---
_id: '12189'
abstract:
- lang: eng
text: Meiotic crossovers (COs) are important for reshuffling genetic information
between homologous chromosomes and they are essential for their correct segregation.
COs are unevenly distributed along chromosomes and the underlying mechanisms controlling
CO localization are not well understood. We previously showed that meiotic COs
are mis-localized in the absence of AXR1, an enzyme involved in the neddylation/rubylation
protein modification pathway in Arabidopsis thaliana. Here, we report that in
axr1-/-, male meiocytes show a strong defect in chromosome pairing whereas the
formation of the telomere bouquet is not affected. COs are also redistributed
towards subtelomeric chromosomal ends where they frequently form clusters, in
contrast to large central regions depleted in recombination. The CO suppressed
regions correlate with DNA hypermethylation of transposable elements (TEs) in
the CHH context in axr1-/- meiocytes. Through examining somatic methylomes, we
found axr1-/- affects DNA methylation in a plant, causing hypermethylation in
all sequence contexts (CG, CHG and CHH) in TEs. Impairment of the main pathways
involved in DNA methylation is epistatic over axr1-/- for DNA methylation in somatic
cells but does not restore regular chromosome segregation during meiosis. Collectively,
our findings reveal that the neddylation pathway not only regulates hormonal perception
and CO distribution but is also, directly or indirectly, a major limiting pathway
of TE DNA methylation in somatic cells.
acknowledgement: The authors wish to thank Cécile Raynaud, Eric Jenczewski, Rajeev
Kumar, Raphaël Mercier and Jean Molinier for critical reading of the manuscript.
article_number: e1008894
article_processing_charge: No
article_type: original
author:
- first_name: Nicolas
full_name: Christophorou, Nicolas
last_name: Christophorou
- first_name: Wenjing
full_name: She, Wenjing
last_name: She
- first_name: Jincheng
full_name: Long, Jincheng
last_name: Long
- first_name: Aurélie
full_name: Hurel, Aurélie
last_name: Hurel
- first_name: Sébastien
full_name: Beaubiat, Sébastien
last_name: Beaubiat
- first_name: Yassir
full_name: Idir, Yassir
last_name: Idir
- first_name: Marina
full_name: Tagliaro-Jahns, Marina
last_name: Tagliaro-Jahns
- first_name: Aurélie
full_name: Chambon, Aurélie
last_name: Chambon
- first_name: Victor
full_name: Solier, Victor
last_name: Solier
- first_name: Daniel
full_name: Vezon, Daniel
last_name: Vezon
- first_name: Mathilde
full_name: Grelon, Mathilde
last_name: Grelon
- first_name: Xiaoqi
full_name: Feng, Xiaoqi
id: e0164712-22ee-11ed-b12a-d80fcdf35958
last_name: Feng
orcid: 0000-0002-4008-1234
- first_name: Nicolas
full_name: Bouché, Nicolas
last_name: Bouché
- first_name: Christine
full_name: Mézard, Christine
last_name: Mézard
citation:
ama: Christophorou N, She W, Long J, et al. AXR1 affects DNA methylation independently
of its role in regulating meiotic crossover localization. PLOS Genetics.
2020;16(6). doi:10.1371/journal.pgen.1008894
apa: Christophorou, N., She, W., Long, J., Hurel, A., Beaubiat, S., Idir, Y., …
Mézard, C. (2020). AXR1 affects DNA methylation independently of its role in regulating
meiotic crossover localization. PLOS Genetics. Public Library of Science
(PLoS). https://doi.org/10.1371/journal.pgen.1008894
chicago: Christophorou, Nicolas, Wenjing She, Jincheng Long, Aurélie Hurel, Sébastien
Beaubiat, Yassir Idir, Marina Tagliaro-Jahns, et al. “AXR1 Affects DNA Methylation
Independently of Its Role in Regulating Meiotic Crossover Localization.” PLOS
Genetics. Public Library of Science (PLoS), 2020. https://doi.org/10.1371/journal.pgen.1008894.
