_license: '1'
intvolume: ' 17'
issue: '1'
keyword:
- cell biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/559898
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: BMC Biology
publication_identifier:
issn:
- 1741-7007
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Changes in ESCRT-III filament geometry drive membrane remodelling and fission
in silico
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 17
year: '2019'
...
---
_id: '7128'
abstract:
- lang: eng
text: Loss of functional cardiomyocytes is a major determinant of heart failure
after myocardial infarction. Previous high throughput screening studies have identified
a few microRNAs (miRNAs) that can induce cardiomyocyte proliferation and stimulate
cardiac regeneration in mice. Here, we show that all of the most effective of
these miRNAs activate nuclear localization of the master transcriptional cofactor
Yes-associated protein (YAP) and induce expression of YAP-responsive genes. In
particular, miR-199a-3p directly targets two mRNAs coding for proteins impinging
on the Hippo pathway, the upstream YAP inhibitory kinase TAOK1, and the E3 ubiquitin
ligase β-TrCP, which leads to YAP degradation. Several of the pro-proliferative
miRNAs (including miR-199a-3p) also inhibit filamentous actin depolymerization
by targeting Cofilin2, a process that by itself activates YAP nuclear translocation.
Thus, activation of YAP and modulation of the actin cytoskeleton are major components
of the pro-proliferative action of miR-199a-3p and other miRNAs that induce cardiomyocyte
proliferation.
article_processing_charge: Yes
article_type: original
author:
- first_name: Consuelo
full_name: Torrini, Consuelo
last_name: Torrini
- first_name: Ryan J
full_name: Cubero, Ryan J
id: 850B2E12-9CD4-11E9-837F-E719E6697425
last_name: Cubero
orcid: 0000-0003-0002-1867
- first_name: Ellen
full_name: Dirkx, Ellen
last_name: Dirkx
- first_name: Luca
full_name: Braga, Luca
last_name: Braga
- first_name: Hashim
full_name: Ali, Hashim
last_name: Ali
- first_name: Giulia
full_name: Prosdocimo, Giulia
last_name: Prosdocimo
- first_name: Maria Ines
full_name: Gutierrez, Maria Ines
last_name: Gutierrez
- first_name: Chiara
full_name: Collesi, Chiara
last_name: Collesi
- first_name: Danilo
full_name: Licastro, Danilo
last_name: Licastro
- first_name: Lorena
full_name: Zentilin, Lorena
last_name: Zentilin
- first_name: Miguel
full_name: Mano, Miguel
last_name: Mano
- first_name: Serena
full_name: Zacchigna, Serena
last_name: Zacchigna
- first_name: Michele
full_name: Vendruscolo, Michele
last_name: Vendruscolo
- first_name: Matteo
full_name: Marsili, Matteo
last_name: Marsili
- first_name: Areejit
full_name: Samal, Areejit
last_name: Samal
- first_name: Mauro
full_name: Giacca, Mauro
last_name: Giacca
citation:
ama: Torrini C, Cubero RJ, Dirkx E, et al. Common regulatory pathways mediate activity
of microRNAs inducing cardiomyocyte proliferation. Cell Reports. 2019;27(9):2759-2771.e5.
doi:10.1016/j.celrep.2019.05.005
apa: Torrini, C., Cubero, R. J., Dirkx, E., Braga, L., Ali, H., Prosdocimo, G.,
… Giacca, M. (2019). Common regulatory pathways mediate activity of microRNAs
inducing cardiomyocyte proliferation. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2019.05.005
chicago: Torrini, Consuelo, Ryan J Cubero, Ellen Dirkx, Luca Braga, Hashim Ali,
Giulia Prosdocimo, Maria Ines Gutierrez, et al. “Common Regulatory Pathways Mediate
Activity of MicroRNAs Inducing Cardiomyocyte Proliferation.” Cell Reports.
Elsevier, 2019. https://doi.org/10.1016/j.celrep.2019.05.005.
ieee: C. Torrini et al., “Common regulatory pathways mediate activity of
microRNAs inducing cardiomyocyte proliferation,” Cell Reports, vol. 27,
no. 9. Elsevier, p. 2759–2771.e5, 2019.
ista: Torrini C, Cubero RJ, Dirkx E, Braga L, Ali H, Prosdocimo G, Gutierrez MI,
Collesi C, Licastro D, Zentilin L, Mano M, Zacchigna S, Vendruscolo M, Marsili
M, Samal A, Giacca M. 2019. Common regulatory pathways mediate activity of microRNAs
inducing cardiomyocyte proliferation. Cell Reports. 27(9), 2759–2771.e5.
mla: Torrini, Consuelo, et al. “Common Regulatory Pathways Mediate Activity of MicroRNAs
Inducing Cardiomyocyte Proliferation.” Cell Reports, vol. 27, no. 9, Elsevier,
2019, p. 2759–2771.e5, doi:10.1016/j.celrep.2019.05.005.
short: C. Torrini, R.J. Cubero, E. Dirkx, L. Braga, H. Ali, G. Prosdocimo, M.I.
Gutierrez, C. Collesi, D. Licastro, L. Zentilin, M. Mano, S. Zacchigna, M. Vendruscolo,
M. Marsili, A. Samal, M. Giacca, Cell Reports 27 (2019) 2759–2771.e5.
date_created: 2019-11-26T22:30:07Z
date_published: 2019-05-28T00:00:00Z
date_updated: 2021-01-12T08:11:56Z
day: '28'
ddc:
- '576'
doi: 10.1016/j.celrep.2019.05.005
extern: '1'
external_id:
pmid:
- '31141697'
file:
- access_level: open_access
checksum: c5d855d07263bfec718673385d0ea2d7
content_type: application/pdf
creator: rcubero
date_created: 2019-11-26T22:30:43Z
date_updated: 2020-07-14T12:47:50Z
file_id: '7129'
file_name: torrini_cellreports_2019.pdf
file_size: 4650750
relation: main_file
file_date_updated: 2020-07-14T12:47:50Z
has_accepted_license: '1'
intvolume: ' 27'
issue: '9'
keyword:
- cardiomyocyte
- cell cycle
- Cofilin2
- cytoskeleton
- Hippo
- microRNA
- regeneration
- YAP
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '05'
oa: 1
oa_version: Published Version
page: 2759-2771.e5
pmid: 1
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte
proliferation
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: 27
year: '2019'
...
