---
_id: '14774'
abstract:
- lang: eng
text: Morphogen gradients impart positional information to cells in a homogenous
tissue field. Fgf8a, a highly conserved growth factor, has been proposed to act
as a morphogen during zebrafish gastrulation. However, technical limitations have
so far prevented direct visualization of the endogenous Fgf8a gradient and confirmation
of its morphogenic activity. Here, we monitor Fgf8a propagation in the developing
neural plate using a CRISPR/Cas9-mediated EGFP knock-in at the endogenous fgf8a
locus. By combining sensitive imaging with single-molecule fluorescence correlation
spectroscopy, we demonstrate that Fgf8a, which is produced at the embryonic margin,
propagates by diffusion through the extracellular space and forms a graded distribution
towards the animal pole. Overlaying the Fgf8a gradient curve with expression profiles
of its downstream targets determines the precise input-output relationship of
Fgf8a-mediated patterning. Manipulation of the extracellular Fgf8a levels alters
the signaling outcome, thus establishing Fgf8a as a bona fide morphogen during
zebrafish gastrulation. Furthermore, by hindering Fgf8a diffusion, we demonstrate
that extracellular diffusion of the protein from the source is crucial for it
to achieve its morphogenic potential.
acknowledgement: "We thank members of the Brand lab, as well as Justina Stark (Ivo
Sbalzarini group, Max Planck Institute of Molecular Cell Biology and Genetics, Dresden,
Germany) for project-related discussions; Darren Gilmour (University of Zurich),
Karuna Sampath (University of Warwick) and Gokul Kesavan (Vowels Lifesciences Private
Limited, Bangalore) for comments on the manuscript; personnel of the CMCB technology
platform, TU Dresden for imaging and image analysis-related support; and Maurizio
Abbate (Technical support, Arivis) for help with image analysis. We are also grateful
to Stapornwongkul and Briscoe for commenting on a preprint version of our work (Stapornwongkul
and Briscoe, 2022).\r\nThis work was supported by the Deutsche Forschungsgemeinschaft
(BR 1746/6-2, BR 1746/11-1 and BR 1746/3 to M.B.), by a Cluster of Excellence ‘Physics
of Life’ seed grant and by institutional funds from Technische Universitat Dresden
(to M.B.). Open Access funding provided by Technische Universitat Dresden. Deposited
in PMC for immediate release."
article_number: dev201559
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Rohit K
full_name: Harish, Rohit K
id: 1bae78aa-ee0e-11ec-9b76-bc42990f409d
last_name: Harish
- first_name: Mansi
full_name: Gupta, Mansi
last_name: Gupta
- first_name: Daniela
full_name: Zöller, Daniela
last_name: Zöller
- first_name: Hella
full_name: Hartmann, Hella
last_name: Hartmann
- first_name: Ali
full_name: Gheisari, Ali
last_name: Gheisari
- first_name: Anja
full_name: Machate, Anja
last_name: Machate
- first_name: Stefan
full_name: Hans, Stefan
last_name: Hans
- first_name: Michael
full_name: Brand, Michael
last_name: Brand
citation:
ama: Harish RK, Gupta M, Zöller D, et al. Real-time monitoring of an endogenous
Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation.
Development. 2023;150(19). doi:10.1242/dev.201559
apa: Harish, R. K., Gupta, M., Zöller, D., Hartmann, H., Gheisari, A., Machate,
A., … Brand, M. (2023). Real-time monitoring of an endogenous Fgf8a gradient attests
to its role as a morphogen during zebrafish gastrulation. Development.
The Company of Biologists. https://doi.org/10.1242/dev.201559
chicago: Harish, Rohit K, Mansi Gupta, Daniela Zöller, Hella Hartmann, Ali Gheisari,
Anja Machate, Stefan Hans, and Michael Brand. “Real-Time Monitoring of an Endogenous
Fgf8a Gradient Attests to Its Role as a Morphogen during Zebrafish Gastrulation.”
Development. The Company of Biologists, 2023. https://doi.org/10.1242/dev.201559.
ieee: R. K. Harish et al., “Real-time monitoring of an endogenous Fgf8a gradient
attests to its role as a morphogen during zebrafish gastrulation,” Development,
vol. 150, no. 19. The Company of Biologists, 2023.
ista: Harish RK, Gupta M, Zöller D, Hartmann H, Gheisari A, Machate A, Hans S, Brand
M. 2023. Real-time monitoring of an endogenous Fgf8a gradient attests to its role
as a morphogen during zebrafish gastrulation. Development. 150(19), dev201559.
mla: Harish, Rohit K., et al. “Real-Time Monitoring of an Endogenous Fgf8a Gradient
Attests to Its Role as a Morphogen during Zebrafish Gastrulation.” Development,
vol. 150, no. 19, dev201559, The Company of Biologists, 2023, doi:10.1242/dev.201559.
short: R.K. Harish, M. Gupta, D. Zöller, H. Hartmann, A. Gheisari, A. Machate, S.
Hans, M. Brand, Development 150 (2023).
date_created: 2024-01-10T09:18:54Z
date_published: 2023-10-01T00:00:00Z
date_updated: 2024-01-10T12:45:25Z
day: '01'
ddc:
- '570'
department:
- _id: AnKi
doi: 10.1242/dev.201559
external_id:
isi:
- '001097449100002'
pmid:
- '37665167'
file:
- access_level: open_access
checksum: 2d6f52dc33260a9b2352b8f28374ba5f
content_type: application/pdf
creator: dernst
date_created: 2024-01-10T12:41:13Z
date_updated: 2024-01-10T12:41:13Z
file_id: '14790'
file_name: 2023_Development_Harish.pdf
file_size: 12836306
relation: main_file
success: 1
file_date_updated: 2024-01-10T12:41:13Z
has_accepted_license: '1'
intvolume: ' 150'
isi: 1
issue: '19'
keyword:
- Developmental Biology
- Molecular Biology
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
status: public
title: Real-time monitoring of an endogenous Fgf8a gradient attests to its role as
a morphogen during zebrafish gastrulation
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: 150
year: '2023'
...
---
_id: '14781'
abstract:
- lang: eng
text: Germ granules, condensates of phase-separated RNA and protein, are organelles
that are essential for germline development in different organisms. The patterning
of the granules and their relevance for germ cell fate are not fully understood.
Combining three-dimensional in vivo structural and functional analyses, we study
the dynamic spatial organization of molecules within zebrafish germ granules.
We find that the localization of RNA molecules to the periphery of the granules,
where ribosomes are localized, depends on translational activity at this location.
In addition, we find that the vertebrate-specific Dead end (Dnd1) protein is essential
for nanos3 RNA localization at the condensates’ periphery. Accordingly, in the
absence of Dnd1, or when translation is inhibited, nanos3 RNA translocates into
the granule interior, away from the ribosomes, a process that is correlated with
the loss of germ cell fate. These findings highlight the relevance of sub-granule
compartmentalization for post-transcriptional control and its importance for preserving
germ cell totipotency.
acknowledgement: We thank Celeste Brennecka for editing and Michal Reichman-Fried
for critical comments on the manuscript. We thank Ursula Jordan, Esther Messerschmidt,
and Ines Sandbote for technical assistance. This work was supported by funding from
the University of Münster (K.J.W., K.T., E.R., A.G., T.G.-T., J.S., and M.G.), the
Max Planck Institute for Molecular Biomedicine (D.Z.), the German Research Foundation
grant CRU 326 (P2) RA863/12-2 (E.R.), Baylor University (K.H. and D.R.), and the
National Institutes of Health grant R35 GM 134910 (D.R.). We thank the referees
for insightful comments that helped improve the manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Kim Joana
full_name: Westerich, Kim Joana
last_name: Westerich
- first_name: Katsiaryna
full_name: Tarbashevich, Katsiaryna
last_name: Tarbashevich
- first_name: Jan
full_name: Schick, Jan
last_name: Schick
- first_name: Antra
full_name: Gupta, Antra
last_name: Gupta
- first_name: Mingzhao
full_name: Zhu, Mingzhao
last_name: Zhu
- first_name: Kenneth
full_name: Hull, Kenneth
last_name: Hull
- first_name: Daniel
full_name: Romo, Daniel
last_name: Romo
- first_name: Dagmar
full_name: Zeuschner, Dagmar
last_name: Zeuschner
- first_name: Mohammad
full_name: Goudarzi, Mohammad
id: 3384113A-F248-11E8-B48F-1D18A9856A87
last_name: Goudarzi
- first_name: Theresa
full_name: Gross-Thebing, Theresa
last_name: Gross-Thebing
- first_name: Erez
full_name: Raz, Erez
last_name: Raz
citation:
ama: Westerich KJ, Tarbashevich K, Schick J, et al. Spatial organization and function
of RNA molecules within phase-separated condensates in zebrafish are controlled
by Dnd1. Developmental Cell. 2023;58(17):1578-1592.e5. doi:10.1016/j.devcel.2023.06.009
apa: Westerich, K. J., Tarbashevich, K., Schick, J., Gupta, A., Zhu, M., Hull, K.,
… Raz, E. (2023). Spatial organization and function of RNA molecules within phase-separated
condensates in zebrafish are controlled by Dnd1. Developmental Cell. Elsevier.
https://doi.org/10.1016/j.devcel.2023.06.009
chicago: Westerich, Kim Joana, Katsiaryna Tarbashevich, Jan Schick, Antra Gupta,
Mingzhao Zhu, Kenneth Hull, Daniel Romo, et al. “Spatial Organization and Function
of RNA Molecules within Phase-Separated Condensates in Zebrafish Are Controlled
by Dnd1.” Developmental Cell. Elsevier, 2023. https://doi.org/10.1016/j.devcel.2023.06.009.
ieee: K. J. Westerich et al., “Spatial organization and function of RNA molecules
within phase-separated condensates in zebrafish are controlled by Dnd1,” Developmental
Cell, vol. 58, no. 17. Elsevier, p. 1578–1592.e5, 2023.
ista: Westerich KJ, Tarbashevich K, Schick J, Gupta A, Zhu M, Hull K, Romo D, Zeuschner
D, Goudarzi M, Gross-Thebing T, Raz E. 2023. Spatial organization and function
of RNA molecules within phase-separated condensates in zebrafish are controlled
by Dnd1. Developmental Cell. 58(17), 1578–1592.e5.
mla: Westerich, Kim Joana, et al. “Spatial Organization and Function of RNA Molecules
within Phase-Separated Condensates in Zebrafish Are Controlled by Dnd1.” Developmental
Cell, vol. 58, no. 17, Elsevier, 2023, p. 1578–1592.e5, doi:10.1016/j.devcel.2023.06.009.
short: K.J. Westerich, K. Tarbashevich, J. Schick, A. Gupta, M. Zhu, K. Hull, D.
