---
_id: '12272'
abstract:
- lang: eng
text: Reading, interpreting and crawling along gradients of chemotactic cues is
one of the most complex questions in cell biology. In this issue, Georgantzoglou
et al. (2022. J. Cell. Biol.https://doi.org/10.1083/jcb.202103207) use in vivo
models to map the temporal sequence of how neutrophils respond to an acutely arising
gradient of chemoattractant.
article_number: e202206127
article_processing_charge: No
article_type: original
author:
- first_name: Julian A
full_name: Stopp, Julian A
id: 489E3F00-F248-11E8-B48F-1D18A9856A87
last_name: Stopp
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Stopp JA, Sixt MK. Plan your trip before you leave: The neutrophils’ search-and-run
journey. Journal of Cell Biology. 2022;221(8). doi:10.1083/jcb.202206127'
apa: 'Stopp, J. A., & Sixt, M. K. (2022). Plan your trip before you leave: The
neutrophils’ search-and-run journey. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.202206127'
chicago: 'Stopp, Julian A, and Michael K Sixt. “Plan Your Trip before You Leave:
The Neutrophils’ Search-and-Run Journey.” Journal of Cell Biology. Rockefeller
University Press, 2022. https://doi.org/10.1083/jcb.202206127.'
ieee: 'J. A. Stopp and M. K. Sixt, “Plan your trip before you leave: The neutrophils’
search-and-run journey,” Journal of Cell Biology, vol. 221, no. 8. Rockefeller
University Press, 2022.'
ista: 'Stopp JA, Sixt MK. 2022. Plan your trip before you leave: The neutrophils’
search-and-run journey. Journal of Cell Biology. 221(8), e202206127.'
mla: 'Stopp, Julian A., and Michael K. Sixt. “Plan Your Trip before You Leave: The
Neutrophils’ Search-and-Run Journey.” Journal of Cell Biology, vol. 221,
no. 8, e202206127, Rockefeller University Press, 2022, doi:10.1083/jcb.202206127.'
short: J.A. Stopp, M.K. Sixt, Journal of Cell Biology 221 (2022).
date_created: 2023-01-16T10:01:08Z
date_published: 2022-07-20T00:00:00Z
date_updated: 2023-12-21T14:30:01Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1083/jcb.202206127
external_id:
isi:
- '000874717200001'
pmid:
- '35856919'
file:
- access_level: open_access
checksum: 6b1620743669679b48b9389bb40f5a11
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T10:39:34Z
date_updated: 2023-01-30T10:39:34Z
file_id: '12451'
file_name: 2022_JourCellBiology_Stopp.pdf
file_size: 969969
relation: main_file
success: 1
file_date_updated: 2023-01-30T10:39:34Z
has_accepted_license: '1'
intvolume: ' 221'
isi: 1
issue: '8'
keyword:
- Cell Biology
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
related_material:
record:
- id: '14697'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: 'Plan your trip before you leave: The neutrophils’ search-and-run journey'
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 221
year: '2022'
...
---
_id: '12283'
abstract:
- lang: eng
text: Neurons extend axons to form the complex circuitry of the mature brain. This
depends on the coordinated response and continuous remodelling of the microtubule
and F-actin networks in the axonal growth cone. Growth cone architecture remains
poorly understood at nanoscales. We therefore investigated mouse hippocampal neuron
growth cones using cryo-electron tomography to directly visualise their three-dimensional
subcellular architecture with molecular detail. Our data showed that the hexagonal
arrays of actin bundles that form filopodia penetrate and terminate deep within
the growth cone interior. We directly observed the modulation of these and other
growth cone actin bundles by alteration of individual F-actin helical structures.
Microtubules with blunt, slightly flared or gently curved ends predominated in
the growth cone, frequently contained lumenal particles and exhibited lattice
defects. Investigation of the effect of absence of doublecortin, a neurodevelopmental
cytoskeleton regulator, on growth cone cytoskeleton showed no major anomalies
in overall growth cone organisation or in F-actin subpopulations. However, our
data suggested that microtubules sustained more structural defects, highlighting
the importance of microtubule integrity during growth cone migration.
acknowledgement: "J.A. was supported by a grant from the Medical Research Council
(MRC), UK (MR/R000352/1) to C.A.M. Cryo-EM data were collected on equipment funded
by the Wellcome Trust, UK (079605/Z/06/Z) and the Biotechnology and Biological Sciences
Research Council (BBSRC) UK (BB/L014211/1). F.F.’s salary and institute were supported
by Inserm (Institut National de la Santé et de la Recherche Médicale), CNRS (Centre
National de la Recherche Scientifique) and Sorbonne Université. F.F.’s group was
particularly supported by Agence Nationale de la\r\nRecherche (ANR-16-CE16-0011-03)
and Seventh Framework Programme (EUHEALTH-\r\n2013, DESIRE, N° 60253; also funding
M.S.’s salary) and the European Cooperation in Science and Technology (COST Action
CA16118). Open Access funding provided by Birkbeck College: Birkbeck University
of London. Deposited in PMC for immediate release."
article_number: '259234'
article_processing_charge: No
article_type: original
author:
- first_name: Joseph
full_name: Atherton, Joseph
last_name: Atherton
- first_name: Melissa A
full_name: Stouffer, Melissa A
id: 4C9372C4-F248-11E8-B48F-1D18A9856A87
last_name: Stouffer
- first_name: Fiona
full_name: Francis, Fiona
last_name: Francis
- first_name: Carolyn A.
full_name: Moores, Carolyn A.
last_name: Moores
citation:
ama: Atherton J, Stouffer MA, Francis F, Moores CA. Visualising the cytoskeletal
machinery in neuronal growth cones using cryo-electron tomography. Journal
of Cell Science. 2022;135(7). doi:10.1242/jcs.259234
apa: Atherton, J., Stouffer, M. A., Francis, F., & Moores, C. A. (2022). Visualising
the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography.
Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.259234
chicago: Atherton, Joseph, Melissa A Stouffer, Fiona Francis, and Carolyn A. Moores.
“Visualising the Cytoskeletal Machinery in Neuronal Growth Cones Using Cryo-Electron
Tomography.” Journal of Cell Science. The Company of Biologists, 2022.
https://doi.org/10.1242/jcs.259234.
ieee: J. Atherton, M. A. Stouffer, F. Francis, and C. A. Moores, “Visualising the
cytoskeletal machinery in neuronal growth cones using cryo-electron tomography,”
Journal of Cell Science, vol. 135, no. 7. The Company of Biologists, 2022.
ista: Atherton J, Stouffer MA, Francis F, Moores CA. 2022. Visualising the cytoskeletal
machinery in neuronal growth cones using cryo-electron tomography. Journal of
Cell Science. 135(7), 259234.
mla: Atherton, Joseph, et al. “Visualising the Cytoskeletal Machinery in Neuronal
Growth Cones Using Cryo-Electron Tomography.” Journal of Cell Science,
vol. 135, no. 7, 259234, The Company of Biologists, 2022, doi:10.1242/jcs.259234.
short: J. Atherton, M.A. Stouffer, F. Francis, C.A. Moores, Journal of Cell Science
135 (2022).
date_created: 2023-01-16T10:03:24Z
date_published: 2022-04-01T00:00:00Z
date_updated: 2023-08-04T10:28:34Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1242/jcs.259234
external_id:
isi:
- '000783840400010'
pmid:
- '35383828'
file:
- access_level: open_access
checksum: 4346ed32cb7c89a8ca051c7da68a9a1c
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T11:41:01Z
date_updated: 2023-01-30T11:41:01Z
file_id: '12461'
file_name: 2022_JourCellBiology_Atherton.pdf
file_size: 13868733
relation: main_file
success: 1
file_date_updated: 2023-01-30T11:41:01Z
has_accepted_license: '1'
intvolume: ' 135'
isi: 1
issue: '7'
keyword:
- Cell Biology
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
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: Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron
tomography
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 135
year: '2022'
...
---
_id: '11052'
abstract:
- lang: eng
text: In order to combat molecular damage, most cellular proteins undergo rapid
turnover. We have previously identified large nuclear protein assemblies that
can persist for years in post-mitotic tissues and are subject to age-related decline.
Here, we report that mitochondria can be long lived in the mouse brain and reveal
that specific mitochondrial proteins have half-lives longer than the average proteome.
These mitochondrial long-lived proteins (mitoLLPs) are core components of the
electron transport chain (ETC) and display increased longevity in respiratory
supercomplexes. We find that COX7C, a mitoLLP that forms a stable contact site
between complexes I and IV, is required for complex IV and supercomplex assembly.
Remarkably, even upon depletion of COX7C transcripts, ETC function is maintained
for days, effectively uncoupling mitochondrial function from ongoing transcription
of its mitoLLPs. Our results suggest that modulating protein longevity within
the ETC is critical for mitochondrial proteome maintenance and the robustness
of mitochondrial function.
article_processing_charge: No
article_type: original
author:
- first_name: Shefali
full_name: Krishna, Shefali
last_name: Krishna
- first_name: Rafael
full_name: Arrojo e Drigo, Rafael
last_name: Arrojo e Drigo
- first_name: Juliana S.
full_name: Capitanio, Juliana S.
last_name: Capitanio
- first_name: Ranjan
full_name: Ramachandra, Ranjan
last_name: Ramachandra
- first_name: Mark
full_name: Ellisman, Mark
last_name: Ellisman
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
M. Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain. Developmental Cell. 2021;56(21):P2952-2965.e9.
doi:10.1016/j.devcel.2021.10.008
apa: Krishna, S., Arrojo e Drigo, R., Capitanio, J. S., Ramachandra, R., Ellisman,
M., & Hetzer, M. (2021). Identification of long-lived proteins in the mitochondria
reveals increased stability of the electron transport chain. Developmental
Cell. Elsevier. https://doi.org/10.1016/j.devcel.2021.10.008
chicago: Krishna, Shefali, Rafael Arrojo e Drigo, Juliana S. Capitanio, Ranjan Ramachandra,
Mark Ellisman, and Martin Hetzer. “Identification of Long-Lived Proteins in the
Mitochondria Reveals Increased Stability of the Electron Transport Chain.” Developmental
Cell. Elsevier, 2021. https://doi.org/10.1016/j.devcel.2021.10.008.
ieee: S. Krishna, R. Arrojo e Drigo, J. S. Capitanio, R. Ramachandra, M. Ellisman,
and M. Hetzer, “Identification of long-lived proteins in the mitochondria reveals
increased stability of the electron transport chain,” Developmental Cell,
vol. 56, no. 21. Elsevier, p. P2952–2965.e9, 2021.