ieee: N. Christophorou et al., “AXR1 affects DNA methylation independently
of its role in regulating meiotic crossover localization,” PLOS Genetics,
vol. 16, no. 6. Public Library of Science (PLoS), 2020.
ista: Christophorou N, She W, Long J, Hurel A, Beaubiat S, Idir Y, Tagliaro-Jahns
M, Chambon A, Solier V, Vezon D, Grelon M, Feng X, Bouché N, Mézard C. 2020. AXR1
affects DNA methylation independently of its role in regulating meiotic crossover
localization. PLOS Genetics. 16(6), e1008894.
mla: Christophorou, Nicolas, et al. “AXR1 Affects DNA Methylation Independently
of Its Role in Regulating Meiotic Crossover Localization.” PLOS Genetics,
vol. 16, no. 6, e1008894, Public Library of Science (PLoS), 2020, doi:10.1371/journal.pgen.1008894.
short: N. Christophorou, W. She, J. Long, A. Hurel, S. Beaubiat, Y. Idir, M. Tagliaro-Jahns,
A. Chambon, V. Solier, D. Vezon, M. Grelon, X. Feng, N. Bouché, C. Mézard, PLOS
Genetics 16 (2020).
date_created: 2023-01-16T09:16:10Z
date_published: 2020-06-29T00:00:00Z
date_updated: 2023-05-08T10:54:39Z
day: '29'
department:
- _id: XiFe
doi: 10.1371/journal.pgen.1008894
extern: '1'
external_id:
pmid:
- '32598340'
intvolume: ' 16'
issue: '6'
keyword:
- Cancer Research
- Genetics (clinical)
- Genetics
- Molecular Biology
- Ecology
- Evolution
- Behavior and Systematics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7351236/
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLOS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science (PLoS)
quality_controlled: '1'
scopus_import: '1'
status: public
title: AXR1 affects DNA methylation independently of its role in regulating meiotic
crossover localization
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2020'
...
---
_id: '7399'
abstract:
- lang: eng
text: Long non-coding (lnc) RNAs are numerous and found throughout the mammalian
genome, and many are thought to be involved in the regulation of gene expression.
However, the majority remain relatively uncharacterised and of uncertain function
making the use of model systems to uncover their mode of action valuable. Imprinted
lncRNAs target and recruit epigenetic silencing factors to a cluster of imprinted
genes on the same chromosome, making them one of the best characterized lncRNAs
for silencing distant genes in cis. In this study we examined silencing of the
distant imprinted gene Slc22a3 by the lncRNA Airn in the Igf2r imprinted cluster
in mouse. Previously we proposed that imprinted lncRNAs may silence distant imprinted
genes by disrupting promoter-enhancer interactions by being transcribed through
the enhancer, which we called the enhancer interference hypothesis. Here we tested
this hypothesis by first using allele-specific chromosome conformation capture
(3C) to detect interactions between the Slc22a3 promoter and the locus of the
Airn lncRNA that silences it on the paternal chromosome. In agreement with the
model, we found interactions enriched on the maternal allele across the entire
Airn gene consistent with multiple enhancer-promoter interactions. Therefore,
to test the enhancer interference hypothesis we devised an approach to delete
the entire Airn gene. However, the deletion showed that there are no essential
enhancers for Slc22a2, Pde10a and Slc22a3 within the Airn gene, strongly indicating
that the Airn RNA rather than its transcription is responsible for silencing distant
imprinted genes. Furthermore, we found that silent imprinted genes were covered
with large blocks of H3K27me3 on the repressed paternal allele. Therefore we propose
an alternative hypothesis whereby the chromosome interactions may initially guide
the lncRNA to target imprinted promoters and recruit repressive chromatin, and
that these interactions are lost once silencing is established.