---
OA_place: publisher
_id: '6891'
abstract:
- lang: eng
text: "While cells of mesenchymal or epithelial origin perform their effector functions
in a purely anchorage dependent manner, cells derived from the hematopoietic lineage
are not committed to operate only within a specific niche. Instead, these cells
are able to function autonomously of the molecular composition in a broad range
of tissue compartments. By this means, cells of the hematopoietic lineage retain
the capacity to disseminate into connective tissue and recirculate between organs,
building the foundation for essential processes such as tissue regeneration or
immune surveillance. \r\nCells of the immune system, specifically leukocytes,
are extraordinarily good at performing this task. These cells are able to flexibly
shift their mode of migration between an adhesion-mediated and an adhesion-independent
manner, instantaneously accommodating for any changes in molecular composition
of the external scaffold. The key component driving directed leukocyte migration
is the chemokine receptor 7, which guides the cell along gradients of chemokine
ligand. Therefore, the physical destination of migrating leukocytes is purely
deterministic, i.e. given by global directional cues such as chemokine gradients.
\r\nNevertheless, these cells typically reside in three-dimensional scaffolds
of inhomogeneous complexity, raising the question whether cells are able to locally
discriminate between multiple optional migration routes. Current literature provides
evidence that leukocytes, specifically dendritic cells, do indeed probe their
surrounding by virtue of multiple explorative protrusions. However, it remains
enigmatic how these cells decide which one is the more favorable route to follow
and what are the key players involved in performing this task. Due to the heterogeneous
environment of most tissues, and the vast adaptability of migrating leukocytes,
at this time it is not clear to what extent leukocytes are able to optimize their
migratory strategy by adapting their level of adhesiveness. And, given the fact
that leukocyte migration is characterized by branched cell shapes in combination
with high migration velocities, it is reasonable to assume that these cells require
fine tuned shape maintenance mechanisms that tightly coordinate protrusion and
adhesion dynamics in a spatiotemporal manner. \r\nTherefore, this study aimed
to elucidate how rapidly migrating leukocytes opt for an ideal migratory path
while maintaining a continuous cell shape and balancing adhesive forces to efficiently
navigate through complex microenvironments. \r\nThe results of this study unraveled
a role for the microtubule cytoskeleton in promoting the decision making process
during path finding and for the first time point towards a microtubule-mediated
function in cell shape maintenance of highly ramified cells such as dendritic
cells. Furthermore, we found that migrating low-adhesive leukocytes are able to
instantaneously adapt to increased tensile load by engaging adhesion receptors.
This response was only occurring tangential to the substrate while adhesive properties
in the vertical direction were not increased. As leukocytes are primed for rapid
migration velocities, these results demonstrate that leukocyte integrins are able
to confer a high level of traction forces parallel to the cell membrane along
the direction of migration without wasting energy in gluing the cell to the substrate.
\r\nThus, the data in the here presented thesis provide new insights into the
pivotal role of cytoskeletal dynamics and the mechanisms of force transduction
during leukocyte migration. \r\nThereby the here presented results help to further
define fundamental principles underlying leukocyte migration and open up potential
therapeutic avenues of clinical relevance.\r\n"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
citation:
ama: Kopf A. The implication of cytoskeletal dynamics on leukocyte migration. 2019.
doi:10.15479/AT:ISTA:6891
apa: Kopf, A. (2019). The implication of cytoskeletal dynamics on leukocyte migration.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6891
chicago: Kopf, Aglaja. “The Implication of Cytoskeletal Dynamics on Leukocyte Migration.”
Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6891.
ieee: A. Kopf, “The implication of cytoskeletal dynamics on leukocyte migration,”
Institute of Science and Technology Austria, 2019.
ista: Kopf A. 2019. The implication of cytoskeletal dynamics on leukocyte migration.
Institute of Science and Technology Austria.
mla: Kopf, Aglaja. The Implication of Cytoskeletal Dynamics on Leukocyte Migration.
Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6891.
short: A. Kopf, The Implication of Cytoskeletal Dynamics on Leukocyte Migration,
Institute of Science and Technology Austria, 2019.
corr_author: '1'
date_created: 2019-09-19T08:19:44Z
date_published: 2019-07-24T00:00:00Z
date_updated: 2026-06-18T17:44:11Z
day: '24'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:6891
file:
- access_level: closed
checksum: 00d100d6468e31e583051e0a006b640c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: akopf
date_created: 2019-10-15T05:28:42Z
date_updated: 2020-10-17T22:30:03Z
embargo_to: open_access
file_id: '6950'
file_name: Kopf_PhD_Thesis.docx
file_size: 74735267
relation: source_file
- access_level: open_access
checksum: 5d1baa899993ae6ca81aebebe1797000
content_type: application/pdf
creator: akopf
date_created: 2019-10-15T05:28:47Z
date_updated: 2020-10-17T22:30:03Z
embargo: 2020-10-16
file_id: '6951'
file_name: Kopf_PhD_Thesis1.pdf
file_size: 52787224
relation: main_file
file_date_updated: 2020-10-17T22:30:03Z
has_accepted_license: '1'
keyword:
- cell biology
- immunology
- leukocyte
- migration
- microfluidics
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: '171'
project:
- _id: 265E2996-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01250-B20
name: Nano-Analytics of Cellular Systems
publication_identifier:
eissn:
- 2663-337X
isbn:
- 978-3-99078-002-2
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
link:
- relation: press_release
url: https://ist.ac.at/en/news/feeling-like-a-cell/
record:
- id: '6877'
relation: part_of_dissertation
status: public
- id: '6328'
relation: part_of_dissertation
status: public
- id: '15'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: The implication of cytoskeletal dynamics on leukocyte migration
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2019'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '6354'
abstract:
- lang: eng
text: Blood platelets are critical for hemostasis and thrombosis, but also play
diverse roles during immune responses. We have recently reported that platelets
migrate at sites of infection in vitro and in vivo. Importantly, platelets use
their ability to migrate to collect and bundle fibrin (ogen)-bound bacteria accomplishing
efficient intravascular bacterial trapping. Here, we describe a method that allows
analyzing platelet migration in vitro, focusing on their ability to collect bacteria
and trap bacteria under flow.