ista: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
M. 2021. Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain. Developmental Cell. 56(21), P2952–2965.e9.
mla: Krishna, Shefali, et al. “Identification of Long-Lived Proteins in the Mitochondria
Reveals Increased Stability of the Electron Transport Chain.” Developmental
Cell, vol. 56, no. 21, Elsevier, 2021, p. P2952–2965.e9, doi:10.1016/j.devcel.2021.10.008.
short: S. Krishna, R. Arrojo e Drigo, J.S. Capitanio, R. Ramachandra, M. Ellisman,
M. Hetzer, Developmental Cell 56 (2021) P2952–2965.e9.
date_created: 2022-04-07T07:43:14Z
date_published: 2021-11-08T00:00:00Z
date_updated: 2022-07-18T08:26:38Z
day: '08'
doi: 10.1016/j.devcel.2021.10.008
extern: '1'
external_id:
pmid:
- '34715012'
intvolume: ' 56'
issue: '21'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa_version: None
page: P2952-2965.e9
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 56
year: '2021'
...
---
_id: '8966'
abstract:
- lang: eng
text: During development, a single cell is transformed into a highly complex organism
through progressive cell division, specification and rearrangement. An important
prerequisite for the emergence of patterns within the developing organism is to
establish asymmetries at various scales, ranging from individual cells to the
entire embryo, eventually giving rise to the different body structures. This becomes
especially apparent during gastrulation, when the earliest major lineage restriction
events lead to the formation of the different germ layers. Traditionally, the
unfolding of the developmental program from symmetry breaking to germ layer formation
has been studied by dissecting the contributions of different signaling pathways
and cellular rearrangements in the in vivo context of intact embryos. Recent efforts,
using the intrinsic capacity of embryonic stem cells to self-assemble and generate
embryo-like structures de novo, have opened new avenues for understanding the
many ways by which an embryo can be built and the influence of extrinsic factors
therein. Here, we discuss and compare divergent and conserved strategies leading
to germ layer formation in embryos as compared to in vitro systems, their upstream
molecular cascades and the role of extrinsic factors in this process.
acknowledgement: We thank Nicoletta Petridou, Diana Pinheiro, Cornelia Schwayer and
Stefania Tavano for feedback on the manuscript. Research in the Heisenberg lab is
supported by an ERC Advanced Grant (MECSPEC 742573) to C.-P.H. A.S. is a recipient
of a DOC Fellowship of the Austrian Academy of Science.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Alexandra
full_name: Schauer, Alexandra
id: 30A536BA-F248-11E8-B48F-1D18A9856A87
last_name: Schauer
orcid: 0000-0001-7659-9142
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Schauer A, Heisenberg C-PJ. Reassembling gastrulation. Developmental Biology.
2021;474:71-81. doi:10.1016/j.ydbio.2020.12.014
apa: Schauer, A., & Heisenberg, C.-P. J. (2021). Reassembling gastrulation.
Developmental Biology. Elsevier. https://doi.org/10.1016/j.ydbio.2020.12.014
chicago: Schauer, Alexandra, and Carl-Philipp J Heisenberg. “Reassembling Gastrulation.”
Developmental Biology. Elsevier, 2021. https://doi.org/10.1016/j.ydbio.2020.12.014.
ieee: A. Schauer and C.-P. J. Heisenberg, “Reassembling gastrulation,” Developmental
Biology, vol. 474. Elsevier, pp. 71–81, 2021.
ista: Schauer A, Heisenberg C-PJ. 2021. Reassembling gastrulation. Developmental
Biology. 474, 71–81.
mla: Schauer, Alexandra, and Carl-Philipp J. Heisenberg. “Reassembling Gastrulation.”
Developmental Biology, vol. 474, Elsevier, 2021, pp. 71–81, doi:10.1016/j.ydbio.2020.12.014.
short: A. Schauer, C.-P.J. Heisenberg, Developmental Biology 474 (2021) 71–81.
date_created: 2020-12-22T09:53:34Z
date_published: 2021-06-01T00:00:00Z
date_updated: 2023-08-07T13:30:01Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1016/j.ydbio.2020.12.014
ec_funded: 1
external_id:
isi:
- '000639461800008'
file:
- access_level: open_access
checksum: fa2a5731fd16ab171b029f32f031c440
content_type: application/pdf
creator: kschuh
date_created: 2021-08-11T10:28:06Z
date_updated: 2021-08-11T10:28:06Z
file_id: '9880'
file_name: 2021_DevBiology_Schauer.pdf
file_size: 1440321
relation: main_file
success: 1
file_date_updated: 2021-08-11T10:28:06Z
has_accepted_license: '1'
intvolume: ' 474'
isi: 1
keyword:
- Developmental Biology
- Cell Biology
- Molecular Biology
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 71-81
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 26B1E39C-B435-11E9-9278-68D0E5697425
grant_number: '25239'
name: 'Mesendoderm specification in zebrafish: The role of extraembryonic tissues'
publication: Developmental Biology
publication_identifier:
issn:
- 0012-1606
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '12891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Reassembling gastrulation
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 474
year: '2021'
...