article_number: e1008268
article_processing_charge: No
article_type: original
author:
- first_name: Daniel
full_name: Andergassen, Daniel
last_name: Andergassen
- first_name: Markus
full_name: Muckenhuber, Markus
last_name: Muckenhuber
- first_name: Philipp C.
full_name: Bammer, Philipp C.
last_name: Bammer
- first_name: Tomasz M.
full_name: Kulinski, Tomasz M.
last_name: Kulinski
- first_name: Hans-Christian
full_name: Theussl, Hans-Christian
last_name: Theussl
- first_name: Takahiko
full_name: Shimizu, Takahiko
last_name: Shimizu
- first_name: Josef M.
full_name: Penninger, Josef M.
last_name: Penninger
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Quanah J.
full_name: Hudson, Quanah J.
last_name: Hudson
citation:
ama: Andergassen D, Muckenhuber M, Bammer PC, et al. The Airn lncRNA does not require
any DNA elements within its locus to silence distant imprinted genes. PLoS
Genetics. 2019;15(7). doi:10.1371/journal.pgen.1008268
apa: Andergassen, D., Muckenhuber, M., Bammer, P. C., Kulinski, T. M., Theussl,
H.-C., Shimizu, T., … Hudson, Q. J. (2019). The Airn lncRNA does not require any
DNA elements within its locus to silence distant imprinted genes. PLoS Genetics.
Public Library of Science. https://doi.org/10.1371/journal.pgen.1008268
chicago: Andergassen, Daniel, Markus Muckenhuber, Philipp C. Bammer, Tomasz M. Kulinski,
Hans-Christian Theussl, Takahiko Shimizu, Josef M. Penninger, Florian Pauler,
and Quanah J. Hudson. “The Airn LncRNA Does Not Require Any DNA Elements within
Its Locus to Silence Distant Imprinted Genes.” PLoS Genetics. Public Library
of Science, 2019. https://doi.org/10.1371/journal.pgen.1008268.
ieee: D. Andergassen et al., “The Airn lncRNA does not require any DNA elements
within its locus to silence distant imprinted genes,” PLoS Genetics, vol.
15, no. 7. Public Library of Science, 2019.
ista: Andergassen D, Muckenhuber M, Bammer PC, Kulinski TM, Theussl H-C, Shimizu
T, Penninger JM, Pauler F, Hudson QJ. 2019. The Airn lncRNA does not require any
DNA elements within its locus to silence distant imprinted genes. PLoS Genetics.
15(7), e1008268.
mla: Andergassen, Daniel, et al. “The Airn LncRNA Does Not Require Any DNA Elements
within Its Locus to Silence Distant Imprinted Genes.” PLoS Genetics, vol.
15, no. 7, e1008268, Public Library of Science, 2019, doi:10.1371/journal.pgen.1008268.
short: D. Andergassen, M. Muckenhuber, P.C. Bammer, T.M. Kulinski, H.-C. Theussl,
T. Shimizu, J.M. Penninger, F. Pauler, Q.J. Hudson, PLoS Genetics 15 (2019).
date_created: 2020-01-29T16:14:07Z
date_published: 2019-07-22T00:00:00Z
date_updated: 2023-10-17T12:30:27Z
day: '22'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1371/journal.pgen.1008268
external_id:
isi:
- '000478689100025'
pmid:
- '31329595'
file:
- access_level: open_access
checksum: 2f51fc91e4a4199827adc51d432ad864
content_type: application/pdf
creator: dernst
date_created: 2020-02-04T10:11:55Z
date_updated: 2020-07-14T12:47:57Z
file_id: '7446'
file_name: 2019_PlosGenetics_Andergassen.pdf
file_size: 2302307
relation: main_file
file_date_updated: 2020-07-14T12:47:57Z
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
issue: '7'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Airn lncRNA does not require any DNA elements within its locus to silence
distant imprinted genes
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: 15
year: '2019'
...