acknowledgement: This protocol was adapted from a previously published study (Gaertner
et al., 2017). We thank Michael Lorenz for his excellent assistance in bacteria
culture. This work was funded by the DFG SFB 914 (S.M. [B02 and Z01]), the DFG SFB
1123 (S.M. [B06]), the DFG FOR 2033 (S.M. and F.G.), the German Centre for Cardiovascular
Research (DZHK) (MHA 1.4VD [S.M.]), FP7 program (project 260309, PRESTIGE [S.M.]),
FöFoLe project 947 (F.G.), the Friedrich-Baur-Stiftung project 41/16 (F.G.), Marie
Sklodowska Curie Individual Fellowship (EU project 747687, LamelliaActin [F.G.]).
article_number: e3018
article_processing_charge: Yes
article_type: original
author:
- first_name: Shuxia
full_name: Fan, Shuxia
last_name: Fan
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
citation:
ama: Fan S, Lorenz M, Massberg S, Gärtner FR. Platelet migration and bacterial trapping
assay under flow. Bio-Protocol. 2018;8(18). doi:10.21769/bioprotoc.3018
apa: Fan, S., Lorenz, M., Massberg, S., & Gärtner, F. R. (2018). Platelet migration
and bacterial trapping assay under flow. Bio-Protocol. Bio-Protocol. https://doi.org/10.21769/bioprotoc.3018
chicago: Fan, Shuxia, Michael Lorenz, Steffen Massberg, and Florian R Gärtner. “Platelet
Migration and Bacterial Trapping Assay under Flow.” Bio-Protocol. Bio-Protocol,
2018. https://doi.org/10.21769/bioprotoc.3018.
ieee: S. Fan, M. Lorenz, S. Massberg, and F. R. Gärtner, “Platelet migration and
bacterial trapping assay under flow,” Bio-Protocol, vol. 8, no. 18. Bio-Protocol,
2018.
ista: Fan S, Lorenz M, Massberg S, Gärtner FR. 2018. Platelet migration and bacterial
trapping assay under flow. Bio-Protocol. 8(18), e3018.
mla: Fan, Shuxia, et al. “Platelet Migration and Bacterial Trapping Assay under
Flow.” Bio-Protocol, vol. 8, no. 18, e3018, Bio-Protocol, 2018, doi:10.21769/bioprotoc.3018.
short: S. Fan, M. Lorenz, S. Massberg, F.R. Gärtner, Bio-Protocol 8 (2018).
corr_author: '1'
date_created: 2019-04-29T09:40:33Z
date_published: 2018-09-20T00:00:00Z
date_updated: 2025-05-20T07:43:06Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.21769/bioprotoc.3018
ec_funded: 1
external_id:
pmid:
- '34395806'
file:
- access_level: open_access
checksum: d4588377e789da7f360b553ae02c5119
content_type: application/pdf
creator: dernst
date_created: 2019-04-30T08:04:33Z
date_updated: 2020-07-14T12:47:28Z
file_id: '6360'
file_name: 2018_BioProtocol_Fan.pdf
file_size: 2928337
relation: main_file
file_date_updated: 2020-07-14T12:47:28Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '18'
keyword:
- Platelets
- Cell migration
- Bacteria
- Shear flow
- Fibrinogen
- E. coli
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Bio-Protocol
publication_identifier:
issn:
- 2331-8325
publication_status: published
publisher: Bio-Protocol
quality_controlled: '1'
status: public
title: Platelet migration and bacterial trapping assay under flow
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: '2018'
...
---
_id: '8440'
abstract:
- lang: eng
text: Mycobacterium tuberculosis can remain dormant in the host, an ability that
explains the failure of many current tuberculosis treatments. Recently, the natural
products cyclomarin, ecumicin, and lassomycin have been shown to efficiently kill
Mycobacterium tuberculosis persisters. Their target is the N-terminal domain of
the hexameric AAA+ ATPase ClpC1, which recognizes, unfolds, and translocates protein
substrates, such as proteins containing phosphorylated arginine residues, to the
ClpP1P2 protease for degradation. Surprisingly, these antibiotics do not inhibit
ClpC1 ATPase activity, and how they cause cell death is still unclear. Here, using
NMR and small-angle X-ray scattering, we demonstrate that arginine-phosphate binding
to the ClpC1 N-terminal domain induces millisecond dynamics. We show that these
dynamics are caused by conformational changes and do not result from unfolding
or oligomerization of this domain. Cyclomarin binding to this domain specifically
blocked these N-terminal dynamics. On the basis of these results, we propose a
mechanism of action involving cyclomarin-induced restriction of ClpC1 dynamics,
which modulates the chaperone enzymatic activity leading eventually to cell death.
article_processing_charge: No
article_type: original
author:
- first_name: Katharina
full_name: Weinhäupl, Katharina
last_name: Weinhäupl
- first_name: Martha
full_name: Brennich, Martha
last_name: Brennich
- first_name: Uli
full_name: Kazmaier, Uli
last_name: Kazmaier
- first_name: Joel
full_name: Lelievre, Joel
last_name: Lelievre
- first_name: Lluis
full_name: Ballell, Lluis
last_name: Ballell
- first_name: Alfred
full_name: Goldberg, Alfred
last_name: Goldberg
- first_name: Paul
full_name: Schanda, Paul
id: 7B541462-FAF6-11E9-A490-E8DFE5697425
last_name: Schanda
orcid: 0000-0002-9350-7606
- first_name: Hugo
full_name: Fraga, Hugo
last_name: Fraga
citation:
ama: Weinhäupl K, Brennich M, Kazmaier U, et al. The antibiotic cyclomarin blocks
arginine-phosphate–induced millisecond dynamics in the N-terminal domain of ClpC1
from Mycobacterium tuberculosis. Journal of Biological Chemistry. 2018;293(22):8379-8393.
doi:10.1074/jbc.ra118.002251
apa: Weinhäupl, K., Brennich, M., Kazmaier, U., Lelievre, J., Ballell, L., Goldberg,
A., … Fraga, H. (2018). The antibiotic cyclomarin blocks arginine-phosphate–induced
millisecond dynamics in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis.