---
_id: '9188'
abstract:
- lang: eng
text: Genomic imprinting is an epigenetic mechanism that results in parental allele-specific
expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental
regulators and play pivotal roles in many biological processes such as nutrient
transfer from the mother to offspring and neuronal development. Imprinted genes
are also involved in human disease, including neurodevelopmental disorders, and
often occur in clusters that are regulated by a common imprint control region
(ICR). In extra-embryonic tissues ICRs can act over large distances, with the
largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical
imprinted expression that shows near exclusive maternal or paternal expression,
widespread biased imprinted expression has been identified mainly in brain. In
this review we discuss recent developments mapping cell type specific imprinted
expression in extra-embryonic tissues and neocortex in the mouse. We highlight
the advantages of using an inducible uniparental chromosome disomy (UPD) system
to generate cells carrying either two maternal or two paternal copies of a specific
chromosome to analyze the functional consequences of genomic imprinting. Mosaic
Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant
induction of UPD sparsely in specific cell types, and thus to over-express or
suppress all imprinted genes on that chromosome. To illustrate the utility of
this technique, we explain how MADM-induced UPD revealed new insights about the
function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs
led to identification of highly cell type specific phenotypes related to perturbed
imprinted expression in the mouse neocortex. Finally, we give an outlook on how
MADM could be used to probe cell type specific imprinted expression in other tissues
in mouse, particularly in extra-embryonic tissues.
acknowledgement: We thank Melissa Stouffer for critically reading the manuscript.
This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung
n[f + b] life science call grant (C13-002) to S.H. and the European Research Council
(ERC) under the European Union's Horizon 2020 research and innovation program (grant
agreement 725780 LinPro) to S.H.
article_number: '104986'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Quanah
full_name: Hudson, Quanah
last_name: Hudson
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome
disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry
International. 2021;145(5). doi:10.1016/j.neuint.2021.104986
apa: Pauler, F., Hudson, Q., Laukoter, S., & Hippenmeyer, S. (2021). Inducible
uniparental chromosome disomy to probe genomic imprinting at single-cell level
in brain and beyond. Neurochemistry International. Elsevier. https://doi.org/10.1016/j.neuint.2021.104986
chicago: Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer.
“Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell
Level in Brain and Beyond.” Neurochemistry International. Elsevier, 2021.
https://doi.org/10.1016/j.neuint.2021.104986.
ieee: F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental
chromosome disomy to probe genomic imprinting at single-cell level in brain and
beyond,” Neurochemistry International, vol. 145, no. 5. Elsevier, 2021.
ista: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental
chromosome disomy to probe genomic imprinting at single-cell level in brain and
beyond. Neurochemistry International. 145(5), 104986.
mla: Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic
Imprinting at Single-Cell Level in Brain and Beyond.” Neurochemistry International,
vol. 145, no. 5, 104986, Elsevier, 2021, doi:10.1016/j.neuint.2021.104986.
short: F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International
145 (2021).
date_created: 2021-02-23T12:31:43Z
date_published: 2021-05-01T00:00:00Z
date_updated: 2023-08-07T13:48:26Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuint.2021.104986
ec_funded: 1
external_id:
isi:
- '000635575000005'
pmid:
- '33600873'
file:
- access_level: open_access
checksum: c6d7a40089cd29e289f9b22e75768304
content_type: application/pdf
creator: kschuh
date_created: 2021-08-11T12:30:38Z
date_updated: 2021-08-11T12:30:38Z
file_id: '9883'
file_name: 2021_NCI_Pauler.pdf
file_size: 7083499
relation: main_file
success: 1
file_date_updated: 2021-08-11T12:30:38Z
has_accepted_license: '1'
intvolume: ' 145'
isi: 1
issue: '5'
keyword:
- Cell Biology
- Cellular and Molecular Neuroscience
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
publication: Neurochemistry International
publication_identifier:
issn:
- 0197-0186
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell
level in brain and beyond
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 145
year: '2021'
...
---
_id: '9379'
abstract:
- lang: eng
text: When B cells encounter membrane-bound antigens, the formation and coalescence
of B cell antigen receptor (BCR) microclusters amplifies BCR signaling. The ability
of B cells to probe the surface of antigen-presenting cells (APCs) and respond
to APC-bound antigens requires remodeling of the actin cytoskeleton. Initial BCR
signaling stimulates actin-related protein (Arp) 2/3 complex-dependent actin polymerization,
which drives B cell spreading as well as the centripetal movement and coalescence
of BCR microclusters at the B cell-APC synapse. Sustained actin polymerization
depends on concomitant actin filament depolymerization, which enables the recycling
of actin monomers and Arp2/3 complexes. Cofilin-mediated severing of actin filaments
is a rate-limiting step in the morphological changes that occur during immune
synapse formation. Hence, regulators of cofilin activity such as WD repeat-containing
protein 1 (Wdr1), LIM domain kinase (LIMK), and coactosin-like 1 (Cotl1) may also
be essential for actin-dependent processes in B cells. Wdr1 enhances cofilin-mediated
actin disassembly. Conversely, Cotl1 competes with cofilin for binding to actin
and LIMK phosphorylates cofilin and prevents it from binding to actin filaments.