Romo, D. Zeuschner, M. Goudarzi, T. Gross-Thebing, E. Raz, Developmental Cell
58 (2023) 1578–1592.e5.
date_created: 2024-01-10T09:41:21Z
date_published: 2023-09-11T00:00:00Z
date_updated: 2024-01-16T08:56:36Z
day: '11'
department:
- _id: Bio
doi: 10.1016/j.devcel.2023.06.009
external_id:
pmid:
- '37463577'
intvolume: ' 58'
issue: '17'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/2023.07.09.548244
month: '09'
oa: 1
oa_version: Preprint
page: 1578-1592.e5
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Spatial organization and function of RNA molecules within phase-separated condensates
in zebrafish are controlled by Dnd1
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 58
year: '2023'
...
---
_id: '12162'
abstract:
- lang: eng
text: Homeostatic balance in the intestinal epithelium relies on a fast cellular
turnover, which is coordinated by an intricate interplay between biochemical signalling,
mechanical forces and organ geometry. We review recent modelling approaches that
have been developed to understand different facets of this remarkable homeostatic
equilibrium. Existing models offer different, albeit complementary, perspectives
on the problem. First, biomechanical models aim to explain the local and global
mechanical stresses driving cell renewal as well as tissue shape maintenance.
Second, compartmental models provide insights into the conditions necessary to
keep a constant flow of cells with well-defined ratios of cell types, and how
perturbations can lead to an unbalance of relative compartment sizes. A third
family of models address, at the cellular level, the nature and regulation of
stem fate choices that are necessary to fuel cellular turnover. We also review
how these different approaches are starting to be integrated together across scales,
to provide quantitative predictions and new conceptual frameworks to think about
the dynamics of cell renewal in complex tissues.
acknowledgement: "This work received funding from the ERC under the European Union’s
Horizon 2020 research and innovation programme (grant agreement No. 851288 to E.H.).\r\nB.
C-M wants to acknowledge the support of the field of excellence Complexity of Life,
in Basic Research and Innovation of the University of Graz."
article_processing_charge: Yes (via OA deal)
article_type: review
author:
- first_name: Bernat
full_name: Corominas-Murtra, Bernat
id: 43BE2298-F248-11E8-B48F-1D18A9856A87
last_name: Corominas-Murtra
orcid: 0000-0001-9806-5643
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
citation:
ama: Corominas-Murtra B, Hannezo EB. Modelling the dynamics of mammalian gut homeostasis.
Seminars in Cell & Developmental Biology. 2023;150-151:58-65. doi:10.1016/j.semcdb.2022.11.005
apa: Corominas-Murtra, B., & Hannezo, E. B. (2023). Modelling the dynamics of
mammalian gut homeostasis. Seminars in Cell & Developmental Biology.
Elsevier. https://doi.org/10.1016/j.semcdb.2022.11.005
chicago: Corominas-Murtra, Bernat, and Edouard B Hannezo. “Modelling the Dynamics
of Mammalian Gut Homeostasis.” Seminars in Cell & Developmental Biology.
Elsevier, 2023. https://doi.org/10.1016/j.semcdb.2022.11.005.
ieee: B. Corominas-Murtra and E. B. Hannezo, “Modelling the dynamics of mammalian
gut homeostasis,” Seminars in Cell & Developmental Biology, vol. 150–151.
Elsevier, pp. 58–65, 2023.
ista: Corominas-Murtra B, Hannezo EB. 2023. Modelling the dynamics of mammalian
gut homeostasis. Seminars in Cell & Developmental Biology. 150–151, 58–65.
mla: Corominas-Murtra, Bernat, and Edouard B. Hannezo. “Modelling the Dynamics of
Mammalian Gut Homeostasis.” Seminars in Cell & Developmental Biology,
vol. 150–151, Elsevier, 2023, pp. 58–65, doi:10.1016/j.semcdb.2022.11.005.
short: B. Corominas-Murtra, E.B. Hannezo, Seminars in Cell & Developmental Biology
150–151 (2023) 58–65.
date_created: 2023-01-12T12:09:47Z
date_published: 2023-12-02T00:00:00Z
date_updated: 2024-01-16T13:22:32Z
day: '02'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1016/j.semcdb.2022.11.005
ec_funded: 1
external_id:
isi:
- '001053522200001'
pmid:
- '36470715'
file:
- access_level: open_access
checksum: c619887cf130f4649bf3035417186004
content_type: application/pdf
creator: dernst
date_created: 2024-01-08T10:16:04Z
date_updated: 2024-01-08T10:16:04Z
file_id: '14741'
file_name: 2023_SeminarsCellDevBiology_CorominasMurtra.pdf
file_size: 1343750
relation: main_file
success: 1
file_date_updated: 2024-01-08T10:16:04Z
has_accepted_license: '1'
isi: 1
keyword:
- Cell Biology
- Developmental Biology
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 58-65
pmid: 1
project:
- _id: 05943252-7A3F-11EA-A408-12923DDC885E
call_identifier: H2020
grant_number: '851288'
name: Design Principles of Branching Morphogenesis
publication: Seminars in Cell & Developmental Biology
publication_identifier:
issn:
- 1084-9521
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Modelling the dynamics of mammalian gut homeostasis
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: 150-151
year: '2023'
...
---
_id: '11460'
abstract:
- lang: eng
text: "Background: Proper cerebral cortical development depends on the tightly orchestrated
migration of newly born neurons from the inner ventricular and subventricular
zones to the outer cortical plate. Any disturbance in this process during prenatal
stages may lead to neuronal migration disorders (NMDs), which can vary in extent
from focal to global. Furthermore, NMDs show a substantial comorbidity with other
neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous
work demonstrated focal neuronal migration defects in mice carrying loss-of-function
alleles of the recognized autism risk gene WDFY3. However, the cellular origins
of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide
critical insight into WDFY3-dependent disease pathology.\r\nMethods: Here, in
an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic
analysis with double markers (MADM). MADM technology enabled us to genetically
distinctly track and phenotypically analyze mutant and wild-type cells concomitantly
in vivo using immunofluorescent techniques.\r\nResults: We revealed a cell autonomous
requirement of WDFY3 for accurate laminar positioning of cortical projection neurons
and elimination of mispositioned cells during early postnatal life. In addition,
we identified significant deviations in dendritic arborization, as well as synaptic
density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant
neurons in Wdfy3-MADM reporter mice at postnatal stages.\r\nLimitations: While
Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD
pathology that remain inaccessible to investigation in humans, like most animal
models, they do not a perfectly replicate all aspects of human ASD biology. The
lack of human data makes it indeterminate whether morphological deviations described
here apply to ASD patients or some of the other neurodevelopmental conditions
associated with WDFY3 mutation.\r\nConclusions: Our genetic approach revealed
several cell autonomous requirements of WDFY3 in neuronal development that could
underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions.
The results are also consistent with findings in other ASD animal models and patients
and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity
in postnatal life."
acknowledgement: "This study was funded by NIMH R21MH115347 to KSZ. KSZ is further
supported by Shriners Hospitals for Children.\r\nWe would like to thank Angelo Harlan
de Crescenzo for early contributions to this project."
article_number: '27'
article_processing_charge: No
article_type: original
author:
- first_name: Zachary A.
full_name: Schaaf, Zachary A.
last_name: Schaaf
- first_name: Lyvin
full_name: Tat, Lyvin
last_name: Tat
- first_name: Noemi
full_name: Cannizzaro, Noemi
last_name: Cannizzaro
- first_name: Ralph
full_name: Green, Ralph
last_name: Green
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Konstantinos S.
full_name: Zarbalis, Konstantinos S.
last_name: Zarbalis
citation:
ama: Schaaf ZA, Tat L, Cannizzaro N, et al. WDFY3 mutation alters laminar position
and morphology of cortical neurons. Molecular Autism. 2022;13. doi:10.1186/s13229-022-00508-3
apa: Schaaf, Z. A., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer,
S., & Zarbalis, K. S. (2022). WDFY3 mutation alters laminar position and morphology
of cortical neurons. Molecular Autism. Springer Nature. https://doi.org/10.1186/s13229-022-00508-3
chicago: Schaaf, Zachary A., Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke,
Simon Hippenmeyer, and Konstantinos S. Zarbalis. “WDFY3 Mutation Alters Laminar
Position and Morphology of Cortical Neurons.” Molecular Autism. Springer
Nature, 2022. https://doi.org/10.1186/s13229-022-00508-3.
ieee: Z. A. Schaaf et al., “WDFY3 mutation alters laminar position and morphology
of cortical neurons,” Molecular Autism, vol. 13. Springer Nature, 2022.
ista: Schaaf ZA, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis
KS. 2022. WDFY3 mutation alters laminar position and morphology of cortical neurons.