Journal of Biological Chemistry. American Society for Biochemistry &
Molecular Biology. https://doi.org/10.1074/jbc.ra118.002251
chicago: Weinhäupl, Katharina, Martha Brennich, Uli Kazmaier, Joel Lelievre, Lluis
Ballell, Alfred Goldberg, Paul Schanda, and Hugo Fraga. “The Antibiotic Cyclomarin
Blocks Arginine-Phosphate–Induced Millisecond Dynamics in the N-Terminal Domain
of ClpC1 from Mycobacterium Tuberculosis.” Journal of Biological Chemistry.
American Society for Biochemistry & Molecular Biology, 2018. https://doi.org/10.1074/jbc.ra118.002251.
ieee: K. Weinhäupl et al., “The antibiotic cyclomarin blocks arginine-phosphate–induced
millisecond dynamics in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis,”
Journal of Biological Chemistry, vol. 293, no. 22. American Society for
Biochemistry & Molecular Biology, pp. 8379–8393, 2018.
ista: Weinhäupl K, Brennich M, Kazmaier U, Lelievre J, Ballell L, Goldberg A, Schanda
P, Fraga H. 2018. The antibiotic cyclomarin blocks arginine-phosphate–induced
millisecond dynamics in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis.
Journal of Biological Chemistry. 293(22), 8379–8393.
mla: Weinhäupl, Katharina, et al. “The Antibiotic Cyclomarin Blocks Arginine-Phosphate–Induced
Millisecond Dynamics in the N-Terminal Domain of ClpC1 from Mycobacterium Tuberculosis.”
Journal of Biological Chemistry, vol. 293, no. 22, American Society for
Biochemistry & Molecular Biology, 2018, pp. 8379–93, doi:10.1074/jbc.ra118.002251.
short: K. Weinhäupl, M. Brennich, U. Kazmaier, J. Lelievre, L. Ballell, A. Goldberg,
P. Schanda, H. Fraga, Journal of Biological Chemistry 293 (2018) 8379–8393.
date_created: 2020-09-18T10:05:18Z
date_published: 2018-06-01T00:00:00Z
date_updated: 2021-01-12T08:19:17Z
day: '01'
doi: 10.1074/jbc.ra118.002251
extern: '1'
intvolume: ' 293'
issue: '22'
keyword:
- Cell Biology
- Biochemistry
- Molecular Biology
language:
- iso: eng
month: '06'
oa_version: None
page: 8379-8393
publication: Journal of Biological Chemistry
publication_identifier:
issn:
- 0021-9258
- 1083-351X
publication_status: published
publisher: American Society for Biochemistry & Molecular Biology
quality_controlled: '1'
status: public
title: The antibiotic cyclomarin blocks arginine-phosphate–induced millisecond dynamics
in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 293
year: '2018'
...
---
_id: '11067'
abstract:
- lang: eng
text: Neural progenitor cells (NeuPCs) possess a unique nuclear architecture that
changes during differentiation. Nucleoporins are linked with cell-type-specific
gene regulation, coupling physical changes in nuclear structure to transcriptional
output; but, whether and how they coordinate with key fate-determining transcription
factors is unclear. Here we show that the nucleoporin Nup153 interacts with Sox2
in adult NeuPCs, where it is indispensable for their maintenance and controls
neuronal differentiation. Genome-wide analyses show that Nup153 and Sox2 bind
and co-regulate hundreds of genes. Binding of Nup153 to gene promoters or transcriptional
end sites correlates with increased or decreased gene expression, respectively,
and inhibiting Nup153 expression alters open chromatin configurations at its target
genes, disrupts genomic localization of Sox2, and promotes differentiation in
vitro and a gliogenic fate switch in vivo. Together, these findings reveal that
nuclear structural proteins may exert bimodal transcriptional effects to control
cell fate.
article_processing_charge: No
article_type: original
author:
- first_name: Tomohisa
full_name: Toda, Tomohisa
last_name: Toda
- first_name: Jonathan Y.
full_name: Hsu, Jonathan Y.
last_name: Hsu
- first_name: Sara B.
full_name: Linker, Sara B.
last_name: Linker
- first_name: Lauren
full_name: Hu, Lauren
last_name: Hu
- first_name: Simon T.
full_name: Schafer, Simon T.
last_name: Schafer
- first_name: Jerome
full_name: Mertens, Jerome
last_name: Mertens
- first_name: Filipe V.
full_name: Jacinto, Filipe V.
last_name: Jacinto
- 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: Fred H.
full_name: Gage, Fred H.
last_name: Gage
citation:
ama: Toda T, Hsu JY, Linker SB, et al. Nup153 interacts with Sox2 to enable bimodal
gene regulation and maintenance of neural progenitor cells. Cell Stem Cell.
