---
_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: '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: '9532'
abstract:
- lang: eng
text: Genomic imprinting, an inherently epigenetic phenomenon defined by parent
of origin-dependent gene expression, is observed in mammals and flowering plants.
Genome-scale surveys of imprinted expression and the underlying differential epigenetic
marks have led to the discovery of hundreds of imprinted plant genes and confirmed
DNA and histone methylation as key regulators of plant imprinting. However, the
biological roles of the vast majority of imprinted plant genes are unknown, and
the evolutionary forces shaping plant imprinting remain rather opaque. Here, we
review the mechanisms of plant genomic imprinting and discuss theories of imprinting
evolution and biological significance in light of recent findings.
article_processing_charge: No
article_type: review
author:
- first_name: Jessica A.
full_name: Rodrigues, Jessica A.
last_name: Rodrigues
- first_name: Daniel
full_name: Zilberman, Daniel
id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1
last_name: Zilberman
orcid: 0000-0002-0123-8649
citation:
ama: Rodrigues JA, Zilberman D. Evolution and function of genomic imprinting in
plants. Genes and Development. 2015;29(24):2517–2531. doi:10.1101/gad.269902.115
apa: Rodrigues, J. A., & Zilberman, D. (2015). Evolution and function of genomic
imprinting in plants. Genes and Development. Cold Spring Harbor Laboratory
Press. https://doi.org/10.1101/gad.269902.115
chicago: Rodrigues, Jessica A., and Daniel Zilberman. “Evolution and Function of
Genomic Imprinting in Plants.” Genes and Development. Cold Spring Harbor
Laboratory Press, 2015. https://doi.org/10.1101/gad.269902.115.
ieee: J. A. Rodrigues and D. Zilberman, “Evolution and function of genomic imprinting
in plants,” Genes and Development, vol. 29, no. 24. Cold Spring Harbor
Laboratory Press, pp. 2517–2531, 2015.
ista: Rodrigues JA, Zilberman D. 2015. Evolution and function of genomic imprinting
in plants. Genes and Development. 29(24), 2517–2531.
mla: Rodrigues, Jessica A., and Daniel Zilberman. “Evolution and Function of Genomic
Imprinting in Plants.” Genes and Development, vol. 29, no. 24, Cold Spring
Harbor Laboratory Press, 2015, pp. 2517–2531, doi:10.1101/gad.269902.115.
short: J.A. Rodrigues, D. Zilberman, Genes and Development 29 (2015) 2517–2531.
date_created: 2021-06-08T09:56:24Z
date_published: 2015-12-15T00:00:00Z
date_updated: 2021-12-14T07:58:15Z
day: '15'
ddc:
- '570'
department:
- _id: DaZi
doi: 10.1101/gad.269902.115
extern: '1'
external_id:
pmid:
- '26680300'
file:
- access_level: open_access
checksum: 086a88cfca4677646da26ed960cb02e9
content_type: application/pdf
creator: asandaue
date_created: 2021-06-08T09:55:10Z
date_updated: 2021-06-08T09:55:10Z
file_id: '9533'
file_name: 2015_GenesAndDevelopment_Rodrigues.pdf
file_size: 1116846
relation: main_file
success: 1
file_date_updated: 2021-06-08T09:55:10Z
has_accepted_license: '1'
intvolume: ' 29'
issue: '24'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 2517–2531
pmid: 1
publication: Genes and Development
publication_identifier:
eissn:
- 1549-5477
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolution and function of genomic imprinting in plants
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
volume: 29
year: '2015'
...
---
_id: '2866'
abstract:
- lang: eng
text: 'Developmental responses to the plant hormone auxin are thought to be mediated
by interacting pairs from two protein families: short-lived inhibitory IAA proteins
and ARF transcription factors binding to auxin-response elements. Monopteros mutants
lacking activating ARF5 and the auxin-insensitive mutant bodenlos fail to initiate
the root meristem during early embryogenesis. Here we show that the bodenlos phenotype
results from an amino-acid exchange in the conserved degradation domain of IAA12.