Molecular Autism. 13, 27.
mla: Schaaf, Zachary A., et al. “WDFY3 Mutation Alters Laminar Position and Morphology
of Cortical Neurons.” Molecular Autism, vol. 13, 27, Springer Nature, 2022,
doi:10.1186/s13229-022-00508-3.
short: Z.A. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer,
K.S. Zarbalis, Molecular Autism 13 (2022).
date_created: 2022-06-23T14:28:55Z
date_published: 2022-06-22T00:00:00Z
date_updated: 2023-08-03T07:21:32Z
day: '22'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1186/s13229-022-00508-3
external_id:
isi:
- '000814641400001'
file:
- access_level: open_access
checksum: 525d2618e855139089bbfc3e3d49d1b2
content_type: application/pdf
creator: dernst
date_created: 2022-06-24T08:22:59Z
date_updated: 2022-06-24T08:22:59Z
file_id: '11461'
file_name: 2022_MolecularAutism_Schaaf.pdf
file_size: 7552298
relation: main_file
success: 1
file_date_updated: 2022-06-24T08:22:59Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
keyword:
- Psychiatry and Mental health
- Developmental Biology
- Developmental Neuroscience
- Molecular Biology
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: Molecular Autism
publication_identifier:
issn:
- 2040-2392
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1186/s13229-023-00539-4
status: public
title: WDFY3 mutation alters laminar position and morphology of cortical neurons
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: 13
year: '2022'
...
---
_id: '12120'
abstract:
- lang: eng
text: Plant root architecture flexibly adapts to changing nitrate (NO3−) availability
in the soil; however, the underlying molecular mechanism of this adaptive development
remains under-studied. To explore the regulation of NO3−-mediated root growth,
we screened for low-nitrate-resistant mutant (lonr) and identified mutants that
were defective in the NAC transcription factor NAC075 (lonr1) as being less sensitive
to low NO3− in terms of primary root growth. We show that NAC075 is a mobile transcription
factor relocating from the root stele tissues to the endodermis based on NO3−
availability. Under low-NO3− availability, the kinase CBL-interacting protein
kinase 1 (CIPK1) is activated, and it phosphorylates NAC075, restricting its movement
from the stele, which leads to the transcriptional regulation of downstream target
WRKY53, consequently leading to adapted root architecture. Our work thus identifies
an adaptive mechanism involving translocation of transcription factor based on
nutrient availability and leading to cell-specific reprogramming of plant root
growth.
acknowledgement: The authors are grateful to Jörg Kudla, Ying Miao, Yu Zheng, Gang
Li, and Jun Zheng for providing published materials and to Wenkun Zhou and Caifu
Jiang for helpful discussions. This work was supported by grants from the National
Key Research and Development Program of China (2021YFF1000500), the National Natural
Science Foundation of China (32170265 and 32022007), the Beijing Municipal Natural
Science Foundation (5192011), and the Chinese Universities Scientific Fund (2022TC153).
article_processing_charge: No
article_type: original
author:
- first_name: Huixin
full_name: Xiao, Huixin
last_name: Xiao
- first_name: Yumei
full_name: Hu, Yumei
last_name: Hu
- first_name: Yaping
full_name: Wang, Yaping
last_name: Wang
- first_name: Jinkui
full_name: Cheng, Jinkui
last_name: Cheng
- first_name: Jinyi
full_name: Wang, Jinyi
last_name: Wang
- first_name: Guojingwei
full_name: Chen, Guojingwei
last_name: Chen
- first_name: Qian
full_name: Li, Qian
last_name: Li
- first_name: Shuwei
full_name: Wang, Shuwei
last_name: Wang
- first_name: Yalu
full_name: Wang, Yalu
last_name: Wang
- first_name: Shao-Shuai
full_name: Wang, Shao-Shuai
last_name: Wang
- first_name: Yi
full_name: Wang, Yi
last_name: Wang
- first_name: Wei
full_name: Xuan, Wei
last_name: Xuan
- first_name: Zhen
full_name: Li, Zhen
last_name: Li
- first_name: Yan
full_name: Guo, Yan
last_name: Guo
- first_name: Zhizhong
full_name: Gong, Zhizhong
last_name: Gong
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Jing
full_name: Zhang, Jing
last_name: Zhang
citation:
ama: Xiao H, Hu Y, Wang Y, et al. Nitrate availability controls translocation of
the transcription factor NAC075 for cell-type-specific reprogramming of root growth.
Developmental Cell. 2022;57(23):2638-2651.e6. doi:10.1016/j.devcel.2022.11.006
apa: Xiao, H., Hu, Y., Wang, Y., Cheng, J., Wang, J., Chen, G., … Zhang, J. (2022).
Nitrate availability controls translocation of the transcription factor NAC075
for cell-type-specific reprogramming of root growth. Developmental Cell.
Elsevier. https://doi.org/10.1016/j.devcel.2022.11.006
chicago: Xiao, Huixin, Yumei Hu, Yaping Wang, Jinkui Cheng, Jinyi Wang, Guojingwei
Chen, Qian Li, et al. “Nitrate Availability Controls Translocation of the Transcription
Factor NAC075 for Cell-Type-Specific Reprogramming of Root Growth.” Developmental
Cell. Elsevier, 2022. https://doi.org/10.1016/j.devcel.2022.11.006.
ieee: H. Xiao et al., “Nitrate availability controls translocation of the
transcription factor NAC075 for cell-type-specific reprogramming of root growth,”
Developmental Cell, vol. 57, no. 23. Elsevier, p. 2638–2651.e6, 2022.
ista: Xiao H, Hu Y, Wang Y, Cheng J, Wang J, Chen G, Li Q, Wang S, Wang Y, Wang
S-S, Wang Y, Xuan W, Li Z, Guo Y, Gong Z, Friml J, Zhang J. 2022. Nitrate availability
controls translocation of the transcription factor NAC075 for cell-type-specific
reprogramming of root growth. Developmental Cell. 57(23), 2638–2651.e6.
mla: Xiao, Huixin, et al. “Nitrate Availability Controls Translocation of the Transcription
Factor NAC075 for Cell-Type-Specific Reprogramming of Root Growth.” Developmental
Cell, vol. 57, no. 23, Elsevier, 2022, p. 2638–2651.e6, doi:10.1016/j.devcel.2022.11.006.
short: H. Xiao, Y. Hu, Y. Wang, J. Cheng, J. Wang, G. Chen, Q. Li, S. Wang, Y. Wang,
S.-S. Wang, Y. Wang, W. Xuan, Z. Li, Y. Guo, Z. Gong, J. Friml, J. Zhang, Developmental
Cell 57 (2022) 2638–2651.e6.
date_created: 2023-01-12T11:57:00Z
date_published: 2022-12-05T00:00:00Z
date_updated: 2023-10-04T08:23:20Z
day: '05'
department:
- _id: JiFr
doi: 10.1016/j.devcel.2022.11.006
external_id:
isi:
- '000919603800005'
pmid:
- '36473460'
intvolume: ' 57'
isi: 1
issue: '23'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '12'
oa_version: None
page: 2638-2651.e6
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nitrate availability controls translocation of the transcription factor NAC075
for cell-type-specific reprogramming of root growth
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 57
year: '2022'
...
---
_id: '12231'
abstract:
- lang: eng
text: Ventral tail bending, which is transient but pronounced, is found in many
chordate embryos and constitutes an interesting model of how tissue interactions
control embryo shape. Here, we identify one key upstream regulator of ventral
tail bending in embryos of the ascidian Ciona. We show that during the early tailbud
stages, ventral epidermal cells exhibit a boat-shaped morphology (boat cell) with
a narrow apical surface where phosphorylated myosin light chain (pMLC) accumulates.
We further show that interfering with the function of the BMP ligand Admp led
to pMLC localizing to the basal instead of the apical side of ventral epidermal
cells and a reduced number of boat cells. Finally, we show that cutting ventral
epidermal midline cells at their apex using an ultraviolet laser relaxed ventral
tail bending. Based on these results, we propose a previously unreported function
for Admp in localizing pMLC to the apical side of ventral epidermal cells, which
causes the tail to bend ventrally by resisting antero-posterior notochord extension
at the ventral side of the tail.
acknowledgement: "iona intestinalis adults were provided by Dr Yutaka Satou (Kyoto
University) and Dr Manabu Yoshida (the University of Tokyo) with support from the
National Bio-Resource Project of AMED, Japan. We thank Dr Hidehiko Hashimoto and
Dr Yuji Mizotani for technical information about 1P-myosin antibody staining. We
thank Dr Kaoru Imai and Dr Yutaka Satou for valuable discussion about Admp and for
the DNA construct of Bmp2/4 under the Dlx.b upstream sequence. We thank Ms Maki
Kogure for constructing the FUSION360 of the intercalating epidermal cell.\r\nThis
work was supported by funding from the Japan Society for the Promotion of Science
(JP16H01451, JP21H00440). Open Access funding provided by Keio University: Keio
Gijuku Daigaku."
article_number: dev200215
article_processing_charge: No
article_type: original
author:
- first_name: Yuki S.
full_name: Kogure, Yuki S.
last_name: Kogure
- first_name: Hiromochi
full_name: Muraoka, Hiromochi
last_name: Muraoka
- first_name: Wataru C.
full_name: Koizumi, Wataru C.
last_name: Koizumi
- first_name: Raphaël
full_name: Gelin-alessi, Raphaël
last_name: Gelin-alessi
- first_name: Benoit G
full_name: Godard, Benoit G
id: 3263621A-F248-11E8-B48F-1D18A9856A87
last_name: Godard
- first_name: Kotaro
full_name: Oka, Kotaro
last_name: Oka
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Kohji
full_name: Hotta, Kohji
last_name: Hotta
citation:
ama: Kogure YS, Muraoka H, Koizumi WC, et al. Admp regulates tail bending by controlling
ventral epidermal cell polarity via phosphorylated myosin localization in Ciona.