We now show that Wdr1 and LIMK have distinct roles in BCR-induced assembly of
the peripheral actin structures that drive B cell spreading, and that cofilin,
Wdr1, and LIMK all contribute to the actin-dependent amplification of BCR signaling
at the immune synapse. Depleting Cotl1 had no effect on these processes. Thus,
the Wdr1-LIMK-cofilin axis is critical for BCR-induced actin remodeling and for
B cell responses to APC-bound antigens.
acknowledgement: We thank the UBC Life Sciences Institute Imaging Facility andthe
UBC Flow Cytometry Facility.
article_number: '649433'
article_processing_charge: No
article_type: original
author:
- first_name: Madison
full_name: Bolger-Munro, Madison
id: 516F03FA-93A3-11EA-A7C5-D6BE3DDC885E
last_name: Bolger-Munro
orcid: 0000-0002-8176-4824
- first_name: Kate
full_name: Choi, Kate
last_name: Choi
- first_name: Faith
full_name: Cheung, Faith
last_name: Cheung
- first_name: Yi Tian
full_name: Liu, Yi Tian
last_name: Liu
- first_name: May
full_name: Dang-Lawson, May
last_name: Dang-Lawson
- first_name: Nikola
full_name: Deretic, Nikola
last_name: Deretic
- first_name: Connor
full_name: Keane, Connor
last_name: Keane
- first_name: Michael R.
full_name: Gold, Michael R.
last_name: Gold
citation:
ama: Bolger-Munro M, Choi K, Cheung F, et al. The Wdr1-LIMK-Cofilin axis controls
B cell antigen receptor-induced actin remodeling and signaling at the immune synapse.
Frontiers in Cell and Developmental Biology. 2021;9. doi:10.3389/fcell.2021.649433
apa: Bolger-Munro, M., Choi, K., Cheung, F., Liu, Y. T., Dang-Lawson, M., Deretic,
N., … Gold, M. R. (2021). The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced
actin remodeling and signaling at the immune synapse. Frontiers in Cell and
Developmental Biology. Frontiers Media. https://doi.org/10.3389/fcell.2021.649433
chicago: Bolger-Munro, Madison, Kate Choi, Faith Cheung, Yi Tian Liu, May Dang-Lawson,
Nikola Deretic, Connor Keane, and Michael R. Gold. “The Wdr1-LIMK-Cofilin Axis
Controls B Cell Antigen Receptor-Induced Actin Remodeling and Signaling at the
Immune Synapse.” Frontiers in Cell and Developmental Biology. Frontiers
Media, 2021. https://doi.org/10.3389/fcell.2021.649433.
ieee: M. Bolger-Munro et al., “The Wdr1-LIMK-Cofilin axis controls B cell
antigen receptor-induced actin remodeling and signaling at the immune synapse,”
Frontiers in Cell and Developmental Biology, vol. 9. Frontiers Media, 2021.
ista: Bolger-Munro M, Choi K, Cheung F, Liu YT, Dang-Lawson M, Deretic N, Keane
C, Gold MR. 2021. The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced
actin remodeling and signaling at the immune synapse. Frontiers in Cell and Developmental
Biology. 9, 649433.
mla: Bolger-Munro, Madison, et al. “The Wdr1-LIMK-Cofilin Axis Controls B Cell Antigen
Receptor-Induced Actin Remodeling and Signaling at the Immune Synapse.” Frontiers
in Cell and Developmental Biology, vol. 9, 649433, Frontiers Media, 2021,
doi:10.3389/fcell.2021.649433.
short: M. Bolger-Munro, K. Choi, F. Cheung, Y.T. Liu, M. Dang-Lawson, N. Deretic,
C. Keane, M.R. Gold, Frontiers in Cell and Developmental Biology 9 (2021).
date_created: 2021-05-09T22:01:37Z
date_published: 2021-04-13T00:00:00Z
date_updated: 2023-10-18T08:19:49Z
day: '13'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.3389/fcell.2021.649433
external_id:
isi:
- '000644419500001'
pmid:
- '33928084'
file:
- access_level: open_access
checksum: 8c8a03575d2f7583f88dc3b658b0976b
content_type: application/pdf
creator: kschuh
date_created: 2021-05-11T15:09:23Z
date_updated: 2021-05-11T15:09:23Z
file_id: '9386'
file_name: 2021_Frontiers_Cell_Bolger-Munro.pdf
file_size: 4076024
relation: main_file
success: 1
file_date_updated: 2021-05-11T15:09:23Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
keyword:
- B cell
- actin
- immune synapse
- cell spreading
- cofilin
- WDR1 (AIP1)
- LIM domain kinase
- B cell receptor (BCR)
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Frontiers in Cell and Developmental Biology
publication_identifier:
eissn:
- 2296-634X
publication_status: published
publisher: Frontiers Media
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced actin remodeling
and signaling at the immune synapse
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: 9
year: '2021'
...
---
_id: '10337'
abstract:
- lang: eng
text: The T cell receptor (TCR) pathway receives, processes, and amplifies the signal
from pathogenic antigens to the activation of T cells. Although major components
in this pathway have been identified, the knowledge on how individual components
cooperate to effectively transduce signals remains limited. Phase separation emerges
as a biophysical principle in organizing signaling molecules into liquid-like
condensates. Here, we report that phospholipase Cγ1 (PLCγ1) promotes phase separation
of LAT, a key adaptor protein in the TCR pathway. PLCγ1 directly cross-links LAT
through its two SH2 domains. PLCγ1 also protects LAT from dephosphorylation by
the phosphatase CD45 and promotes LAT-dependent ERK activation and SLP76 phosphorylation.
Intriguingly, a nonmonotonic effect of PLCγ1 on LAT clustering was discovered.