BODENLOS and MONOPTEROS interact in the yeast two-hybrid assay and the two genes
are coexpressed in early embryogenesis, suggesting that BODENLOS inhibits MONOPTEROS
action in root meristem initiation.'
acknowledgement: "We thank C. Maulbetsch for isolating BDL cDNA clones; T. Berleth
and J. Friml for providing clones for in situ probes; K. Harter for making available
the parsley protoplast system; and J. Friml, N. Geldner, M. Griffith, C. Schwechheimer,
D. Weigel, and D. Weijers for helpful comments and critical reading of the manuscript.
This work was supported by Sonderforschungsbereich 446 “Mechanismen des Zellverhaltens
bei Eukaryoten.”\r\n\r\nThe publication costs of this article were defrayed in part
by payment of page charges. This article must therefore be hereby marked “advertisement”
in accordance with 18 USC section 1734 solely to indicate this fact."
article_processing_charge: No
article_type: original
author:
- first_name: Thorsten
full_name: Hamann, Thorsten
last_name: Hamann
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Isabel
full_name: Bäurle, Isabel
last_name: Bäurle
- first_name: Marika
full_name: Kientz, Marika
last_name: Kientz
- first_name: Gerd
full_name: Jürgens, Gerd
last_name: Jürgens
citation:
ama: Hamann T, Benková E, Bäurle I, Kientz M, Jürgens G. The Arabidopsis BODENLOS
gene encodes an auxin response protein inhibiting MONOPTEROS-mediated embryo patterning.
Genes and Development. 2002;16(13):1610-1615. doi:10.1101/gad.229402
apa: Hamann, T., Benková, E., Bäurle, I., Kientz, M., & Jürgens, G. (2002).
The Arabidopsis BODENLOS gene encodes an auxin response protein inhibiting MONOPTEROS-mediated
embryo patterning. Genes and Development. Cold Spring Harbor Laboratory
Press. https://doi.org/10.1101/gad.229402
chicago: Hamann, Thorsten, Eva Benková, Isabel Bäurle, Marika Kientz, and Gerd Jürgens.
“The Arabidopsis BODENLOS Gene Encodes an Auxin Response Protein Inhibiting MONOPTEROS-Mediated
Embryo Patterning.” Genes and Development. Cold Spring Harbor Laboratory
Press, 2002. https://doi.org/10.1101/gad.229402.
ieee: T. Hamann, E. Benková, I. Bäurle, M. Kientz, and G. Jürgens, “The Arabidopsis
BODENLOS gene encodes an auxin response protein inhibiting MONOPTEROS-mediated
embryo patterning,” Genes and Development, vol. 16, no. 13. Cold Spring
Harbor Laboratory Press, pp. 1610–1615, 2002.
ista: Hamann T, Benková E, Bäurle I, Kientz M, Jürgens G. 2002. The Arabidopsis
BODENLOS gene encodes an auxin response protein inhibiting MONOPTEROS-mediated
embryo patterning. Genes and Development. 16(13), 1610–1615.
mla: Hamann, Thorsten, et al. “The Arabidopsis BODENLOS Gene Encodes an Auxin Response
Protein Inhibiting MONOPTEROS-Mediated Embryo Patterning.” Genes and Development,
vol. 16, no. 13, Cold Spring Harbor Laboratory Press, 2002, pp. 1610–15, doi:10.1101/gad.229402.
short: T. Hamann, E. Benková, I. Bäurle, M. Kientz, G. Jürgens, Genes and Development
16 (2002) 1610–1615.
date_created: 2018-12-11T12:00:01Z
date_published: 2002-07-01T00:00:00Z
date_updated: 2023-07-18T08:26:58Z
day: '01'
doi: 10.1101/gad.229402
extern: '1'
external_id:
pmid:
- '12101120'
intvolume: ' 16'
issue: '13'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC186366/
month: '07'
oa: 1
oa_version: Published Version
page: 1610 - 1615
pmid: 1
publication: Genes and Development
publication_identifier:
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory Press
publist_id: '3921'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Arabidopsis BODENLOS gene encodes an auxin response protein inhibiting
MONOPTEROS-mediated embryo patterning
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 16
year: '2002'
...