Development. 2022;149(21). doi:10.1242/dev.200215
apa: Kogure, Y. S., Muraoka, H., Koizumi, W. C., Gelin-alessi, R., Godard, B. G.,
Oka, K., … Hotta, K. (2022). Admp regulates tail bending by controlling ventral
epidermal cell polarity via phosphorylated myosin localization in Ciona. Development.
The Company of Biologists. https://doi.org/10.1242/dev.200215
chicago: Kogure, Yuki S., Hiromochi Muraoka, Wataru C. Koizumi, Raphaël Gelin-alessi,
Benoit G Godard, Kotaro Oka, Carl-Philipp J Heisenberg, and Kohji Hotta. “Admp
Regulates Tail Bending by Controlling Ventral Epidermal Cell Polarity via Phosphorylated
Myosin Localization in Ciona.” Development. The Company of Biologists,
2022. https://doi.org/10.1242/dev.200215.
ieee: Y. S. Kogure et al., “Admp regulates tail bending by controlling ventral
epidermal cell polarity via phosphorylated myosin localization in Ciona,” Development,
vol. 149, no. 21. The Company of Biologists, 2022.
ista: Kogure YS, Muraoka H, Koizumi WC, Gelin-alessi R, Godard BG, Oka K, Heisenberg
C-PJ, Hotta K. 2022. Admp regulates tail bending by controlling ventral epidermal
cell polarity via phosphorylated myosin localization in Ciona. Development. 149(21),
dev200215.
mla: Kogure, Yuki S., et al. “Admp Regulates Tail Bending by Controlling Ventral
Epidermal Cell Polarity via Phosphorylated Myosin Localization in Ciona.” Development,
vol. 149, no. 21, dev200215, The Company of Biologists, 2022, doi:10.1242/dev.200215.
short: Y.S. Kogure, H. Muraoka, W.C. Koizumi, R. Gelin-alessi, B.G. Godard, K. Oka,
C.-P.J. Heisenberg, K. Hotta, Development 149 (2022).
date_created: 2023-01-16T09:50:12Z
date_published: 2022-11-01T00:00:00Z
date_updated: 2023-08-04T09:33:24Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1242/dev.200215
external_id:
isi:
- '000903991700002'
pmid:
- '36227591'
file:
- access_level: open_access
checksum: 871b9c58eb79b9e60752de25a46938d6
content_type: application/pdf
creator: dernst
date_created: 2023-01-27T10:36:50Z
date_updated: 2023-01-27T10:36:50Z
file_id: '12423'
file_name: 2022_Development_Kogure.pdf
file_size: 9160451
relation: main_file
success: 1
file_date_updated: 2023-01-27T10:36:50Z
has_accepted_license: '1'
intvolume: ' 149'
isi: 1
issue: '21'
keyword:
- Developmental Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Admp regulates tail bending by controlling ventral epidermal cell polarity
via phosphorylated myosin localization in Ciona
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: 149
year: '2022'
...
---
_id: '12238'
abstract:
- lang: eng
text: Upon the initiation of collective cell migration, the cells at the free edge
are specified as leader cells; however, the mechanism underlying the leader cell
specification remains elusive. Here, we show that lamellipodial extension after
the release from mechanical confinement causes sustained extracellular signal-regulated
kinase (ERK) activation and underlies the leader cell specification. Live-imaging
of Madin-Darby canine kidney (MDCK) cells and mouse epidermis through the use
of Förster resonance energy transfer (FRET)-based biosensors showed that leader
cells exhibit sustained ERK activation in a hepatocyte growth factor (HGF)-dependent
manner. Meanwhile, follower cells exhibit oscillatory ERK activation waves in
an epidermal growth factor (EGF) signaling-dependent manner. Lamellipodial extension
at the free edge increases the cellular sensitivity to HGF. The HGF-dependent
ERK activation, in turn, promotes lamellipodial extension, thereby forming a positive
feedback loop between cell extension and ERK activation and specifying the cells
at the free edge as the leader cells. Our findings show that the integration of
physical and biochemical cues underlies the leader cell specification during collective
cell migration.
acknowledgement: We thank the members of the Matsuda Laboratory for their helpful
discussion and encouragement, and we thank K. Hirano and K. Takakura for their technical
assistance. This work was supported by the Kyoto University Live Imaging Center.
Financial support was provided in the form of JSPS KAKENHI grants (nos. 17J02107
and 20K22653 to N.H., and 20H05898 and 19H00993 to M.M.), a JST CREST grant (no.
JPMJCR1654 to M.M.), a Moonshot R&D grant (no. JPMJPS2022-11 to M.M.), Generalitat
de Catalunya and the CERCA Programme (no. SGR-2017-01602 to X.T.), MICCINN/FEDER
(no. PGC2018-099645-B-I00 to X.T.), and European Research Council (no. Adv-883739
to X.T.). IBEC is a recipient of a Severo Ochoa Award of Excellence from the MINECO.
This work was partly supported by an Extramural Collaborative Research Grant of
Cancer Research Institute, Kanazawa University.
article_processing_charge: No
article_type: original
author:
- first_name: Naoya
full_name: Hino, Naoya
id: 5299a9ce-7679-11eb-a7bc-d1e62b936307
last_name: Hino
- first_name: Kimiya
full_name: Matsuda, Kimiya
last_name: Matsuda
- first_name: Yuya
full_name: Jikko, Yuya
last_name: Jikko
- first_name: Gembu
full_name: Maryu, Gembu
last_name: Maryu
- first_name: Katsuya
full_name: Sakai, Katsuya
last_name: Sakai
- first_name: Ryu
full_name: Imamura, Ryu
last_name: Imamura
- first_name: Shinya
full_name: Tsukiji, Shinya
last_name: Tsukiji
- first_name: Kazuhiro
full_name: Aoki, Kazuhiro
last_name: Aoki
- first_name: Kenta
full_name: Terai, Kenta
last_name: Terai
- first_name: Tsuyoshi
full_name: Hirashima, Tsuyoshi
last_name: Hirashima
- first_name: Xavier
full_name: Trepat, Xavier
last_name: Trepat
- first_name: Michiyuki
full_name: Matsuda, Michiyuki
last_name: Matsuda
citation:
ama: Hino N, Matsuda K, Jikko Y, et al. A feedback loop between lamellipodial extension
and HGF-ERK signaling specifies leader cells during collective cell migration.
Developmental Cell. 2022;57(19):2290-2304.e7. doi:10.1016/j.devcel.2022.09.003
apa: Hino, N., Matsuda, K., Jikko, Y., Maryu, G., Sakai, K., Imamura, R., … Matsuda,
M. (2022). A feedback loop between lamellipodial extension and HGF-ERK signaling
specifies leader cells during collective cell migration. Developmental Cell.
Elsevier. https://doi.org/10.1016/j.devcel.2022.09.003
chicago: Hino, Naoya, Kimiya Matsuda, Yuya Jikko, Gembu Maryu, Katsuya Sakai, Ryu
Imamura, Shinya Tsukiji, et al. “A Feedback Loop between Lamellipodial Extension
and HGF-ERK Signaling Specifies Leader Cells during Collective Cell Migration.”
Developmental Cell. Elsevier, 2022. https://doi.org/10.1016/j.devcel.2022.09.003.
ieee: N. Hino et al., “A feedback loop between lamellipodial extension and
HGF-ERK signaling specifies leader cells during collective cell migration,” Developmental
Cell, vol. 57, no. 19. Elsevier, p. 2290–2304.e7, 2022.
ista: Hino N, Matsuda K, Jikko Y, Maryu G, Sakai K, Imamura R, Tsukiji S, Aoki K,
Terai K, Hirashima T, Trepat X, Matsuda M. 2022. A feedback loop between lamellipodial
extension and HGF-ERK signaling specifies leader cells during collective cell
migration. Developmental Cell. 57(19), 2290–2304.e7.
mla: Hino, Naoya, et al. “A Feedback Loop between Lamellipodial Extension and HGF-ERK
Signaling Specifies Leader Cells during Collective Cell Migration.” Developmental
Cell, vol. 57, no. 19, Elsevier, 2022, p. 2290–2304.e7, doi:10.1016/j.devcel.2022.09.003.
short: N. Hino, K. Matsuda, Y. Jikko, G. Maryu, K. Sakai, R. Imamura, S. Tsukiji,
K. Aoki, K. Terai, T. Hirashima, X. Trepat, M. Matsuda, Developmental Cell 57
(2022) 2290–2304.e7.
date_created: 2023-01-16T09:51:39Z
date_published: 2022-10-01T00:00:00Z
date_updated: 2023-08-04T09:38:53Z
day: '01'
department:
- _id: CaHe
doi: 10.1016/j.devcel.2022.09.003
external_id:
isi:
- '000898428700006'
pmid:
- '36174555'
intvolume: ' 57'
isi: 1
issue: '19'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '10'
oa_version: None
page: 2290-2304.e7
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A feedback loop between lamellipodial extension and HGF-ERK signaling specifies
leader cells during collective cell migration
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 57
year: '2022'
...
---
_id: '12245'
abstract:
- lang: eng
text: MicroRNAs (miRs) have an important role in tuning dynamic gene expression.
However, the mechanism by which they are quantitatively controlled is unknown.