---
_id: '5998'
abstract:
- lang: eng
text: Genome amplification and cellular senescence are commonly associated with
pathological processes. While physiological roles for polyploidization and senescence
have been described in mouse development, controversy exists over their significance
in humans. Here, we describe tetraploidization and senescence as phenomena of
normal human placenta development. During pregnancy, placental extravillous trophoblasts
(EVTs) invade the pregnant endometrium, termed decidua, to establish an adapted
microenvironment required for the developing embryo. This process is critically
dependent on continuous cell proliferation and differentiation, which is thought
to follow the classical model of cell cycle arrest prior to terminal differentiation.
Strikingly, flow cytometry and DNAseq revealed that EVT formation is accompanied
with a genome-wide polyploidization, independent of mitotic cycles. DNA replication
in these cells was analysed by a fluorescent cell-cycle indicator reporter system,
cell cycle marker expression and EdU incorporation. Upon invasion into the decidua,
EVTs widely lose their replicative potential and enter a senescent state characterized
by high senescence-associated (SA) β-galactosidase activity, induction of a SA
secretory phenotype as well as typical metabolic alterations. Furthermore, we
show that the shift from endocycle-dependent genome amplification to growth arrest
is disturbed in androgenic complete hydatidiform moles (CHM), a hyperplastic pregnancy
disorder associated with increased risk of developing choriocarinoma. Senescence
is decreased in CHM-EVTs, accompanied by exacerbated endoreduplication and hyperploidy.
We propose induction of cellular senescence as a ploidy-limiting mechanism during
normal human placentation and unravel a link between excessive polyploidization
and reduced senescence in CHM.
article_number: e1007698
article_processing_charge: No
author:
- first_name: Philipp
full_name: Velicky, Philipp
id: 39BDC62C-F248-11E8-B48F-1D18A9856A87
last_name: Velicky
orcid: 0000-0002-2340-7431
- first_name: Gudrun
full_name: Meinhardt, Gudrun
last_name: Meinhardt
- first_name: Kerstin
full_name: Plessl, Kerstin
last_name: Plessl
- first_name: Sigrid
full_name: Vondra, Sigrid
last_name: Vondra
- first_name: Tamara
full_name: Weiss, Tamara
last_name: Weiss
- first_name: Peter
full_name: Haslinger, Peter
last_name: Haslinger
- first_name: Thomas
full_name: Lendl, Thomas
last_name: Lendl
- first_name: Karin
full_name: Aumayr, Karin
last_name: Aumayr
- first_name: Mario
full_name: Mairhofer, Mario
last_name: Mairhofer
- first_name: Xiaowei
full_name: Zhu, Xiaowei
last_name: Zhu
- first_name: Birgit
full_name: Schütz, Birgit
last_name: Schütz
- first_name: Roberta L.
full_name: Hannibal, Roberta L.
last_name: Hannibal
- first_name: Robert
full_name: Lindau, Robert
last_name: Lindau
- first_name: Beatrix
full_name: Weil, Beatrix
last_name: Weil
- first_name: Jan
full_name: Ernerudh, Jan
last_name: Ernerudh
- first_name: Jürgen
full_name: Neesen, Jürgen
last_name: Neesen
- first_name: Gerda
full_name: Egger, Gerda
last_name: Egger
- first_name: Mario
full_name: Mikula, Mario
last_name: Mikula
- first_name: Clemens
full_name: Röhrl, Clemens
last_name: Röhrl
- first_name: Alexander E.
full_name: Urban, Alexander E.
last_name: Urban
- first_name: Julie
full_name: Baker, Julie
last_name: Baker
- first_name: Martin
full_name: Knöfler, Martin
last_name: Knöfler
- first_name: Jürgen
full_name: Pollheimer, Jürgen
last_name: Pollheimer
citation:
ama: Velicky P, Meinhardt G, Plessl K, et al. Genome amplification and cellular
senescence are hallmarks of human placenta development. PLOS Genetics.