---
_id: '2982'
abstract:
- lang: eng
text: Polar auxin transport is crucial for the regulation of auxin action and required
for some light-regulated responses during plant development. We have found that
two mutants of Arabidopsis - doc1, which displays altered expression of light-regulated
genes, and tir3, known for its reduced auxin transport - have similar defects
and define mutations in a single gene that we have renamed BIG. BIG is very similar
to the Drosophila gene Calossin/Pushover, a member of a gene family also present
in Caenorhabditis elegans and human genomes. The protein encoded by BIG is extraordinary
in size, 560 kD, and contains several putative Zn-finger domains. Expression-profiling
experiments indicate that altered expression of multiple light-regulated genes
in doc1 mutants can be suppressed by elevated levels of auxin caused by overexpression
of an auxin biosynthetic gene, suggesting that normal auxin distribution is required
to maintain low-level expression of these genes in the dark. Double mutants of
tir3 with the auxin mutants pin1, pid, and axr1 display severe defects in auxin-dependent
growth of the inflorescence. Chemical inhibitors of auxin transport change the
intracellular localization of the auxin efflux carrier PIN1 in doc1/tir3 mutants,
supporting the idea that BIG is required for normal auxin efflux.
acknowledgement: "We thank Kim Hanson and Melissa McCarthy for technical support,
and Adan Colon-Carmona, Jianming Li, and Karin Schumacher for their help in generating
and identifying the doc1-3 T-DNA line. Seeds of ap3-1 and a cosmid library were
supplied by the ABRC stock center. Jennifer Nemhauser made useful comments concerning
this manuscript. This work was supported by grants from the Department of Energy
(DE-FG03-89ER13993) and the National Science Foundation (MCB96-31390) to J.C., by
grants from the Department of Energy (DE-FG02-98ER20313) and the National Institutes
of Health (GM43644) to M.E., by a grant from DAAD to J.F., by a grant from DFG to
K.P., and by a Marsden grant of New Zealand to J.P. and K.S. J.C. is an Associate
Investigator of the Howard Hughes Medical Institute (HHMI), and Y.Z. is a HHMI fellow
of the Life Sciences Research Foundation.\r\n\r\nThe publication costs of this article
were defrayed in part by payment of page charges. This article must therefore be
hereby marked “advertisement” in accordance with 18 USC section 1734 solely to indicate
this fact."
article_processing_charge: No
article_type: original
author:
- first_name: Pedro
full_name: Gil, Pedro
last_name: Gil
- first_name: Elizabeth
full_name: Dewey, Elizabeth
last_name: Dewey
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Yunde
full_name: Zhao, Yunde
last_name: Zhao
- first_name: Kimberley
full_name: Snowden, Kimberley
last_name: Snowden
- first_name: Jo
full_name: Putterill, Jo
last_name: Putterill
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
- first_name: Mark
full_name: Estelle, Mark
last_name: Estelle
- first_name: Joanne
full_name: Chory, Joanne
last_name: Chory
citation:
ama: 'Gil P, Dewey E, Friml J, et al. BIG: A calossin-like protein required for
polar auxin transport in Arabidopsis. Genes and Development. 2001;15(15):1985-1997.
doi:10.1101/gad.905201'
apa: 'Gil, P., Dewey, E., Friml, J., Zhao, Y., Snowden, K., Putterill, J., … Chory,
J. (2001). BIG: A calossin-like protein required for polar auxin transport in
Arabidopsis. Genes and Development. Cold Spring Harbor Laboratory Press.
https://doi.org/10.1101/gad.905201'
chicago: 'Gil, Pedro, Elizabeth Dewey, Jiří Friml, Yunde Zhao, Kimberley Snowden,
Jo Putterill, Klaus Palme, Mark Estelle, and Joanne Chory. “BIG: A Calossin-like
Protein Required for Polar Auxin Transport in Arabidopsis.” Genes and Development.
Cold Spring Harbor Laboratory Press, 2001. https://doi.org/10.1101/gad.905201.'
ieee: 'P. Gil et al., “BIG: A calossin-like protein required for polar auxin
transport in Arabidopsis,” Genes and Development, vol. 15, no. 15. Cold
Spring Harbor Laboratory Press, pp. 1985–1997, 2001.'
ista: 'Gil P, Dewey E, Friml J, Zhao Y, Snowden K, Putterill J, Palme K, Estelle
M, Chory J. 2001. BIG: A calossin-like protein required for polar auxin transport
in Arabidopsis. Genes and Development. 15(15), 1985–1997.'
mla: 'Gil, Pedro, et al. “BIG: A Calossin-like Protein Required for Polar Auxin
Transport in Arabidopsis.” Genes and Development, vol. 15, no. 15, Cold
Spring Harbor Laboratory Press, 2001, pp. 1985–97, doi:10.1101/gad.905201.'