We show that the amount of mature miR-9, a key regulator of neuronal development,
increases during zebrafish neurogenesis in a sharp stepwise manner. We characterize
the spatiotemporal profile of seven distinct microRNA primary transcripts (pri-mir)-9s
that produce the same mature miR-9 and show that they are sequentially expressed
during hindbrain neurogenesis. Expression of late-onset pri-mir-9-1 is added on
to, rather than replacing, the expression of early onset pri-mir-9-4 and -9-5
in single cells. CRISPR/Cas9 mutation of the late-onset pri-mir-9-1 prevents the
developmental increase of mature miR-9, reduces late neuronal differentiation
and fails to downregulate Her6 at late stages. Mathematical modelling shows that
an adaptive network containing Her6 is insensitive to linear increases in miR-9
but responds to stepwise increases of miR-9. We suggest that a sharp stepwise
increase of mature miR-9 is created by sequential and additive temporal activation
of distinct loci. This may be a strategy to overcome adaptation and facilitate
a transition of Her6 to a new dynamic regime or steady state.
acknowledgement: "We are grateful to Dr Tom Pettini for the advice on smiFISH technique
and Dr Laure Bally-Cuif for sharing plasmids. The authors also thank the Biological
Services Facility, Bioimaging and Systems Microscopy Facilities of the University
of Manchester for technical support.\r\nThis work was supported by a Wellcome Trust
Senior Research Fellowship (090868/Z/09/Z) and a Wellcome Trust Investigator Award
(224394/Z/21/Z) to N.P. and a Medical Research Council Career Development Award
to C.S.M. (MR/V032534/1). J.B. was supported by a Wellcome Trust Four-Year PhD Studentship
in Basic Science (219992/Z/19/Z). Open Access funding provided by The University
of Manchester. Deposited in PMC for immediate release."
article_number: dev200474
article_processing_charge: No
article_type: original
author:
- first_name: Ximena
full_name: Soto, Ximena
last_name: Soto
- first_name: Joshua
full_name: Burton, Joshua
last_name: Burton
- first_name: Cerys S.
full_name: Manning, Cerys S.
last_name: Manning
- first_name: Thomas
full_name: Minchington, Thomas
id: 7d1648cb-19e9-11eb-8e7a-f8c037fb3e3f
last_name: Minchington
- first_name: Robert
full_name: Lea, Robert
last_name: Lea
- first_name: Jessica
full_name: Lee, Jessica
last_name: Lee
- first_name: Jochen
full_name: Kursawe, Jochen
last_name: Kursawe
- first_name: Magnus
full_name: Rattray, Magnus
last_name: Rattray
- first_name: Nancy
full_name: Papalopulu, Nancy
last_name: Papalopulu
citation:
ama: Soto X, Burton J, Manning CS, et al. Sequential and additive expression of
miR-9 precursors control timing of neurogenesis. Development. 2022;149(19).
doi:10.1242/dev.200474
apa: Soto, X., Burton, J., Manning, C. S., Minchington, T., Lea, R., Lee, J., …
Papalopulu, N. (2022). Sequential and additive expression of miR-9 precursors
control timing of neurogenesis. Development. The Company of Biologists.
https://doi.org/10.1242/dev.200474
chicago: Soto, Ximena, Joshua Burton, Cerys S. Manning, Thomas Minchington, Robert
Lea, Jessica Lee, Jochen Kursawe, Magnus Rattray, and Nancy Papalopulu. “Sequential
and Additive Expression of MiR-9 Precursors Control Timing of Neurogenesis.” Development.
The Company of Biologists, 2022. https://doi.org/10.1242/dev.200474.
ieee: X. Soto et al., “Sequential and additive expression of miR-9 precursors
control timing of neurogenesis,” Development, vol. 149, no. 19. The Company
of Biologists, 2022.
ista: Soto X, Burton J, Manning CS, Minchington T, Lea R, Lee J, Kursawe J, Rattray
M, Papalopulu N. 2022. Sequential and additive expression of miR-9 precursors
control timing of neurogenesis. Development. 149(19), dev200474.
mla: Soto, Ximena, et al. “Sequential and Additive Expression of MiR-9 Precursors
Control Timing of Neurogenesis.” Development, vol. 149, no. 19, dev200474,
The Company of Biologists, 2022, doi:10.1242/dev.200474.
short: X. Soto, J. Burton, C.S. Manning, T. Minchington, R. Lea, J. Lee, J. Kursawe,
M. Rattray, N. Papalopulu, Development 149 (2022).
date_created: 2023-01-16T09:53:17Z
date_published: 2022-10-01T00:00:00Z
date_updated: 2023-08-04T09:41:08Z
day: '01'
ddc:
- '570'
department:
- _id: AnKi
doi: 10.1242/dev.200474
external_id:
isi:
- '000918161000003'
pmid:
- '36189829'
file:
- access_level: open_access
checksum: d7c29b74e9e4032308228cc704a30e88
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T08:35:44Z
date_updated: 2023-01-30T08:35:44Z
file_id: '12438'
file_name: 2022_Development_Soto.pdf
file_size: 9348839
relation: main_file
success: 1
file_date_updated: 2023-01-30T08:35:44Z
has_accepted_license: '1'
intvolume: ' 149'
isi: 1
issue: '19'
keyword:
- Developmental Biology
- Molecular Biology
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
eissn:
- 1477-9129
issn:
- 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
related_material:
link:
- relation: software
url: ' https://github.com/burtonjosh/StepwiseMir9'
scopus_import: '1'
status: public
title: Sequential and additive expression of miR-9 precursors control timing of neurogenesis
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: 149
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: '11057'
abstract:
- lang: eng
text: During mitosis, transcription of genomic DNA is dramatically reduced, before
it is reactivated during nuclear reformation in anaphase/telophase. Many aspects
of the underlying principles that mediate transcriptional memory and reactivation
in the daughter cells remain unclear. Here, we used ChIP-seq on synchronized cells
at different stages after mitosis to generate genome-wide maps of histone modifications.
Combined with EU-RNA-seq and Hi-C analyses, we found that during prometaphase,
promoters, enhancers, and insulators retain H3K4me3 and H3K4me1, while losing
H3K27ac. Enhancers globally retaining mitotic H3K4me1 or locally retaining mitotic
H3K27ac are associated with cell type-specific genes and their transcription factors
for rapid transcriptional activation. As cells exit mitosis, promoters regain
H3K27ac, which correlates with transcriptional reactivation. Insulators also gain
H3K27ac and CCCTC-binding factor (CTCF) in anaphase/telophase. This increase of
H3K27ac in anaphase/telophase is required for posttranscriptional activation and
may play a role in the establishment of topologically associating domains (TADs).
Together, our results suggest that the genome is reorganized in a sequential order,
in which histone methylations occur first in prometaphase, histone acetylation,
and CTCF in anaphase/telophase, transcription in cytokinesis, and long-range chromatin
interactions in early G1. We thus provide insights into the histone modification
landscape that allows faithful reestablishment of the transcriptional program
and TADs during cell division.
article_processing_charge: No
article_type: original
author:
- first_name: Hyeseon
full_name: Kang, Hyeseon
last_name: Kang
- first_name: Maxim N.
full_name: Shokhirev, Maxim N.
last_name: Shokhirev
- first_name: Zhichao
full_name: Xu, Zhichao
last_name: Xu
- first_name: Sahaana
full_name: Chandran, Sahaana
last_name: Chandran
- first_name: Jesse R.
full_name: Dixon, Jesse R.
last_name: Dixon
- 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: Kang H, Shokhirev MN, Xu Z, Chandran S, Dixon JR, Hetzer M. Dynamic regulation
of histone modifications and long-range chromosomal interactions during postmitotic
transcriptional reactivation. Genes & Development. 2020;34(13-14):913-930.
doi:10.1101/gad.335794.119
apa: Kang, H., Shokhirev, M. N., Xu, Z., Chandran, S., Dixon, J. R., & Hetzer,
M. (2020). Dynamic regulation of histone modifications and long-range chromosomal
interactions during postmitotic transcriptional reactivation. Genes & Development.
Cold Spring Harbor Laboratory Press. https://doi.org/10.1101/gad.335794.119
chicago: Kang, Hyeseon, Maxim N. Shokhirev, Zhichao Xu, Sahaana Chandran, Jesse
R. Dixon, and Martin Hetzer. “Dynamic Regulation of Histone Modifications and
Long-Range Chromosomal Interactions during Postmitotic Transcriptional Reactivation.”
Genes & Development. Cold Spring Harbor Laboratory Press, 2020. https://doi.org/10.1101/gad.335794.119.
ieee: H. Kang, M. N. Shokhirev, Z. Xu, S. Chandran, J. R. Dixon, and M. Hetzer,
“Dynamic regulation of histone modifications and long-range chromosomal interactions
during postmitotic transcriptional reactivation,” Genes & Development,
vol. 34, no. 13–14. Cold Spring Harbor Laboratory Press, pp. 913–930, 2020.
ista: Kang H, Shokhirev MN, Xu Z, Chandran S, Dixon JR, Hetzer M. 2020. Dynamic
regulation of histone modifications and long-range chromosomal interactions during
postmitotic transcriptional reactivation. Genes & Development. 34(13–14),
913–930.
mla: Kang, Hyeseon, et al. “Dynamic Regulation of Histone Modifications and Long-Range
Chromosomal Interactions during Postmitotic Transcriptional Reactivation.” Genes
& Development, vol. 34, no. 13–14, Cold Spring Harbor Laboratory Press,
2020, pp. 913–30, doi:10.1101/gad.335794.119.
short: H. Kang, M.N. Shokhirev, Z. Xu, S. Chandran, J.R. Dixon, M. Hetzer, Genes
& Development 34 (2020) 913–930.
date_created: 2022-04-07T07:44:09Z
date_published: 2020-04-28T00:00:00Z
date_updated: 2022-07-18T08:31:08Z
day: '28'
ddc:
- '570'
doi: 10.1101/gad.335794.119
extern: '1'
external_id:
pmid:
- '32499403'
file:
- access_level: open_access
checksum: 84e92d40e67936c739628315c238daf9
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T07:12:33Z
date_updated: 2022-04-08T07:12:33Z
file_id: '11136'
file_name: 2020_GenesDevelopment_Kang.pdf
file_size: 4406772
relation: main_file
success: 1
file_date_updated: 2022-04-08T07:12:33Z
has_accepted_license: '1'
intvolume: ' 34'
issue: 13-14
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 913-930
pmid: 1
publication: Genes & Development
publication_identifier:
issn:
- 0890-9369
- 1549-5477
publication_status: published
publisher: Cold Spring Harbor Laboratory Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dynamic regulation of histone modifications and long-range chromosomal interactions
during postmitotic transcriptional reactivation
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 34
year: '2020'
...