2018;14(10). doi:10.1371/journal.pgen.1007698
apa: Velicky, P., Meinhardt, G., Plessl, K., Vondra, S., Weiss, T., Haslinger, P.,
… Pollheimer, J. (2018). Genome amplification and cellular senescence are hallmarks
of human placenta development. PLOS Genetics. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1007698
chicago: Velicky, Philipp, Gudrun Meinhardt, Kerstin Plessl, Sigrid Vondra, Tamara
Weiss, Peter Haslinger, Thomas Lendl, et al. “Genome Amplification and Cellular
Senescence Are Hallmarks of Human Placenta Development.” PLOS Genetics.
Public Library of Science, 2018. https://doi.org/10.1371/journal.pgen.1007698.
ieee: P. Velicky et al., “Genome amplification and cellular senescence are
hallmarks of human placenta development,” PLOS Genetics, vol. 14, no. 10.
Public Library of Science, 2018.
ista: Velicky P, Meinhardt G, Plessl K, Vondra S, Weiss T, Haslinger P, Lendl T,
Aumayr K, Mairhofer M, Zhu X, Schütz B, Hannibal RL, Lindau R, Weil B, Ernerudh
J, Neesen J, Egger G, Mikula M, Röhrl C, Urban AE, Baker J, Knöfler M, Pollheimer
J. 2018. Genome amplification and cellular senescence are hallmarks of human placenta
development. PLOS Genetics. 14(10), e1007698.
mla: Velicky, Philipp, et al. “Genome Amplification and Cellular Senescence Are
Hallmarks of Human Placenta Development.” PLOS Genetics, vol. 14, no. 10,
e1007698, Public Library of Science, 2018, doi:10.1371/journal.pgen.1007698.
short: P. Velicky, G. Meinhardt, K. Plessl, S. Vondra, T. Weiss, P. Haslinger, T.
Lendl, K. Aumayr, M. Mairhofer, X. Zhu, B. Schütz, R.L. Hannibal, R. Lindau, B.
Weil, J. Ernerudh, J. Neesen, G. Egger, M. Mikula, C. Röhrl, A.E. Urban, J. Baker,
M. Knöfler, J. Pollheimer, PLOS Genetics 14 (2018).
date_created: 2019-02-14T13:07:45Z
date_published: 2018-10-12T00:00:00Z
date_updated: 2023-09-19T14:31:43Z
day: '12'
ddc:
- '570'
department:
- _id: JoDa
doi: 10.1371/journal.pgen.1007698
external_id:
isi:
- '000449328500025'
file:
- access_level: open_access
checksum: 34aa9a5972f61889c19f18be8ee787a0
content_type: application/pdf
creator: kschuh
date_created: 2019-02-14T13:14:35Z
date_updated: 2020-07-14T12:47:15Z
file_id: '6000'
file_name: 2018_PLOS_Velicky.pdf
file_size: 4592947
relation: main_file
file_date_updated: 2020-07-14T12:47:15Z
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
issue: '10'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
publication: PLOS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Genome amplification and cellular senescence are hallmarks of human placenta
development
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 14
year: '2018'
...
---
_id: '6111'
abstract:
- lang: eng
text: 'Neurons develop elaborate morphologies that provide a model for understanding
cellular architecture. By studying C. elegans sensory dendrites, we previously
identified genes that act to promote the extension of ciliated sensory dendrites
during embryogenesis. Interestingly, the nonciliated dendrite of the oxygen-sensing
neuron URX is not affected by these genes, suggesting it develops through a distinct
mechanism. Here, we use a visual forward genetic screen to identify mutants that
affect URX dendrite morphogenesis. We find that disruption of the MAP kinase MAPK-15
or the βH-spectrin SMA-1 causes a phenotype opposite to what we had seen before:
dendrites extend normally during embryogenesis but begin to overgrow as the animals
reach adulthood, ultimately extending up to 150% of their normal length. SMA-1
is broadly expressed and acts non-cell-autonomously, while MAPK-15 is expressed
in many sensory neurons including URX and acts cell-autonomously. MAPK-15 acts
at the time of overgrowth, localizes at the dendrite ending, and requires its
kinase activity, suggesting it acts locally in time and space to constrain dendrite
growth. Finally, we find that the oxygen-sensing guanylate cyclase GCY-35, which
normally localizes at the dendrite ending, is localized throughout the overgrown
region, and that overgrowth can be suppressed by overexpressing GCY-35 or by genetically
mimicking elevated cGMP signaling. These results suggest that overgrowth may correspond
to expansion of a sensory compartment at the dendrite ending, reminiscent of the
remodeling of sensory cilia or dendritic spines. Thus, in contrast to established
pathways that promote dendrite growth during early development, our results reveal
a distinct mechanism that constrains dendrite growth throughout the life of the
animal, possibly by controlling the size of a sensory compartment at the dendrite
ending.'