short: P. Gil, E. Dewey, J. Friml, Y. Zhao, K. Snowden, J. Putterill, K. Palme,
M. Estelle, J. Chory, Genes and Development 15 (2001) 1985–1997.
date_created: 2018-12-11T12:00:41Z
date_published: 2001-08-01T00:00:00Z
date_updated: 2023-05-16T11:59:47Z
day: '01'
doi: 10.1101/gad.905201
extern: '1'
external_id:
pmid:
- '11485992'
intvolume: ' 15'
issue: '15'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC312751/
month: '08'
oa: 1
oa_version: Published Version
page: 1985 - 1997
pmid: 1
publication: Genes and Development
publication_identifier:
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory Press
publist_id: '3720'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'BIG: A calossin-like protein required for polar auxin transport in Arabidopsis'
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 15
year: '2001'
...
---
_id: '4200'
abstract:
- lang: eng
text: Zebrafish embryos homozygous for the masterblind (mb1) mutation exhibit a
striking phenotype in which the eyes and telencephalon are reduced or absent and
diencephalic fates expand to the front of the brain. Here we show that mb1(-/-)
embryos carry an amino-acid change at a conserved site in the Wnt pathway scaffolding
protein, Axin1. The amino-acid substitution present in the mbl allele abolishes
the binding of Axin to Gsk3 and affects Tcf-dependent transcription. Therefore,
Gsk3 activity may be decreased in mbl(-/-) embryos and in support of this possibility,
overexpression of either wild-type Axin1 or Gsk3 beta can restore eye and telencephalic
fates to mb1(-/-) embryos. Our data reveal a crucial role for Axin1-dependent
inhibition of the Wnt pathway in the early regional subdivision of the anterior
neural plate into telencephalic, diencephalic, and eye-forming territories.
acknowledgement: "We thank many colleagues who provided reagents that enabled us to
test axin1 and several other genes as candidates for the mbl mutation. In particular,
we are indebted to Masahiko Hibi, Ken Irvine, Antonio Jacinto, Yun-Jin Jiang, Julian
Lewis, and Tom Vogt for help and advice. We thank Ajay Chitnis and Dana Zivkovic
for providing information prior to publication. This study was supported primarily
by grants from the EMBO and EC to C.P.H., Wellcome Trust and EC to S.W.W., from
the MRC to D.S., from Naito to M.T., from the DHGP to G.J.R. and R.G., and from
the CRC/ICR to T.D. P.C. was supported by a PhD studentship from Fundação para a
Ciência e Tecnologia, Programa PRAXIS XXI. S.W.W. is a Wellcome Trust Senior Research
Fellow.\r\n\r\nThe publication costs of this article were defrayed in part by payment
of page charges. This article must therefore be hereby marked “advertisement” in
accordance with 18 USC section 1734 solely to indicate this fact."
article_processing_charge: No
article_type: original
author:
- 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: Corinne
full_name: Houart, Corinne
last_name: Houart
- first_name: Masaya
full_name: Take Uchi, Masaya
last_name: Take Uchi
- first_name: Gerd
full_name: Rauch, Gerd
last_name: Rauch
- first_name: Neville
full_name: Young, Neville
last_name: Young
- first_name: Pedro
full_name: Coutinho, Pedro
last_name: Coutinho
- first_name: Ichiro
full_name: Masai, Ichiro
last_name: Masai
- first_name: Luca
full_name: Caneparo, Luca
last_name: Caneparo
- first_name: Miguel
full_name: Concha, Miguel
last_name: Concha
- first_name: Robert
full_name: Geisler, Robert
last_name: Geisler
- first_name: Trevor
full_name: Dale, Trevor
last_name: Dale
- first_name: Stephen
full_name: Wilson, Stephen
last_name: Wilson
- first_name: Derek
full_name: Stemple, Derek
last_name: Stemple
citation:
ama: Heisenberg C-PJ, Houart C, Take Uchi M, et al. A mutation in the Gsk3-binding
domain of zebrafish Masterblind/Axin1 leads to a fate transformation of telencephalon
and eyes to diencephalon. Genes and Development. 2001;15(11):1427-1434.