---
_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: '11063'
abstract:
- lang: eng
text: The total number of nuclear pore complexes (NPCs) per nucleus varies greatly
between different cell types and is known to change during cell differentiation
and cell transformation. However, the underlying mechanisms that control how many
nuclear transport channels are assembled into a given nuclear envelope remain
unclear. Here, we report that depletion of the NPC basket protein Tpr, but not
Nup153, dramatically increases the total NPC number in various cell types. This
negative regulation of Tpr occurs via a phosphorylation cascade of extracellular
signal-regulated kinase (ERK), the central kinase of the mitogen-activated protein
kinase (MAPK) pathway. Tpr serves as a scaffold for ERK to phosphorylate the nucleoporin
(Nup) Nup153, which is critical for early stages of NPC biogenesis. Our results
reveal a critical role of the Nup Tpr in coordinating signal transduction pathways
during cell proliferation and the dynamic organization of the nucleus.
article_processing_charge: No
article_type: original
author:
- first_name: Asako
full_name: McCloskey, Asako
last_name: McCloskey
- first_name: Arkaitz
full_name: Ibarra, Arkaitz
last_name: Ibarra
- 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: McCloskey A, Ibarra A, Hetzer M. Tpr regulates the total number of nuclear
pore complexes per cell nucleus. Genes & Development. 2018;32(19-20):1321-1331.
doi:10.1101/gad.315523.118
apa: McCloskey, A., Ibarra, A., & Hetzer, M. (2018). Tpr regulates the total
number of nuclear pore complexes per cell nucleus. Genes & Development.
Cold Spring Harbor Laboratory. https://doi.org/10.1101/gad.315523.118
chicago: McCloskey, Asako, Arkaitz Ibarra, and Martin Hetzer. “Tpr Regulates the
Total Number of Nuclear Pore Complexes per Cell Nucleus.” Genes & Development.
Cold Spring Harbor Laboratory, 2018. https://doi.org/10.1101/gad.315523.118.
ieee: A. McCloskey, A. Ibarra, and M. Hetzer, “Tpr regulates the total number of
nuclear pore complexes per cell nucleus,” Genes & Development, vol.
32, no. 19–20. Cold Spring Harbor Laboratory, pp. 1321–1331, 2018.
ista: McCloskey A, Ibarra A, Hetzer M. 2018. Tpr regulates the total number of nuclear
pore complexes per cell nucleus. Genes & Development. 32(19–20), 1321–1331.
mla: McCloskey, Asako, et al. “Tpr Regulates the Total Number of Nuclear Pore Complexes
per Cell Nucleus.” Genes & Development, vol. 32, no. 19–20, Cold Spring
Harbor Laboratory, 2018, pp. 1321–31, doi:10.1101/gad.315523.118.
short: A. McCloskey, A. Ibarra, M. Hetzer, Genes & Development 32 (2018) 1321–1331.
date_created: 2022-04-07T07:45:30Z
date_published: 2018-09-18T00:00:00Z
date_updated: 2022-07-18T08:32:32Z
day: '18'
doi: 10.1101/gad.315523.118
extern: '1'
external_id:
pmid:
- '30228202'
intvolume: ' 32'
issue: 19-20
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/gad.315523.118
month: '09'
oa: 1
oa_version: Published Version
page: 1321-1331
pmid: 1
publication: Genes & Development
publication_identifier:
issn:
- 0890-9369
- 1549-5477
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: Tpr regulates the total number of nuclear pore complexes per cell nucleus
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 32
year: '2018'
...
---
_id: '11066'
abstract:
- lang: eng
text: Recent studies have shown that a subset of nucleoporins (Nups) can detach
from the nuclear pore complex and move into the nuclear interior to regulate transcription.
One such dynamic Nup, called Nup98, has been implicated in gene activation in
healthy cells and has been shown to drive leukemogenesis when mutated in patients
with acute myeloid leukemia (AML). Here we show that in hematopoietic cells, Nup98
binds predominantly to transcription start sites to recruit the Wdr82–Set1A/COMPASS
(complex of proteins associated with Set1) complex, which is required for deposition
of the histone 3 Lys4 trimethyl (H3K4me3)-activating mark. Depletion of Nup98
or Wdr82 abolishes Set1A recruitment to chromatin and subsequently ablates H3K4me3
at adjacent promoters. Furthermore, expression of a Nup98 fusion protein implicated
in aggressive AML causes mislocalization of H3K4me3 at abnormal regions and up-regulation
of associated genes. Our findings establish a function of Nup98 in hematopoietic
gene activation and provide mechanistic insight into which Nup98 leukemic fusion
proteins promote AML.
article_processing_charge: No
article_type: original
author:
- first_name: Tobias M.
full_name: Franks, Tobias M.
last_name: Franks
- first_name: Asako
full_name: McCloskey, Asako
last_name: McCloskey
- first_name: Maxim Nikolaievich
full_name: Shokhirev, Maxim Nikolaievich
last_name: Shokhirev
- first_name: Chris
full_name: Benner, Chris
last_name: Benner
- first_name: Annie
full_name: Rathore, Annie
last_name: Rathore
- 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: Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. Nup98
recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation
in hematopoietic progenitor cells. Genes & Development. 2017;31(22):2222-2234.
doi:10.1101/gad.306753.117
apa: Franks, T. M., McCloskey, A., Shokhirev, M. N., Benner, C., Rathore, A., &
Hetzer, M. (2017). Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters
to regulate H3K4 trimethylation in hematopoietic progenitor cells. Genes &
Development. Cold Spring Harbor Laboratory. https://doi.org/10.1101/gad.306753.117
chicago: Franks, Tobias M., Asako McCloskey, Maxim Nikolaievich Shokhirev, Chris
Benner, Annie Rathore, and Martin Hetzer. “Nup98 Recruits the Wdr82–Set1A/COMPASS
Complex to Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor
Cells.” Genes & Development. Cold Spring Harbor Laboratory, 2017. https://doi.org/10.1101/gad.306753.117.
ieee: T. M. Franks, A. McCloskey, M. N. Shokhirev, C. Benner, A. Rathore, and M.
Hetzer, “Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate
H3K4 trimethylation in hematopoietic progenitor cells,” Genes & Development,
vol. 31, no. 22. Cold Spring Harbor Laboratory, pp. 2222–2234, 2017.
ista: Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. 2017.
Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation
in hematopoietic progenitor cells. Genes & Development. 31(22), 2222–2234.
mla: Franks, Tobias M., et al. “Nup98 Recruits the Wdr82–Set1A/COMPASS Complex to
Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor Cells.”
Genes & Development, vol. 31, no. 22, Cold Spring Harbor Laboratory,
2017, pp. 2222–34, doi:10.1101/gad.306753.117.
short: T.M. Franks, A. McCloskey, M.N. Shokhirev, C. Benner, A. Rathore, M. Hetzer,
Genes & Development 31 (2017) 2222–2234.
date_created: 2022-04-07T07:45:59Z
date_published: 2017-12-21T00:00:00Z
date_updated: 2022-07-18T08:33:05Z
day: '21'
doi: 10.1101/gad.306753.117
extern: '1'
external_id:
pmid:
- '29269482'
intvolume: ' 31'
issue: '22'
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/gad.306753.117
month: '12'
oa: 1
oa_version: Published Version
page: 2222-2234
pmid: 1
publication: Genes & Development
publication_identifier:
issn:
- 0890-9369
- 1549-5477
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4
trimethylation in hematopoietic progenitor cells
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 31
year: '2017'
...
---
_id: '11070'
abstract:
- lang: eng
text: The organization of the genome in the three-dimensional space of the nucleus
is coupled with cell type-specific gene expression. However, how nuclear architecture
influences transcription that governs cell identity remains unknown. Here, we
show that nuclear pore complex (NPC) components Nup93 and Nup153 bind superenhancers
(SE), regulatory structures that drive the expression of key genes that specify
cell identity. We found that nucleoporin-associated SEs localize preferentially
to the nuclear periphery, and absence of Nup153 and Nup93 results in dramatic
transcriptional changes of SE-associated genes. Our results reveal a crucial role
of NPC components in the regulation of cell type-specifying genes and highlight
nuclear architecture as a regulatory layer of genome functions in cell fate.
article_processing_charge: No
article_type: original
author:
- first_name: Arkaitz
full_name: Ibarra, Arkaitz
last_name: Ibarra
- first_name: Chris
full_name: Benner, Chris
last_name: Benner
- first_name: Swati
full_name: Tyagi, Swati
last_name: Tyagi
- first_name: Jonah
full_name: Cool, Jonah
last_name: Cool
- 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: Ibarra A, Benner C, Tyagi S, Cool J, Hetzer M. Nucleoporin-mediated regulation
of cell identity genes. Genes & Development. 2016;30(20):2253-2258.
doi:10.1101/gad.287417.116
apa: Ibarra, A., Benner, C., Tyagi, S., Cool, J., & Hetzer, M. (2016). Nucleoporin-mediated
regulation of cell identity genes. Genes & Development. Cold Spring
Harbor Laboratory. https://doi.org/10.1101/gad.287417.116
chicago: Ibarra, Arkaitz, Chris Benner, Swati Tyagi, Jonah Cool, and Martin Hetzer.