Computer simulations, based on patchy particles, revealed how the cluster size
is regulated by protein compositions. Together, these results define a critical
function of PLCγ1 in promoting phase separation of the LAT complex and TCR signal
transduction.
acknowledgement: Charles H. Hood Foundation (NO AWARD) ; Rally Foundation (NO AWARD)
article_number: e202009154
article_processing_charge: No
article_type: original
author:
- first_name: Longhui
full_name: Zeng, Longhui
last_name: Zeng
- first_name: Ivan
full_name: Palaia, Ivan
last_name: Palaia
- first_name: Anđela
full_name: Šarić, Anđela
id: bf63d406-f056-11eb-b41d-f263a6566d8b
last_name: Šarić
orcid: 0000-0002-7854-2139
- first_name: Xiaolei
full_name: Su, Xiaolei
last_name: Su
citation:
ama: Zeng L, Palaia I, Šarić A, Su X. PLCγ1 promotes phase separation of T cell
signaling components. Journal of Cell Biology. 2021;220(6). doi:10.1083/jcb.202009154
apa: Zeng, L., Palaia, I., Šarić, A., & Su, X. (2021). PLCγ1 promotes phase
separation of T cell signaling components. Journal of Cell Biology. Rockefeller
University Press. https://doi.org/10.1083/jcb.202009154
chicago: Zeng, Longhui, Ivan Palaia, Anđela Šarić, and Xiaolei Su. “PLCγ1 Promotes
Phase Separation of T Cell Signaling Components.” Journal of Cell Biology.
Rockefeller University Press, 2021. https://doi.org/10.1083/jcb.202009154.
ieee: L. Zeng, I. Palaia, A. Šarić, and X. Su, “PLCγ1 promotes phase separation
of T cell signaling components,” Journal of Cell Biology, vol. 220, no.
6. Rockefeller University Press, 2021.
ista: Zeng L, Palaia I, Šarić A, Su X. 2021. PLCγ1 promotes phase separation of
T cell signaling components. Journal of Cell Biology. 220(6), e202009154.
mla: Zeng, Longhui, et al. “PLCγ1 Promotes Phase Separation of T Cell Signaling
Components.” Journal of Cell Biology, vol. 220, no. 6, e202009154, Rockefeller
University Press, 2021, doi:10.1083/jcb.202009154.
short: L. Zeng, I. Palaia, A. Šarić, X. Su, Journal of Cell Biology 220 (2021).
date_created: 2021-11-25T15:21:30Z
date_published: 2021-04-30T00:00:00Z
date_updated: 2021-11-25T15:33:08Z
day: '30'
doi: 10.1083/jcb.202009154
extern: '1'
external_id:
pmid:
- '33929486'
intvolume: ' 220'
issue: '6'
keyword:
- cell biology
language:
- iso: eng
month: '04'
oa_version: None
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: PLCγ1 promotes phase separation of T cell signaling components
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 220
year: '2021'
...
---
_id: '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.
date_created: 2021-08-29T12:36:50Z
date_published: 2021-09-02T00:00:00Z
date_updated: 2023-09-22T09:58:30Z
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
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2021'
...
---
_id: '9986'
abstract:
- lang: eng
text: Size control is a fundamental question in biology, showing incremental complexity
in plants, whose cells possess a rigid cell wall. The phytohormone auxin is a
vital growth regulator with central importance for differential growth control.
Our results indicate that auxin-reliant growth programs affect the molecular complexity
of xyloglucans, the major type of cell wall hemicellulose in eudicots. Auxin-dependent
induction and repression of growth coincide with reduced and enhanced molecular
complexity of xyloglucans, respectively. In agreement with a proposed function
in growth control, genetic interference with xyloglucan side decorations distinctly
modulates auxin-dependent differential growth rates. Our work proposes that auxin-dependent
growth programs have a spatially defined effect on xyloglucan’s molecular structure,
which in turn affects cell wall mechanics and specifies differential, gravitropic
hypocotyl growth.
acknowledgement: "We are grateful to Paul Knox, Markus Pauly, Malcom O’Neill, and
Ignacio Zarra for providing published material; the BOKU-VIBT Imaging Center for
access and M. Debreczeny for expertise; J.I. Thaker and Georg Seifert for critical
reading.\r\n"
article_number: '9222'
article_processing_charge: Yes
article_type: original
author:
- first_name: Silvia Melina
full_name: Velasquez, Silvia Melina
last_name: Velasquez
- first_name: Xiaoyuan
full_name: Guo, Xiaoyuan
last_name: Guo
- first_name: Marçal
full_name: Gallemi, Marçal
id: 460C6802-F248-11E8-B48F-1D18A9856A87
last_name: Gallemi
orcid: 0000-0003-4675-6893
- first_name: Bibek
full_name: Aryal, Bibek
last_name: Aryal
- first_name: Peter
full_name: Venhuizen, Peter
last_name: Venhuizen
- first_name: Elke
full_name: Barbez, Elke
last_name: Barbez
- first_name: Kai Alexander
full_name: Dünser, Kai Alexander
last_name: Dünser
- first_name: Martin
full_name: Darino, Martin
last_name: Darino
- first_name: Aleš
full_name: Pӗnčík, Aleš
last_name: Pӗnčík
- first_name: Ondřej
full_name: Novák, Ondřej
last_name: Novák
- first_name: Maria
full_name: Kalyna, Maria
last_name: Kalyna
- first_name: Gregory
full_name: Mouille, Gregory
last_name: Mouille
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Rishikesh P.
full_name: Bhalerao, Rishikesh P.
last_name: Bhalerao
- first_name: Jozef
full_name: Mravec, Jozef
last_name: Mravec
- first_name: Jürgen
full_name: Kleine-Vehn, Jürgen
last_name: Kleine-Vehn
citation:
ama: Velasquez SM, Guo X, Gallemi M, et al. Xyloglucan remodeling defines auxin-dependent
differential tissue expansion in plants. International Journal of Molecular
Sciences. 2021;22(17). doi:10.3390/ijms22179222
apa: Velasquez, S. M., Guo, X., Gallemi, M., Aryal, B., Venhuizen, P., Barbez, E.,
… Kleine-Vehn, J. (2021). Xyloglucan remodeling defines auxin-dependent differential
tissue expansion in plants. International Journal of Molecular Sciences.