doi:10.1101/gad.194301
apa: Heisenberg, C.-P. J., Houart, C., Take Uchi, M., Rauch, G., Young, N., Coutinho,
P., … Stemple, D. (2001). A mutation in the Gsk3-binding domain of zebrafish Masterblind/Axin1
leads to a fate transformation of telencephalon and eyes to diencephalon. Genes
and Development. Cold Spring Harbor Laboratory Press. https://doi.org/10.1101/gad.194301
chicago: Heisenberg, Carl-Philipp J, Corinne Houart, Masaya Take Uchi, Gerd Rauch,
Neville Young, Pedro Coutinho, Ichiro Masai, et al. “A Mutation in the Gsk3-Binding
Domain of Zebrafish Masterblind/Axin1 Leads to a Fate Transformation of Telencephalon
and Eyes to Diencephalon.” Genes and Development. Cold Spring Harbor Laboratory
Press, 2001. https://doi.org/10.1101/gad.194301.
ieee: C.-P. J. Heisenberg et al., “A mutation in the Gsk3-binding domain
of zebrafish Masterblind/Axin1 leads to a fate transformation of telencephalon
and eyes to diencephalon,” Genes and Development, vol. 15, no. 11. Cold
Spring Harbor Laboratory Press, pp. 1427–1434, 2001.
ista: Heisenberg C-PJ, Houart C, Take Uchi M, Rauch G, Young N, Coutinho P, Masai
I, Caneparo L, Concha M, Geisler R, Dale T, Wilson S, Stemple D. 2001. A mutation
in the Gsk3-binding domain of zebrafish Masterblind/Axin1 leads to a fate transformation
of telencephalon and eyes to diencephalon. Genes and Development. 15(11), 1427–1434.
mla: Heisenberg, Carl-Philipp J., et al. “A Mutation in the Gsk3-Binding Domain
of Zebrafish Masterblind/Axin1 Leads to a Fate Transformation of Telencephalon
and Eyes to Diencephalon.” Genes and Development, vol. 15, no. 11, Cold
Spring Harbor Laboratory Press, 2001, pp. 1427–34, doi:10.1101/gad.194301.
short: C.-P.J. Heisenberg, C. Houart, M. Take Uchi, G. Rauch, N. Young, P. Coutinho,
I. Masai, L. Caneparo, M. Concha, R. Geisler, T. Dale, S. Wilson, D. Stemple,
Genes and Development 15 (2001) 1427–1434.
date_created: 2018-12-11T12:07:33Z
date_published: 2001-06-01T00:00:00Z
date_updated: 2023-05-10T12:27:02Z
day: '01'
doi: 10.1101/gad.194301
extern: '1'
external_id:
pmid:
- '11390362'
intvolume: ' 15'
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC312705/
month: '06'
oa: 1
oa_version: Published Version
page: 1427 - 1434
pmid: 1
publication: Genes and Development
publication_identifier:
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory Press
publist_id: '1916'
quality_controlled: '1'
status: public
title: A mutation in the Gsk3-binding domain of zebrafish Masterblind/Axin1 leads
to a fate transformation of telencephalon and eyes to diencephalon
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 15
year: '2001'
...
---
_id: '2535'
abstract:
- lang: eng
text: We report the molecular characterization of two novel rat helix-loop-helix
(HLH) proteins, designated HES-1 and HES-3, that show structural homology to the
Drosophila hairy and Enhancer of split [E(spl)] proteins, both of which are required
for normal neurogenesis. HES-1 mRNA, expressed in various tissues of both embryos
and adults, is present at a high level in the epithelial cells, including the
embryonal neuroepithelial cells, as well as in the mesoderm-derived tissues such
as the embryonal muscle. In contrast, HES-3 mRNA is produced exclusively in cerebellar
Purkinje cells. HES-1 represses transcription by binding to the N box, which is
a recognition sequence of E(spl) proteins. Interestingly, neither HES-1 nor HES-3
alone interacts efficiently with the E box, but each protein decreases the transcription
induced by E-box-binding HLH activators such as E47. Furthermore, HES-1 also inhibits
the functions of MyoD and MASH1 and effectively diminishes the myogenic conversion
of C3H10T1/2 cells induced by MyoD. These results suggest that HES-1 may play
an important role in mammalian development by negatively acting on the two different
sequences while HES-3 acts as a repressor in a specific type of neurons.