“Nucleoporin-Mediated Regulation of Cell Identity Genes.” Genes & Development.
Cold Spring Harbor Laboratory, 2016. https://doi.org/10.1101/gad.287417.116.
ieee: A. Ibarra, C. Benner, S. Tyagi, J. Cool, and M. Hetzer, “Nucleoporin-mediated
regulation of cell identity genes,” Genes & Development, vol. 30, no.
20. Cold Spring Harbor Laboratory, pp. 2253–2258, 2016.
ista: Ibarra A, Benner C, Tyagi S, Cool J, Hetzer M. 2016. Nucleoporin-mediated
regulation of cell identity genes. Genes & Development. 30(20), 2253–2258.
mla: Ibarra, Arkaitz, et al. “Nucleoporin-Mediated Regulation of Cell Identity Genes.”
Genes & Development, vol. 30, no. 20, Cold Spring Harbor Laboratory,
2016, pp. 2253–58, doi:10.1101/gad.287417.116.
short: A. Ibarra, C. Benner, S. Tyagi, J. Cool, M. Hetzer, Genes & Development
30 (2016) 2253–2258.
date_created: 2022-04-07T07:48:08Z
date_published: 2016-11-02T00:00:00Z
date_updated: 2022-07-18T08:33:49Z
day: '02'
doi: 10.1101/gad.287417.116
extern: '1'
external_id:
pmid:
- '27807035'
intvolume: ' 30'
issue: '20'
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/gad.287417.116
month: '11'
oa: 1
oa_version: Published Version
page: 2253-2258
pmid: 1
publication: Genes & Development
publication_identifier:
eissn:
- 1549-5477
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nucleoporin-mediated regulation of cell identity genes
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 30
year: '2016'
...
---
_id: '11071'
abstract:
- lang: eng
text: Nuclear pore complexes (NPCs) emerged as nuclear transport channels in eukaryotic
cells ∼1.5 billion years ago. While the primary role of NPCs is to regulate nucleo–cytoplasmic
transport, recent research suggests that certain NPC proteins have additionally
acquired the role of affecting gene expression at the nuclear periphery and in
the nucleoplasm in metazoans. Here we identify a widely expressed variant of the
transmembrane nucleoporin (Nup) Pom121 (named sPom121, for “soluble Pom121”) that
arose by genomic rearrangement before the divergence of hominoids. sPom121 lacks
the nuclear membrane-anchoring domain and thus does not localize to the NPC. Instead,
sPom121 colocalizes and interacts with nucleoplasmic Nup98, a previously identified
transcriptional regulator, at gene promoters to control transcription of its target
genes in human cells. Interestingly, sPom121 transcripts appear independently
in several mammalian species, suggesting convergent innovation of Nup-mediated
transcription regulation during mammalian evolution. Our findings implicate alternate
transcription initiation as a mechanism to increase the functional diversity of
NPC components.
article_processing_charge: No
article_type: original
author:
- first_name: Tobias M.
full_name: Franks, Tobias M.
last_name: Franks
- first_name: Chris
full_name: Benner, Chris
last_name: Benner
- first_name: Iñigo
full_name: Narvaiza, Iñigo
last_name: Narvaiza
- first_name: Maria C.N.
full_name: Marchetto, Maria C.N.
last_name: Marchetto
- first_name: Janet M.
full_name: Young, Janet M.
last_name: Young
- first_name: Harmit S.
full_name: Malik, Harmit S.
last_name: Malik
- first_name: Fred H.
full_name: Gage, Fred H.
last_name: Gage
- 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: Franks TM, Benner C, Narvaiza I, et al. Evolution of a transcriptional regulator
from a transmembrane nucleoporin. Genes & Development. 2016;30(10):1155-1171.
doi:10.1101/gad.280941.116
apa: Franks, T. M., Benner, C., Narvaiza, I., Marchetto, M. C. N., Young, J. M.,
Malik, H. S., … Hetzer, M. (2016). Evolution of a transcriptional regulator from
a transmembrane nucleoporin. Genes & Development. Cold Spring Harbor
Laboratory. https://doi.org/10.1101/gad.280941.116
chicago: Franks, Tobias M., Chris Benner, Iñigo Narvaiza, Maria C.N. Marchetto,
Janet M. Young, Harmit S. Malik, Fred H. Gage, and Martin Hetzer. “Evolution of
a Transcriptional Regulator from a Transmembrane Nucleoporin.” Genes &
Development. Cold Spring Harbor Laboratory, 2016. https://doi.org/10.1101/gad.280941.116.
ieee: T. M. Franks et al., “Evolution of a transcriptional regulator from
a transmembrane nucleoporin,” Genes & Development, vol. 30, no. 10.
Cold Spring Harbor Laboratory, pp. 1155–1171, 2016.
ista: Franks TM, Benner C, Narvaiza I, Marchetto MCN, Young JM, Malik HS, Gage FH,
Hetzer M. 2016. Evolution of a transcriptional regulator from a transmembrane
nucleoporin. Genes & Development. 30(10), 1155–1171.
mla: Franks, Tobias M., et al. “Evolution of a Transcriptional Regulator from a
Transmembrane Nucleoporin.” Genes & Development, vol. 30, no. 10, Cold
Spring Harbor Laboratory, 2016, pp. 1155–71, doi:10.1101/gad.280941.116.
short: T.M. Franks, C. Benner, I. Narvaiza, M.C.N. Marchetto, J.M. Young, H.S. Malik,
F.H. Gage, M. Hetzer, Genes & Development 30 (2016) 1155–1171.
date_created: 2022-04-07T07:48:20Z
date_published: 2016-05-19T00:00:00Z
date_updated: 2022-07-18T08:33:50Z
day: '19'
doi: 10.1101/gad.280941.116
extern: '1'
external_id:
pmid:
- '27198230'
intvolume: ' 30'
issue: '10'
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/gad.280941.116
month: '05'
oa: 1
oa_version: Published Version
page: 1155-1171
pmid: 1
publication: Genes & Development
publication_identifier:
eissn:
- 1549-5477
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolution of a transcriptional regulator from a transmembrane nucleoporin
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 30
year: '2016'
...
---
_id: '11076'
abstract:
- lang: eng
text: Nuclear pore complexes (NPCs) are composed of several copies of ∼30 different
proteins called nucleoporins (Nups). NPCs penetrate the nuclear envelope (NE)
and regulate the nucleocytoplasmic trafficking of macromolecules. Beyond this
vital role, NPC components influence genome functions in a transport-independent
manner. Nups play an evolutionarily conserved role in gene expression regulation
that, in metazoans, extends into the nuclear interior. Additionally, in proliferative
cells, Nups play a crucial role in genome integrity maintenance and mitotic progression.
Here we discuss genome-related functions of Nups and their impact on essential
DNA metabolism processes such as transcription, chromosome duplication, and segregation.
article_processing_charge: No
article_type: original
author:
- first_name: Arkaitz
full_name: Ibarra, Arkaitz
last_name: Ibarra
- 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: Ibarra A, Hetzer M. Nuclear pore proteins and the control of genome functions.
Genes & Development. 2015;29(4):337-349. doi:10.1101/gad.256495.114
apa: Ibarra, A., & Hetzer, M. (2015). Nuclear pore proteins and the control
of genome functions. Genes & Development. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/gad.256495.114
chicago: Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control
of Genome Functions.” Genes & Development. Cold Spring Harbor Laboratory,
2015. https://doi.org/10.1101/gad.256495.114.
ieee: A. Ibarra and M. Hetzer, “Nuclear pore proteins and the control of genome
functions,” Genes & Development, vol. 29, no. 4. Cold Spring Harbor
Laboratory, pp. 337–349, 2015.
ista: Ibarra A, Hetzer M. 2015. Nuclear pore proteins and the control of genome
functions. Genes & Development. 29(4), 337–349.
mla: Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control
of Genome Functions.” Genes & Development, vol. 29, no. 4, Cold Spring
Harbor Laboratory, 2015, pp. 337–49, doi:10.1101/gad.256495.114.
short: A. Ibarra, M. Hetzer, Genes & Development 29 (2015) 337–349.
date_created: 2022-04-07T07:49:21Z
date_published: 2015-02-01T00:00:00Z
date_updated: 2022-07-18T08:43:20Z
day: '01'
doi: 10.1101/gad.256495.114
extern: '1'
external_id:
pmid:
- '25691464'
intvolume: ' 29'
issue: '4'
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/gad.256495.114
month: '02'
oa: 1
oa_version: Published Version
page: 337-349
pmid: 1
publication: Genes & Development
publication_identifier:
eissn:
- 1549-5477
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nuclear pore proteins and the control of genome functions
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 29
year: '2015'
...
---
_id: '11077'
abstract:
- lang: eng
text: Nucleoporins (Nups) are a family of proteins best known as the constituent
building blocks of nuclear pore complexes (NPCs), membrane-embedded channels that
mediate nuclear transport across the nuclear envelope. Recent evidence suggests
that several Nups have additional roles in controlling the activation and silencing
of developmental genes; however, the mechanistic details of these functions remain
poorly understood. Here, we show that depletion of Nup153 in mouse embryonic stem
cells (mESCs) causes the derepression of developmental genes and induction of
early differentiation. This loss of stem cell identity is not associated with
defects in the nuclear import of key pluripotency factors. Rather, Nup153 binds
around the transcriptional start site (TSS) of developmental genes and mediates
the recruitment of the polycomb-repressive complex 1 (PRC1) to a subset of its
target loci. Our results demonstrate a chromatin-associated role of Nup153 in
maintaining stem cell pluripotency by functioning in mammalian epigenetic gene
silencing.
article_processing_charge: No
article_type: original
author:
- first_name: Filipe V.
full_name: Jacinto, Filipe V.
last_name: Jacinto
- first_name: Chris
full_name: Benner, Chris
last_name: Benner
- 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: Jacinto FV, Benner C, Hetzer M. The nucleoporin Nup153 regulates embryonic
stem cell pluripotency through gene silencing. Genes & Development.