MDPI. https://doi.org/10.3390/ijms22179222
chicago: Velasquez, Silvia Melina, Xiaoyuan Guo, Marçal Gallemi, Bibek Aryal, Peter
Venhuizen, Elke Barbez, Kai Alexander Dünser, et al. “Xyloglucan Remodeling Defines
Auxin-Dependent Differential Tissue Expansion in Plants.” International Journal
of Molecular Sciences. MDPI, 2021. https://doi.org/10.3390/ijms22179222.
ieee: S. M. Velasquez et al., “Xyloglucan remodeling defines auxin-dependent
differential tissue expansion in plants,” International Journal of Molecular
Sciences, vol. 22, no. 17. MDPI, 2021.
ista: Velasquez SM, Guo X, Gallemi M, Aryal B, Venhuizen P, Barbez E, Dünser KA,
Darino M, Pӗnčík A, Novák O, Kalyna M, Mouille G, Benková E, Bhalerao RP, Mravec
J, Kleine-Vehn J. 2021. Xyloglucan remodeling defines auxin-dependent differential
tissue expansion in plants. International Journal of Molecular Sciences. 22(17),
9222.
mla: Velasquez, Silvia Melina, et al. “Xyloglucan Remodeling Defines Auxin-Dependent
Differential Tissue Expansion in Plants.” International Journal of Molecular
Sciences, vol. 22, no. 17, 9222, MDPI, 2021, doi:10.3390/ijms22179222.
short: S.M. Velasquez, X. Guo, M. Gallemi, B. Aryal, P. Venhuizen, E. Barbez, K.A.
Dünser, M. Darino, A. Pӗnčík, O. Novák, M. Kalyna, G. Mouille, E. Benková, R.P.
Bhalerao, J. Mravec, J. Kleine-Vehn, International Journal of Molecular Sciences
22 (2021).
date_created: 2021-09-05T22:01:24Z
date_published: 2021-08-26T00:00:00Z
date_updated: 2023-10-31T19:29:38Z
day: '26'
ddc:
- '575'
department:
- _id: EvBe
doi: 10.3390/ijms22179222
external_id:
isi:
- '000694347100001'
pmid:
- '34502129'
file:
- access_level: open_access
checksum: 6b7055cf89f1b7ed8594c3fdf56f000b
content_type: application/pdf
creator: cchlebak
date_created: 2021-09-06T12:50:19Z
date_updated: 2021-09-07T09:04:53Z
file_id: '9988'
file_name: 2021_IntJMolecularSciences_Velasquez.pdf
file_size: 2162247
relation: main_file
file_date_updated: 2021-09-07T09:04:53Z
has_accepted_license: '1'
intvolume: ' 22'
isi: 1
issue: '17'
keyword:
- auxin
- growth
- cell wall
- xyloglucans
- hypocotyls
- gravitropism
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: International Journal of Molecular Sciences
publication_identifier:
eissn:
- 1422-0067
issn:
- 1661-6596
publication_status: published
publisher: MDPI
quality_controlled: '1'
scopus_import: '1'
status: public
title: Xyloglucan remodeling defines auxin-dependent differential tissue expansion
in plants
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: 22
year: '2021'
...
---
_id: '9999'
abstract:
- lang: eng
text: 'The developmental strategies used by progenitor cells to endure a safe journey
from their induction place towards the site of terminal differentiation are still
poorly understood. Here we uncovered a progenitor cell allocation mechanism that
stems from an incomplete process of epithelial delamination that allows progenitors
to coordinate their movement with adjacent extra-embryonic tissues. Progenitors
of the zebrafish laterality organ originate from the surface epithelial enveloping
layer by an apical constriction process of cell delamination. During this process,
progenitors retain long-term apical contacts that enable the epithelial layer
to pull a subset of progenitors along their way towards the vegetal pole. The
remaining delaminated progenitors follow apically-attached progenitors’ movement
by a co-attraction mechanism, avoiding sequestration by the adjacent endoderm,
ensuring their fate and collective allocation at the differentiation site. Thus,
we reveal that incomplete delamination serves as a cellular platform for coordinated
tissue movements during development. Impact Statement: Incomplete delamination
serves as a cellular platform for coordinated tissue movements during development,
guiding newly formed progenitor cell groups to the differentiation site.'
article_number: e66483
article_processing_charge: Yes
article_type: original
author:
- first_name: Eduardo
full_name: Pulgar, Eduardo
last_name: Pulgar
- first_name: Cornelia
full_name: Schwayer, Cornelia
id: 3436488C-F248-11E8-B48F-1D18A9856A87
last_name: Schwayer
orcid: 0000-0001-5130-2226
- first_name: Néstor
full_name: Guerrero, Néstor
last_name: Guerrero
- first_name: Loreto
full_name: López, Loreto
last_name: López
- first_name: Susana
full_name: Márquez, Susana
last_name: Márquez
- first_name: Steffen
full_name: Härtel, Steffen
last_name: Härtel
- first_name: Rodrigo
full_name: Soto, Rodrigo
last_name: Soto
- first_name: Carl Philipp
full_name: Heisenberg, Carl Philipp
last_name: Heisenberg
- first_name: Miguel L.
full_name: Concha, Miguel L.
last_name: Concha
citation:
ama: Pulgar E, Schwayer C, Guerrero N, et al. Apical contacts stemming from incomplete
delamination guide progenitor cell allocation through a dragging mechanism. eLife.