2017;21(5):618-634.e7. doi:10.1016/j.stem.2017.08.012
apa: Toda, T., Hsu, J. Y., Linker, S. B., Hu, L., Schafer, S. T., Mertens, J., …
Gage, F. H. (2017). Nup153 interacts with Sox2 to enable bimodal gene regulation
and maintenance of neural progenitor cells. Cell Stem Cell. Elsevier. https://doi.org/10.1016/j.stem.2017.08.012
chicago: Toda, Tomohisa, Jonathan Y. Hsu, Sara B. Linker, Lauren Hu, Simon T. Schafer,
Jerome Mertens, Filipe V. Jacinto, Martin Hetzer, and Fred H. Gage. “Nup153 Interacts
with Sox2 to Enable Bimodal Gene Regulation and Maintenance of Neural Progenitor
Cells.” Cell Stem Cell. Elsevier, 2017. https://doi.org/10.1016/j.stem.2017.08.012.
ieee: T. Toda et al., “Nup153 interacts with Sox2 to enable bimodal gene
regulation and maintenance of neural progenitor cells,” Cell Stem Cell,
vol. 21, no. 5. Elsevier, p. 618–634.e7, 2017.
ista: Toda T, Hsu JY, Linker SB, Hu L, Schafer ST, Mertens J, Jacinto FV, Hetzer
M, Gage FH. 2017. Nup153 interacts with Sox2 to enable bimodal gene regulation
and maintenance of neural progenitor cells. Cell Stem Cell. 21(5), 618–634.e7.
mla: Toda, Tomohisa, et al. “Nup153 Interacts with Sox2 to Enable Bimodal Gene Regulation
and Maintenance of Neural Progenitor Cells.” Cell Stem Cell, vol. 21, no.
5, Elsevier, 2017, p. 618–634.e7, doi:10.1016/j.stem.2017.08.012.
short: T. Toda, J.Y. Hsu, S.B. Linker, L. Hu, S.T. Schafer, J. Mertens, F.V. Jacinto,
M. Hetzer, F.H. Gage, Cell Stem Cell 21 (2017) 618–634.e7.
date_created: 2022-04-07T07:46:12Z
date_published: 2017-11-02T00:00:00Z
date_updated: 2022-07-18T08:33:07Z
day: '02'
doi: 10.1016/j.stem.2017.08.012
extern: '1'
external_id:
pmid:
- '28919367'
intvolume: ' 21'
issue: '5'
keyword:
- Cell Biology
- Genetics
- Molecular Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.stem.2017.08.012
month: '11'
oa: 1
oa_version: Published Version
page: 618-634.e7
pmid: 1
publication: Cell Stem Cell
publication_identifier:
issn:
- 1934-5909
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance
of neural progenitor cells
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 21
year: '2017'
...
---
_id: '15155'
abstract:
- lang: eng
text: The C-terminal transactivation domain (TAD) of BMAL1 (brain and muscle ARNT-like
1) is a regulatory hub for transcriptional coactivators and repressors that compete
for binding and, consequently, contributes to period determination of the mammalian
circadian clock. Here, we report the discovery of two distinct conformational
states that slowly exchange within the dynamic TAD to control timing. This binary
switch results from cis/trans isomerization about a highly conserved Trp-Pro imide
bond in a region of the TAD that is required for normal circadian timekeeping.
Both cis and trans isomers interact with transcriptional regulators, suggesting
that isomerization could serve a role in assembling regulatory complexes in vivo.
Toward this end, we show that locking the switch into the trans isomer leads to
shortened circadian periods. Furthermore, isomerization is regulated by the cyclophilin
family of peptidyl-prolyl isomerases, highlighting the potential for regulation
of BMAL1 protein dynamics in period determination.
article_processing_charge: No
article_type: original
author:
- first_name: Chelsea L.
full_name: Gustafson, Chelsea L.
last_name: Gustafson
- first_name: Nicole C.
full_name: Parsley, Nicole C.
last_name: Parsley
- first_name: Hande
full_name: Asimgil, Hande
last_name: Asimgil
- first_name: Hsiau-Wei
full_name: Lee, Hsiau-Wei
last_name: Lee
- first_name: Christopher
full_name: Ahlbach, Christopher
last_name: Ahlbach
- first_name: Alicia Kathleen
full_name: Michael, Alicia Kathleen
id: 6437c950-2a03-11ee-914d-d6476dd7b75c
last_name: Michael
- first_name: Haiyan
full_name: Xu, Haiyan
last_name: Xu
- first_name: Owen L.
full_name: Williams, Owen L.
last_name: Williams
- first_name: Tara L.
full_name: Davis, Tara L.
last_name: Davis
- first_name: Andrew C.
full_name: Liu, Andrew C.
last_name: Liu
- first_name: Carrie L.
full_name: Partch, Carrie L.
last_name: Partch
citation:
ama: Gustafson CL, Parsley NC, Asimgil H, et al. A slow conformational switch in
the BMAL1 transactivation domain modulates circadian rhythms. Molecular Cell.
2017;66(4):447-457.e7. doi:10.1016/j.molcel.2017.04.011
apa: Gustafson, C. L., Parsley, N. C., Asimgil, H., Lee, H.-W., Ahlbach, C., Michael,
A. K., … Partch, C. L. (2017). A slow conformational switch in the BMAL1 transactivation
domain modulates circadian rhythms. Molecular Cell. Elsevier. https://doi.org/10.1016/j.molcel.2017.04.011
chicago: Gustafson, Chelsea L., Nicole C. Parsley, Hande Asimgil, Hsiau-Wei Lee,
Christopher Ahlbach, Alicia K. Michael, Haiyan Xu, et al. “A Slow Conformational
Switch in the BMAL1 Transactivation Domain Modulates Circadian Rhythms.” Molecular
Cell. Elsevier, 2017. https://doi.org/10.1016/j.molcel.2017.04.011.
ieee: C. L. Gustafson et al., “A slow conformational switch in the BMAL1
transactivation domain modulates circadian rhythms,” Molecular Cell, vol.
66, no. 4. Elsevier, p. 447–457.e7, 2017.
ista: Gustafson CL, Parsley NC, Asimgil H, Lee H-W, Ahlbach C, Michael AK, Xu H,
Williams OL, Davis TL, Liu AC, Partch CL. 2017. A slow conformational switch in
the BMAL1 transactivation domain modulates circadian rhythms. Molecular Cell.