2015;29(12):1224-1238. doi:10.1101/gad.260919.115
apa: Jacinto, F. V., Benner, C., & Hetzer, M. (2015). The nucleoporin Nup153
regulates embryonic stem cell pluripotency through gene silencing. Genes &
Development. Cold Spring Harbor Laboratory. https://doi.org/10.1101/gad.260919.115
chicago: Jacinto, Filipe V., Chris Benner, and Martin Hetzer. “The Nucleoporin Nup153
Regulates Embryonic Stem Cell Pluripotency through Gene Silencing.” Genes &
Development. Cold Spring Harbor Laboratory, 2015. https://doi.org/10.1101/gad.260919.115.
ieee: F. V. Jacinto, C. Benner, and M. Hetzer, “The nucleoporin Nup153 regulates
embryonic stem cell pluripotency through gene silencing,” Genes & Development,
vol. 29, no. 12. Cold Spring Harbor Laboratory, pp. 1224–1238, 2015.
ista: Jacinto FV, Benner C, Hetzer M. 2015. The nucleoporin Nup153 regulates embryonic
stem cell pluripotency through gene silencing. Genes & Development. 29(12),
1224–1238.
mla: Jacinto, Filipe V., et al. “The Nucleoporin Nup153 Regulates Embryonic Stem
Cell Pluripotency through Gene Silencing.” Genes & Development, vol.
29, no. 12, Cold Spring Harbor Laboratory, 2015, pp. 1224–38, doi:10.1101/gad.260919.115.
short: F.V. Jacinto, C. Benner, M. Hetzer, Genes & Development 29 (2015) 1224–1238.
date_created: 2022-04-07T07:49:31Z
date_published: 2015-06-16T00:00:00Z
date_updated: 2022-07-18T08:43:51Z
day: '16'
doi: 10.1101/gad.260919.115
extern: '1'
external_id:
pmid:
- '26080816'
intvolume: ' 29'
issue: '12'
keyword:
- Developmental Biology
- Genetics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/gad.260919.115
month: '06'
oa: 1
oa_version: Published Version
page: 1224-1238
pmid: 1
publication: Genes & Development
publication_identifier:
eissn:
- 1549-5477
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory
quality_controlled: '1'
scopus_import: '1'
status: public
title: The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene
silencing
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 29
year: '2015'
...
---
_id: '10815'
abstract:
- lang: eng
text: In the last several decades, developmental biology has clarified the molecular
mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated
that the “tool-kit genes” essential for regulating developmental processes are
not only highly conserved among species, but are also used as systems at various
times and places in an organism to control distinct developmental events. Therefore,
mutations in many of these tool-kit genes may cause congenital diseases involving
morphological abnormalities. This link between genes and abnormal morphological
phenotypes underscores the importance of understanding how cells behave and contribute
to morphogenesis as a result of gene function. Recent improvements in live imaging
and in quantitative analyses of cellular dynamics will advance our understanding
of the cellular pathogenesis of congenital diseases associated with aberrant morphologies.
In these studies, it is critical to select an appropriate model organism for the
particular phenomenon of interest.
acknowledgement: The authors thank all the members of the Division of Morphogenesis,
National Institute for Basic Biology, for their contributions to the research, their
encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical
reading of the manuscript. We also thank the Model Animal Research and Spectrography
and Bioimaging Facilities, NIBB Core Research Facilities, for technical support.
M.H. was supported by a research fellowship from the Japan Society for the Promotion
of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid
for Scientific Research on Innovative Areas from the Ministry of Education, Culture,
Sports, Science, and Technology (MEXT), Japan, to N.U.
article_processing_charge: No
article_type: original
author:
- first_name: Masakazu
full_name: Hashimoto, Masakazu
last_name: Hashimoto
- first_name: Hitoshi
full_name: Morita, Hitoshi
id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87
last_name: Morita
- first_name: Naoto
full_name: Ueno, Naoto
last_name: Ueno
citation:
ama: Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development
underlying congenital diseases. Congenital Anomalies. 2014;54(1):1-7. doi:10.1111/cga.12039
apa: Hashimoto, M., Morita, H., & Ueno, N. (2014). Molecular and cellular mechanisms
of development underlying congenital diseases. Congenital Anomalies. Wiley.
https://doi.org/10.1111/cga.12039
chicago: Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular
Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies.
Wiley, 2014. https://doi.org/10.1111/cga.12039.
ieee: M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of
development underlying congenital diseases,” Congenital Anomalies, vol.
54, no. 1. Wiley, pp. 1–7, 2014.
ista: Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of
development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7.
mla: Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development
Underlying Congenital Diseases.” Congenital Anomalies, vol. 54, no. 1,
Wiley, 2014, pp. 1–7, doi:10.1111/cga.12039.
short: M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7.
date_created: 2022-03-04T08:17:25Z
date_published: 2014-02-01T00:00:00Z
date_updated: 2022-03-04T08:26:05Z
day: '01'
department:
- _id: CaHe
doi: 10.1111/cga.12039
external_id:
pmid:
- '24666178'
intvolume: ' 54'
issue: '1'
keyword:
- Developmental Biology
- Embryology
- General Medicine
- Pediatrics
- Perinatology
- and Child Health
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1111/cga.12039
month: '02'
oa: 1
oa_version: None
page: 1-7
pmid: 1
publication: Congenital Anomalies
publication_identifier:
issn:
- 0914-3505
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Molecular and cellular mechanisms of development underlying congenital diseases
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 54
year: '2014'
...
---
_id: '11093'
abstract:
- lang: eng
text: Nuclear pore complexes (NPCs) are built from ∼30 different proteins called
nucleoporins or Nups. Previous studies have shown that several Nups exhibit cell-type-specific
expression and that mutations in NPC components result in tissue-specific diseases.
Here we show that a specific change in NPC composition is required for both myogenic
and neuronal differentiation. The transmembrane nucleoporin Nup210 is absent in
proliferating myoblasts and embryonic stem cells (ESCs) but becomes expressed
and incorporated into NPCs during cell differentiation. Preventing Nup210 production
by RNAi blocks myogenesis and the differentiation of ESCs into neuroprogenitors.
We found that the addition of Nup210 to NPCs does not affect nuclear transport
but is required for the induction of genes that are essential for cell differentiation.
Our results identify a single change in NPC composition as an essential step in
cell differentiation and establish a role for Nup210 in gene expression regulation
and cell fate determination.
article_processing_charge: No
article_type: original
author:
- first_name: Maximiliano A.
full_name: D'Angelo, Maximiliano A.
last_name: D'Angelo
- first_name: J. Sebastian
full_name: Gomez-Cavazos, J. Sebastian
last_name: Gomez-Cavazos
- first_name: Arianna
full_name: Mei, Arianna
last_name: Mei
- first_name: Daniel H.
full_name: Lackner, Daniel H.
last_name: Lackner
- 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: D’Angelo MA, Gomez-Cavazos JS, Mei A, Lackner DH, Hetzer M. A change in nuclear
pore complex composition regulates cell differentiation. Developmental Cell.
2012;22(2):446-458. doi:10.1016/j.devcel.2011.11.021
apa: D’Angelo, M. A., Gomez-Cavazos, J. S., Mei, A., Lackner, D. H., & Hetzer,
M. (2012). A change in nuclear pore complex composition regulates cell differentiation.
Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2011.11.021
chicago: D’Angelo, Maximiliano A., J. Sebastian Gomez-Cavazos, Arianna Mei, Daniel H.
Lackner, and Martin Hetzer. “A Change in Nuclear Pore Complex Composition Regulates
Cell Differentiation.” Developmental Cell. Elsevier, 2012. https://doi.org/10.1016/j.devcel.2011.11.021.
ieee: M. A. D’Angelo, J. S. Gomez-Cavazos, A. Mei, D. H. Lackner, and M. Hetzer,
“A change in nuclear pore complex composition regulates cell differentiation,”
Developmental Cell, vol. 22, no. 2. Elsevier, pp. 446–458, 2012.
ista: D’Angelo MA, Gomez-Cavazos JS, Mei A, Lackner DH, Hetzer M. 2012. A change
in nuclear pore complex composition regulates cell differentiation. Developmental
Cell. 22(2), 446–458.
mla: D’Angelo, Maximiliano A., et al. “A Change in Nuclear Pore Complex Composition
Regulates Cell Differentiation.” Developmental Cell, vol. 22, no. 2, Elsevier,
2012, pp. 446–58, doi:10.1016/j.devcel.2011.11.021.
short: M.A. D’Angelo, J.S. Gomez-Cavazos, A. Mei, D.H. Lackner, M. Hetzer, Developmental
Cell 22 (2012) 446–458.
date_created: 2022-04-07T07:52:10Z
date_published: 2012-01-19T00:00:00Z
date_updated: 2022-07-18T08:53:16Z
day: '19'
doi: 10.1016/j.devcel.2011.11.021
extern: '1'
external_id:
pmid:
- '22264802'
intvolume: ' 22'
issue: '2'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.devcel.2011.11.021
month: '01'
oa: 1
oa_version: Published Version
page: 446-458
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A change in nuclear pore complex composition regulates cell differentiation
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 22
year: '2012'
...