article_number: e1007435
author:
- first_name: Ian G.
full_name: McLachlan, Ian G.
last_name: McLachlan
- first_name: Isabel
full_name: Beets, Isabel
last_name: Beets
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
- first_name: Maxwell G.
full_name: Heiman, Maxwell G.
last_name: Heiman
citation:
ama: McLachlan IG, Beets I, de Bono M, Heiman MG. A neuronal MAP kinase constrains
growth of a Caenorhabditis elegans sensory dendrite throughout the life of the
organism. PLOS Genetics. 2018;14(6). doi:10.1371/journal.pgen.1007435
apa: McLachlan, I. G., Beets, I., de Bono, M., & Heiman, M. G. (2018). A neuronal
MAP kinase constrains growth of a Caenorhabditis elegans sensory dendrite throughout
the life of the organism. PLOS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007435
chicago: McLachlan, Ian G., Isabel Beets, Mario de Bono, and Maxwell G. Heiman.
“A Neuronal MAP Kinase Constrains Growth of a Caenorhabditis Elegans Sensory Dendrite
throughout the Life of the Organism.” PLOS Genetics. Public Library of
Science, 2018. https://doi.org/10.1371/journal.pgen.1007435.
ieee: I. G. McLachlan, I. Beets, M. de Bono, and M. G. Heiman, “A neuronal MAP kinase
constrains growth of a Caenorhabditis elegans sensory dendrite throughout the
life of the organism,” PLOS Genetics, vol. 14, no. 6. Public Library of
Science, 2018.
ista: McLachlan IG, Beets I, de Bono M, Heiman MG. 2018. A neuronal MAP kinase constrains
growth of a Caenorhabditis elegans sensory dendrite throughout the life of the
organism. PLOS Genetics. 14(6), e1007435.
mla: McLachlan, Ian G., et al. “A Neuronal MAP Kinase Constrains Growth of a Caenorhabditis
Elegans Sensory Dendrite throughout the Life of the Organism.” PLOS Genetics,
vol. 14, no. 6, e1007435, Public Library of Science, 2018, doi:10.1371/journal.pgen.1007435.
short: I.G. McLachlan, I. Beets, M. de Bono, M.G. Heiman, PLOS Genetics 14 (2018).
date_created: 2019-03-19T13:09:28Z
date_published: 2018-06-07T00:00:00Z
date_updated: 2021-01-12T08:06:11Z
day: '07'
ddc:
- '570'
doi: 10.1371/journal.pgen.1007435
extern: '1'
external_id:
pmid:
- '29879119'
file:
- access_level: open_access
checksum: 622036b945365dbc575bea2768aa9bc8
content_type: application/pdf
creator: kschuh
date_created: 2019-03-19T13:18:01Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6112'
file_name: 2018_PLOS_McLachlan.pdf
file_size: 13011506
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 14'
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLOS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
status: public
title: A neuronal MAP kinase constrains growth of a Caenorhabditis elegans sensory
dendrite throughout the life of the organism
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2018'
...