66(4), 447–457.e7.
mla: Gustafson, Chelsea L., et al. “A Slow Conformational Switch in the BMAL1 Transactivation
Domain Modulates Circadian Rhythms.” Molecular Cell, vol. 66, no. 4, Elsevier,
2017, p. 447–457.e7, doi:10.1016/j.molcel.2017.04.011.
short: C.L. Gustafson, N.C. Parsley, H. Asimgil, H.-W. Lee, C. Ahlbach, A.K. Michael,
H. Xu, O.L. Williams, T.L. Davis, A.C. Liu, C.L. Partch, Molecular Cell 66 (2017)
447–457.e7.
date_created: 2024-03-21T07:56:01Z
date_published: 2017-05-18T00:00:00Z
date_updated: 2024-03-25T12:19:20Z
day: '18'
doi: 10.1016/j.molcel.2017.04.011
extern: '1'
intvolume: ' 66'
issue: '4'
keyword:
- Cell Biology
- Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.molcel.2017.04.011
month: '05'
oa: 1
oa_version: Published Version
page: 447-457.e7
publication: Molecular Cell
publication_identifier:
issn:
- 1097-2765
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A slow conformational switch in the BMAL1 transactivation domain modulates
circadian rhythms
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 66
year: '2017'
...
---
_id: '5560'
abstract:
- lang: eng
text: "This repository contains the data collected for the manuscript \"Biased partitioning
of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity\".\r\nThe
data is compressed into a single archive. Within the archive, different folders
correspond to figures of the main text and the SI of the related publication.\r\nData
is saved as plain text, with each folder containing a separate readme file describing
the format. Typically, the data is from fluorescence microscopy measurements of
single cells growing in a microfluidic \"mother machine\" device, and consists
of relevant values (primarily arbitrary unit or normalized fluorescence measurements,
and division times / growth rates) after raw microscopy images have been processed,
segmented, and their features extracted, as described in the methods section of
the related publication."
article_processing_charge: No
author:
- first_name: Tobias
full_name: Bergmiller, Tobias
id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
last_name: Bergmiller
orcid: 0000-0001-5396-4346
- first_name: Anna M
full_name: Andersson, Anna M
id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87
last_name: Andersson
orcid: 0000-0003-2912-6769
- first_name: Kathrin
full_name: Tomasek, Kathrin
id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
last_name: Tomasek
orcid: 0000-0003-3768-877X
- first_name: Enrique
full_name: Balleza, Enrique
last_name: Balleza
- first_name: Daniel
full_name: Kiviet, Daniel
last_name: Kiviet
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Gasper
full_name: Tkacik, Gasper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkacik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multi-drug
efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity. 2017. doi:10.15479/AT:ISTA:53
apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild,
R., … Guet, C. C. (2017). Biased partitioning of the multi-drug efflux pump AcrAB-TolC
underlies long-lived phenotypic heterogeneity. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:53
chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza,
Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning
of the Multi-Drug Efflux Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity.”
Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:53.
ieee: T. Bergmiller et al., “Biased partitioning of the multi-drug efflux
pump AcrAB-TolC underlies long-lived phenotypic heterogeneity.” Institute of Science
and Technology Austria, 2017.
ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik
G, Guet CC. 2017. Biased partitioning of the multi-drug efflux pump AcrAB-TolC
underlies long-lived phenotypic heterogeneity, Institute of Science and Technology
Austria, 10.15479/AT:ISTA:53.
mla: Bergmiller, Tobias, et al. Biased Partitioning of the Multi-Drug Efflux
Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity. Institute of
Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:53.
short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild,
G. Tkačik, C.C. Guet, (2017).
datarep_id: '53'
date_created: 2018-12-12T12:31:32Z
date_published: 2017-03-10T00:00:00Z
date_updated: 2025-09-11T07:05:03Z
day: '10'
ddc:
- '571'
department:
- _id: CaGu
- _id: GaTk
- _id: Bio
doi: 10.15479/AT:ISTA:53
file:
- access_level: open_access
checksum: d77859af757ac8025c50c7b12b52eaf3
content_type: application/zip
creator: system
date_created: 2018-12-12T13:02:38Z
date_updated: 2020-07-14T12:47:03Z
file_id: '5603'
file_name: IST-2017-53-v1+1_Data_MDE.zip
file_size: 6773204
relation: main_file
file_date_updated: 2020-07-14T12:47:03Z
has_accepted_license: '1'
keyword:
- single cell microscopy
- mother machine microfluidic device
- AcrAB-TolC pump
- multi-drug efflux
- Escherichia coli
license: https://creativecommons.org/publicdomain/zero/1.0/
month: '03'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '665'
relation: research_paper
status: public
status: public
title: Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived
phenotypic heterogeneity
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '5570'
abstract:
- lang: eng
text: Matlab script to calculate the forward migration indexes (/) from
TrackMate spot-statistics files.
article_processing_charge: No
author:
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
citation:
ama: Hauschild R. Forward migration indexes. 2017. doi:10.15479/AT:ISTA:75
apa: Hauschild, R. (2017). Forward migration indexes. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:75
chicago: Hauschild, Robert. “Forward Migration Indexes.” Institute of Science and
Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:75.
ieee: R. Hauschild, “Forward migration indexes.” Institute of Science and Technology
Austria, 2017.
ista: Hauschild R. 2017. Forward migration indexes, Institute of Science and Technology
Austria, 10.15479/AT:ISTA:75.
mla: Hauschild, Robert. Forward Migration Indexes. Institute of Science and
Technology Austria, 2017, doi:10.15479/AT:ISTA:75.
short: R. Hauschild, (2017).
datarep_id: '75'
date_created: 2018-12-12T12:31:35Z
date_published: 2017-10-04T00:00:00Z
date_updated: 2024-02-21T13:47:14Z
day: '04'
ddc:
- '570'
department:
- _id: Bio
doi: 10.15479/AT:ISTA:75
file:
- access_level: open_access
checksum: cb7a2fa622460eca6231d659ce590e32
content_type: application/octet-stream
creator: system
date_created: 2018-12-12T13:02:29Z
date_updated: 2020-07-14T12:47:04Z
file_id: '5596'
file_name: IST-2017-75-v1+1_FMI.m
file_size: 799
relation: main_file
file_date_updated: 2020-07-14T12:47:04Z
has_accepted_license: '1'
keyword:
- Cell migration
- tracking
- forward migration index
- FMI
month: '10'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
status: public
title: Forward migration indexes
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_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: 2024-10-14T11:20:38Z
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 215
year: '2016'
...