acknowledgement: "We thank Professor Noboru Mizuno for his kind help with in situ
hybridization experiments, Akira Uesugi and Dr. Chihiro\r\nAkazawa for photographic
assistance, Drs. Elizabeth Knust and Jose A. Campos-Ortega for communicating their
unpublished results, Dr. Shinji Fushiki for useful discussion, Dr. Mikio Nishizawa
and Professor Shigekazu Nagata for pMNT, Dr. David Baltimore for the E47 expression
vector, Drs. Yoichiro Nabeshima and Atsuko Fujisawa for the MyoD expression vector
and the reporter plasmid with the MCK enhancer, and Dr. Makoto Ishibashi for his
help in isolating the human E47 eDNA clone. This work was supported in part by research
grants from the Ministry of Education, Science, and Culture of Japan. The publication
costs of this article were defrayed in part by payment of page charges. This article
must therefore be hereby marked \"advertisement\" in accordance with 18 USC section
1734 solely to indicate this fact. \r\n"
article_processing_charge: No
article_type: original
author:
- first_name: Yoshiki
full_name: Sasai, Yoshiki
last_name: Sasai
- first_name: Ryoichiro
full_name: Kageyama, Ryoichiro
last_name: Kageyama
- first_name: Yoshiaki
full_name: Tagawa, Yoshiaki
last_name: Tagawa
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Shigetada
full_name: Nakanishi, Shigetada
last_name: Nakanishi
citation:
ama: Sasai Y, Kageyama R, Tagawa Y, Shigemoto R, Nakanishi S. Two mammalian helix-loop-helix
factors structurally related to Drosophila hairy and Enhancer of split. Genes
and Development. 1992;6(12 B):2620-2634. doi:10.1101/gad.6.12b.2620
apa: Sasai, Y., Kageyama, R., Tagawa, Y., Shigemoto, R., & Nakanishi, S. (1992).
Two mammalian helix-loop-helix factors structurally related to Drosophila hairy
and Enhancer of split. Genes and Development. Cold Spring Harbor Laboratory
Press. https://doi.org/10.1101/gad.6.12b.2620
chicago: Sasai, Yoshiki, Ryoichiro Kageyama, Yoshiaki Tagawa, Ryuichi Shigemoto,
and Shigetada Nakanishi. “Two Mammalian Helix-Loop-Helix Factors Structurally
Related to Drosophila Hairy and Enhancer of Split.” Genes and Development.
Cold Spring Harbor Laboratory Press, 1992. https://doi.org/10.1101/gad.6.12b.2620.
ieee: Y. Sasai, R. Kageyama, Y. Tagawa, R. Shigemoto, and S. Nakanishi, “Two mammalian
helix-loop-helix factors structurally related to Drosophila hairy and Enhancer
of split,” Genes and Development, vol. 6, no. 12 B. Cold Spring Harbor
Laboratory Press, pp. 2620–2634, 1992.
ista: Sasai Y, Kageyama R, Tagawa Y, Shigemoto R, Nakanishi S. 1992. Two mammalian
helix-loop-helix factors structurally related to Drosophila hairy and Enhancer
of split. Genes and Development. 6(12 B), 2620–2634.
mla: Sasai, Yoshiki, et al. “Two Mammalian Helix-Loop-Helix Factors Structurally
Related to Drosophila Hairy and Enhancer of Split.” Genes and Development,
vol. 6, no. 12 B, Cold Spring Harbor Laboratory Press, 1992, pp. 2620–34, doi:10.1101/gad.6.12b.2620.
short: Y. Sasai, R. Kageyama, Y. Tagawa, R. Shigemoto, S. Nakanishi, Genes and Development
6 (1992) 2620–2634.
date_created: 2018-12-11T11:58:15Z
date_published: 1992-01-01T00:00:00Z
date_updated: 2022-03-17T14:52:29Z
day: '01'
doi: 10.1101/gad.6.12b.2620
extern: '1'
external_id:
pmid:
- '1340473'
intvolume: ' 6'
issue: 12 B
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://genesdev.cshlp.org/content/6/12b/2620
month: '01'
oa: 1
oa_version: Published Version
page: 2620 - 2634
pmid: 1
publication: Genes and Development
publication_identifier:
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory Press
publist_id: '4364'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Two mammalian helix-loop-helix factors structurally related to Drosophila hairy
and Enhancer of split
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 6
year: '1992'
...