---
_id: '7599'
abstract:
- lang: eng
text: Normal leaf margin development is important for leaf morphogenesis and contributes
to diverse leaf shapes in higher plants. We here show the crucial roles of an
atypical type II phosphatidylinositol 4-kinase, PI4Kγ5, in Arabidopsis leaf margin
development. PI4Kγ5 presents a dynamics expression pattern along with leaf development
and a T-DNA mutant lacking PI4Kγ5, pi4kγ5–1, presents serrated leaves, which is
resulted from the accelerated cell division and increased auxin concentration
at serration tips. Studies revealed that PI4Kγ5 interacts with and phosphorylates
a membrane-bound NAC transcription factor, ANAC078. Previous studies demonstrated
that membrane-bound transcription factors regulate gene transcription by undergoing
proteolytic process to translocate into nucleus, and ANAC078 undergoes proteolysis
by cleaving off the transmembrane region and carboxyl terminal. Western blot analysis
indeed showed that ANAC078 deleting of carboxyl terminal is significantly reduced
in pi4kγ5–1, indicating that PI4Kγ5 is important for the cleavage of ANAC078.
This is consistent with the subcellular localization observation showing that
fluorescence by GFP-ANAC078 is detected at plasma membrane but not nucleus in
pi4kγ5–1 mutant and that expression of ANAC078 deleting of carboxyl terminal,
driven by PI4Kγ5 promoter, could rescue the leaf serration defects of pi4kγ5–1.
Further analysis showed that ANAC078 suppresses the auxin synthesis by directly
binding and regulating the expression of auxin synthesis-related genes. These
results indicate that PI4Kγ5 interacts with ANAC078 to negatively regulate auxin
synthesis and hence influences cell proliferation and leaf development, providing
informative clues for the regulation of in situ auxin synthesis and cell division,
as well as the cleavage and functional mechanism of membrane-bound transcription
factors.
article_number: e1006252
article_processing_charge: No
article_type: original
author:
- first_name: Yong
full_name: Tang, Yong
last_name: Tang
- first_name: Chun-Yan
full_name: Zhao, Chun-Yan
last_name: Zhao
- first_name: Shutang
full_name: Tan, Shutang
id: 2DE75584-F248-11E8-B48F-1D18A9856A87
last_name: Tan
orcid: 0000-0002-0471-8285
- first_name: Hong-Wei
full_name: Xue, Hong-Wei
last_name: Xue
citation:
ama: Tang Y, Zhao C-Y, Tan S, Xue H-W. Arabidopsis type II phosphatidylinositol
4-kinase PI4Kγ5 regulates auxin biosynthesis and leaf margin development through
interacting with membrane-bound transcription factor ANAC078. PLOS Genetics.
2016;12(8). doi:10.1371/journal.pgen.1006252
apa: Tang, Y., Zhao, C.-Y., Tan, S., & Xue, H.-W. (2016). Arabidopsis type II
phosphatidylinositol 4-kinase PI4Kγ5 regulates auxin biosynthesis and leaf margin
development through interacting with membrane-bound transcription factor ANAC078.
PLOS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1006252
chicago: Tang, Yong, Chun-Yan Zhao, Shutang Tan, and Hong-Wei Xue. “Arabidopsis
Type II Phosphatidylinositol 4-Kinase PI4Kγ5 Regulates Auxin Biosynthesis and
Leaf Margin Development through Interacting with Membrane-Bound Transcription
Factor ANAC078.” PLOS Genetics. Public Library of Science, 2016. https://doi.org/10.1371/journal.pgen.1006252.
ieee: Y. Tang, C.-Y. Zhao, S. Tan, and H.-W. Xue, “Arabidopsis type II phosphatidylinositol
4-kinase PI4Kγ5 regulates auxin biosynthesis and leaf margin development through
interacting with membrane-bound transcription factor ANAC078,” PLOS Genetics,
vol. 12, no. 8. Public Library of Science, 2016.
ista: Tang Y, Zhao C-Y, Tan S, Xue H-W. 2016. Arabidopsis type II phosphatidylinositol
4-kinase PI4Kγ5 regulates auxin biosynthesis and leaf margin development through
interacting with membrane-bound transcription factor ANAC078. PLOS Genetics. 12(8),
e1006252.
mla: Tang, Yong, et al. “Arabidopsis Type II Phosphatidylinositol 4-Kinase PI4Kγ5
Regulates Auxin Biosynthesis and Leaf Margin Development through Interacting with
Membrane-Bound Transcription Factor ANAC078.” PLOS Genetics, vol. 12, no.