---
_id: '5555'
abstract:
- lang: eng
text: This FIJI script calculates the population average of the migration speed
as a function of time of all cells from wide field microscopy movies.
article_processing_charge: No
author:
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
citation:
ama: Hauschild R. Fiji script to determine average speed and direction of migration
of cells. 2016. doi:10.15479/AT:ISTA:44
apa: Hauschild, R. (2016). Fiji script to determine average speed and direction
of migration of cells. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:44
chicago: Hauschild, Robert. “Fiji Script to Determine Average Speed and Direction
of Migration of Cells.” Institute of Science and Technology Austria, 2016. https://doi.org/10.15479/AT:ISTA:44.
ieee: R. Hauschild, “Fiji script to determine average speed and direction of migration
of cells.” Institute of Science and Technology Austria, 2016.
ista: Hauschild R. 2016. Fiji script to determine average speed and direction of
migration of cells, Institute of Science and Technology Austria, 10.15479/AT:ISTA:44.
mla: Hauschild, Robert. Fiji Script to Determine Average Speed and Direction
of Migration of Cells. Institute of Science and Technology Austria, 2016,
doi:10.15479/AT:ISTA:44.
short: R. Hauschild, (2016).
datarep_id: '44'
date_created: 2018-12-12T12:31:31Z
date_published: 2016-07-08T00:00:00Z
date_updated: 2024-02-21T13:50:06Z
day: '08'
ddc:
- '570'
department:
- _id: Bio
doi: 10.15479/AT:ISTA:44
file:
- access_level: open_access
checksum: 9f96cddbcd4ed689f48712ffe234d5e5
content_type: application/zip
creator: system
date_created: 2018-12-12T13:03:03Z
date_updated: 2020-07-14T12:47:02Z
file_id: '5621'
file_name: IST-2016-44-v1+1_migrationAnalyzer.zip
file_size: 20692
relation: main_file
file_date_updated: 2020-07-14T12:47:02Z
has_accepted_license: '1'
keyword:
- cell migration
- wide field microscopy
- FIJI
month: '07'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
status: public
title: Fiji script to determine average speed and direction of migration of cells
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2016'
...
---
OA_type: closed access
_id: '22510'
abstract:
- lang: eng
text: This study advances mechanistic interpretation of predictability challenges
in hydro-geomorphology related to the role of soil moisture spatial variability.
Using model formulations describing the physics of overland flow, variably saturated
subsurface flow, and erosion and sediment transport, this study explores (1) why
a basin with the same mean soil moisture can exhibit distinctly different spatial
moisture distributions, (2) whether these varying distributions lead to non-unique
hydro-geomorphic responses, and (3) what controls non-uniqueness in relation to
the response type. Two sets of numerical experiments are carried out with two
physically-based models, HYDRUS and tRIBS+VEGGIE+FEaST, and their outputs are
analyzed with respect to pre-storm moisture state. The results demonstrate that
distinct spatial moisture distributions for the same mean wetness arise because
near-surface soil moisture dynamics exhibit different degrees of coupling with
deeper-soil moisture and the process of subsurface drainage. The consequences
of such variations are different depending on the type of hydrological response.
Specifically, if the predominant runoff response is of infiltration excess type,
the degree of non-uniqueness is related to the spatial distribution of near-surface
moisture. If runoff is governed by subsurface stormflow, the extent of deep moisture
contributing area and its “readiness to drain” determine the response characteristics.
Because the processes of erosion and sediment transport superimpose additional
controls over factors governing runoff generation and overland flow, non-uniqueness
of the geomorphic response can be highly dampened or enhanced. The explanation
is sediment composed by multi-size particles can alternate states of mobilization
or surface shielding and the transient behavior is inherently intertwined with
the availability of mobile particles. We conclude that complex nonlinear dynamics
of hydro-geomorphic processes are inherent expressions of physical interactions.
As complete knowledge of watershed properties, states, or forcings will always
present the ultimate, if ever resolvable, challenge, deterministic predictability
will remain handicapped. Coupling of uncertainty quantification methods and space-time
physics-based approaches will need to evolve to facilitate mechanistic interpretations
and informed practical applications.
article_processing_charge: No
article_type: original
author:
- first_name: Jongho
full_name: Kim, Jongho
last_name: Kim
- first_name: M. Chase
full_name: Dwelle, M. Chase
last_name: Dwelle
- first_name: Stephanie K.
full_name: Kampf, Stephanie K.
last_name: Kampf
- first_name: Simone
full_name: Fatichi, Simone
id: cf8e546b-a9b0-11f0-a43b-aa89ed1b56d6
last_name: Fatichi
- first_name: Valeriy Y.
full_name: Ivanov, Valeriy Y.
last_name: Ivanov
citation:
ama: Kim J, Dwelle MC, Kampf SK, Fatichi S, Ivanov VY. On the non-uniqueness of
the hydro-geomorphic responses in a zero-order catchment with respect to soil
moisture. Advances in Water Resources. 2016;92:73-89. doi:10.1016/j.advwatres.2016.03.019
apa: Kim, J., Dwelle, M. C., Kampf, S. K., Fatichi, S., & Ivanov, V. Y. (2016).
On the non-uniqueness of the hydro-geomorphic responses in a zero-order catchment
with respect to soil moisture. Advances in Water Resources. Elsevier. https://doi.org/10.1016/j.advwatres.2016.03.019
chicago: Kim, Jongho, M. Chase Dwelle, Stephanie K. Kampf, Simone Fatichi, and Valeriy
Y. Ivanov. “On the Non-Uniqueness of the Hydro-Geomorphic Responses in a Zero-Order
Catchment with Respect to Soil Moisture.” Advances in Water Resources.