2021;10. doi:10.7554/eLife.66483
apa: Pulgar, E., Schwayer, C., Guerrero, N., López, L., Márquez, S., Härtel, S.,
… Concha, M. L. (2021). Apical contacts stemming from incomplete delamination
guide progenitor cell allocation through a dragging mechanism. ELife. eLife
Sciences Publications. https://doi.org/10.7554/eLife.66483
chicago: Pulgar, Eduardo, Cornelia Schwayer, Néstor Guerrero, Loreto López, Susana
Márquez, Steffen Härtel, Rodrigo Soto, Carl Philipp Heisenberg, and Miguel L.
Concha. “Apical Contacts Stemming from Incomplete Delamination Guide Progenitor
Cell Allocation through a Dragging Mechanism.” ELife. eLife Sciences Publications,
2021. https://doi.org/10.7554/eLife.66483.
ieee: E. Pulgar et al., “Apical contacts stemming from incomplete delamination
guide progenitor cell allocation through a dragging mechanism,” eLife,
vol. 10. eLife Sciences Publications, 2021.
ista: Pulgar E, Schwayer C, Guerrero N, López L, Márquez S, Härtel S, Soto R, Heisenberg
CP, Concha ML. 2021. Apical contacts stemming from incomplete delamination guide
progenitor cell allocation through a dragging mechanism. eLife. 10, e66483.
mla: Pulgar, Eduardo, et al. “Apical Contacts Stemming from Incomplete Delamination
Guide Progenitor Cell Allocation through a Dragging Mechanism.” ELife,
vol. 10, e66483, eLife Sciences Publications, 2021, doi:10.7554/eLife.66483.
short: E. Pulgar, C. Schwayer, N. Guerrero, L. López, S. Márquez, S. Härtel, R.
Soto, C.P. Heisenberg, M.L. Concha, ELife 10 (2021).
date_created: 2021-09-12T22:01:23Z
date_published: 2021-08-27T00:00:00Z
date_updated: 2023-08-14T06:53:33Z
day: '27'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.7554/eLife.66483
ec_funded: 1
external_id:
isi:
- '000700428500001'
pmid:
- '34448451'
file:
- access_level: open_access
checksum: a3f82b0499cc822ac1eab48a01f3f57e
content_type: application/pdf
creator: dernst
date_created: 2022-05-13T08:03:37Z
date_updated: 2022-05-13T08:03:37Z
file_id: '11371'
file_name: 2021_eLife_Pulgar.pdf
file_size: 9010446
relation: main_file
success: 1
file_date_updated: 2022-05-13T08:03:37Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
keyword:
- cell delamination
- apical constriction
- dragging
- mechanical forces
- collective 18 locomotion
- dorsal forerunner cells
- zebrafish
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Apical contacts stemming from incomplete delamination guide progenitor cell
allocation through a dragging mechanism
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '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: 2021-01-12T08:19:02Z
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 18
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: 2023-09-05T15:41:48Z
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'
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: '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
- 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).
date_created: 2020-09-29T13:24:06Z
date_published: 2020-12-01T00:00:00Z
date_updated: 2024-03-25T23:30:04Z
day: '01'
ddc:
- '570'
department:
- _id: FlSc
doi: 10.1016/j.jsb.2020.107633
external_id:
isi:
- '000600997800008'
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
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 212
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: 2022-07-18T08:31:52Z
day: '04'
ddc:
- '570'
doi: 10.1083/jcb.201809123
extern: '1'
external_id:
pmid:
- '30552100'
file:
- access_level: open_access
checksum: 7964ebbf833b0b35f9fba840eea9531d
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T08:26:32Z
date_updated: 2022-04-08T08:26:32Z
file_id: '11139'
file_name: 2019_JCB_Toyama.pdf
file_size: 2503838
relation: main_file
success: 1
file_date_updated: 2022-04-08T08:26:32Z
has_accepted_license: '1'
intvolume: ' 218'
issue: '2'
keyword:
- Cell Biology
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 433-444
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Visualization of long-lived proteins reveals age mosaicism within nuclei of
postmitotic cells
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 218
year: '2019'
...
---
_id: '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: 2022-07-18T08:32:30Z
day: '06'
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: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 30
year: '2019'
...
---
_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.
date_created: 2019-09-19T08:19:44Z
date_published: 2019-07-24T00:00:00Z
date_updated: 2023-10-18T08:49:17Z
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: '6328'
relation: part_of_dissertation
status: public
- id: '15'
relation: part_of_dissertation
status: public
- id: '6877'
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
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
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'
...
---
_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: '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: '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: ' FöFoLe project 947 (F.G.), the Friedrich-Baur-Stiftung project
41/16 (F.G.)'
article_number: e3018
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).
date_created: 2019-04-29T09:40:33Z
date_published: 2018-09-20T00:00:00Z
date_updated: 2021-01-12T08:07:12Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.21769/bioprotoc.3018
ec_funded: 1
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
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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2018'
...