Elsevier, 2016. https://doi.org/10.1016/j.advwatres.2016.03.019.
ieee: J. Kim, M. C. Dwelle, S. K. Kampf, S. Fatichi, and V. Y. Ivanov, “On the non-uniqueness
of the hydro-geomorphic responses in a zero-order catchment with respect to soil
moisture,” Advances in Water Resources, vol. 92. Elsevier, pp. 73–89, 2016.
ista: Kim J, Dwelle MC, Kampf SK, Fatichi S, Ivanov VY. 2016. On the non-uniqueness
of the hydro-geomorphic responses in a zero-order catchment with respect to soil
moisture. Advances in Water Resources. 92, 73–89.
mla: Kim, Jongho, et al. “On the Non-Uniqueness of the Hydro-Geomorphic Responses
in a Zero-Order Catchment with Respect to Soil Moisture.” Advances in Water
Resources, vol. 92, Elsevier, 2016, pp. 73–89, doi:10.1016/j.advwatres.2016.03.019.
short: J. Kim, M.C. Dwelle, S.K. Kampf, S. Fatichi, V.Y. Ivanov, Advances in Water
Resources 92 (2016) 73–89.
das_tickbox: '1'
date_created: 2026-07-27T12:30:24Z
date_published: 2016-07-01T00:00:00Z
date_updated: 2026-08-06T07:50:36Z
day: '01'
doi: 10.1016/j.advwatres.2016.03.019
extern: '1'
intvolume: ' 92'
keyword:
- Soil moisture
- Spatial heterogeneity
- Hydrological response
- Geomorphic response
- Non-uniqueness
- Hydraulic connectivity
language:
- iso: eng
month: '07'
oa_version: None
page: 73-89
publication: Advances in Water Resources
publication_identifier:
issn:
- 0309-1708
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: On the non-uniqueness of the hydro-geomorphic responses in a zero-order catchment
with respect to soil moisture
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 92
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: 2024-10-14T11:22:26Z
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 208
year: '2015'
...
---
_id: '11078'
abstract:
- lang: eng
text: Aging is associated with the decline of protein, cell, and organ function.
Here, we use an integrated approach to characterize gene expression, bulk translation,
and cell biology in the brains and livers of young and old rats. We identify 468
differences in protein abundance between young and old animals. The majority are
a consequence of altered translation output, that is, the combined effect of changes
in transcript abundance and translation efficiency. In addition, we identify 130
proteins whose overall abundance remains unchanged but whose sub-cellular localization,
phosphorylation state, or splice-form varies. While some protein-level differences
appear to be a generic property of the rats’ chronological age, the majority are
specific to one organ. These may be a consequence of the organ’s physiology or
the chronological age of the cells within the tissue. Taken together, our study
provides an initial view of the proteome at the molecular, sub-cellular, and organ
level in young and old rats.
article_processing_charge: No
article_type: original
author:
- first_name: Alessandro
full_name: Ori, Alessandro
last_name: Ori
- first_name: Brandon H.
full_name: Toyama, Brandon H.
last_name: Toyama
- first_name: Michael S.
full_name: Harris, Michael S.
last_name: Harris
- first_name: Thomas
full_name: Bock, Thomas
last_name: Bock
- first_name: Murat
full_name: Iskar, Murat
last_name: Iskar
- first_name: Peer
full_name: Bork, Peer
last_name: Bork
- first_name: Nicholas T.
full_name: Ingolia, Nicholas T.
last_name: Ingolia
- 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: Martin
full_name: Beck, Martin
last_name: Beck
citation:
ama: Ori A, Toyama BH, Harris MS, et al. Integrated transcriptome and proteome analyses
reveal organ-specific proteome deterioration in old rats. Cell Systems.
2015;1(3):P224-237. doi:10.1016/j.cels.2015.08.012
apa: Ori, A., Toyama, B. H., Harris, M. S., Bock, T., Iskar, M., Bork, P., … Beck,
M. (2015). Integrated transcriptome and proteome analyses reveal organ-specific
proteome deterioration in old rats. Cell Systems. Elsevier. https://doi.org/10.1016/j.cels.2015.08.012
chicago: Ori, Alessandro, Brandon H. Toyama, Michael S. Harris, Thomas Bock, Murat
Iskar, Peer Bork, Nicholas T. Ingolia, Martin Hetzer, and Martin Beck. “Integrated
Transcriptome and Proteome Analyses Reveal Organ-Specific Proteome Deterioration
in Old Rats.” Cell Systems. Elsevier, 2015. https://doi.org/10.1016/j.cels.2015.08.012.
ieee: A. Ori et al., “Integrated transcriptome and proteome analyses reveal
organ-specific proteome deterioration in old rats,” Cell Systems, vol.
1, no. 3. Elsevier, pp. P224-237, 2015.
ista: Ori A, Toyama BH, Harris MS, Bock T, Iskar M, Bork P, Ingolia NT, Hetzer M,
Beck M. 2015. Integrated transcriptome and proteome analyses reveal organ-specific
proteome deterioration in old rats. Cell Systems. 1(3), P224-237.
mla: Ori, Alessandro, et al. “Integrated Transcriptome and Proteome Analyses Reveal
Organ-Specific Proteome Deterioration in Old Rats.” Cell Systems, vol.
1, no. 3, Elsevier, 2015, pp. P224-237, doi:10.1016/j.cels.2015.08.012.
short: A. Ori, B.H. Toyama, M.S. Harris, T. Bock, M. Iskar, P. Bork, N.T. Ingolia,
M. Hetzer, M. Beck, Cell Systems 1 (2015) P224-237.
date_created: 2022-04-07T07:49:39Z
date_published: 2015-09-23T00:00:00Z
date_updated: 2024-10-14T11:23:01Z
day: '23'
doi: 10.1016/j.cels.2015.08.012
extern: '1'
external_id:
pmid:
- '27135913'
intvolume: ' 1'
issue: '3'
keyword:
- Cell Biology
- Histology
- Pathology and Forensic Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cels.2015.08.012
month: '09'
oa: 1
oa_version: Published Version
page: P224-237
pmid: 1
publication: Cell Systems
publication_identifier:
issn:
- 2405-4712
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Integrated transcriptome and proteome analyses reveal organ-specific proteome
deterioration in old rats
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2015'
...