8, e1006252, Public Library of Science, 2016, doi:10.1371/journal.pgen.1006252.
short: Y. Tang, C.-Y. Zhao, S. Tan, H.-W. Xue, PLOS Genetics 12 (2016).
date_created: 2020-03-21T16:08:33Z
date_published: 2016-08-16T00:00:00Z
date_updated: 2021-01-12T08:14:25Z
day: '16'
ddc:
- '580'
doi: 10.1371/journal.pgen.1006252
extern: '1'
file:
- access_level: open_access
checksum: ff0ab9a6bed11cda800a6e59820866a0
content_type: application/pdf
creator: dernst
date_created: 2020-03-23T12:15:31Z
date_updated: 2020-07-14T12:48:01Z
file_id: '7612'
file_name: 2016_PlosGenetics_Tang.PDF
file_size: 3266119
relation: main_file
file_date_updated: 2020-07-14T12:48:01Z
has_accepted_license: '1'
intvolume: ' 12'
issue: '8'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
publication: PLOS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
status: public
title: Arabidopsis type II phosphatidylinositol 4-kinase PI4Kγ5 regulates auxin biosynthesis
and leaf margin development through interacting with membrane-bound transcription
factor ANAC078
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: 12
year: '2016'
...
---
_id: '6124'
abstract:
- lang: eng
text: Despite the importance of G-protein coupled receptors (GPCRs) their biogenesis
is poorly understood. Like vertebrates, C. elegans uses a large family of GPCRs
as chemoreceptors. A subset of these receptors, such as ODR-10, requires the odr-4
and odr-8 genes to be appropriately localized to sensory cilia. The odr-4 gene
encodes a conserved tail-anchored transmembrane protein; the molecular identity
of odr-8 is unknown. Here, we show that odr-8 encodes the C. elegans ortholog
of Ufm1-specific protease 2 (UfSP2). UfSPs are cysteine proteases identified biochemically
by their ability to liberate the ubiquitin-like modifier Ufm1 from its pro-form
and protein conjugates. ODR-8/UfSP2 and ODR-4 are expressed in the same set of
twelve chemosensory neurons, and physically interact at the ER membrane. ODR-4
also binds ODR-10, suggesting that an ODR-4/ODR-8 complex promotes GPCR folding,
maturation, or export from the ER. The physical interaction between human ODR4
and UfSP2 suggests that this complex's role in GPCR biogenesis may be evolutionarily
conserved. Unexpectedly, mutant versions of ODR-8/UfSP2 lacking catalytic residues
required for protease activity can rescue all odr-8 mutant phenotypes tested.
Moreover, deleting C. elegans ufm-1 does not alter chemoreceptor traffic to cilia,
either in wild type or in odr-8 mutants. Thus, UfSP2 proteins have protease- and
Ufm1-independent functions in GPCR biogenesis.
article_number: e1004082
author:
- first_name: Changchun
full_name: Chen, Changchun
last_name: Chen
- first_name: Eisuke
full_name: Itakura, Eisuke
last_name: Itakura
- first_name: Katherine P.
full_name: Weber, Katherine P.
last_name: Weber
- first_name: Ramanujan S.
full_name: Hegde, Ramanujan S.
last_name: Hegde
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: Chen C, Itakura E, Weber KP, Hegde RS, de Bono M. An ER complex of ODR-4 and
ODR-8/Ufm1 specific protease 2 promotes GPCR maturation by a Ufm1-independent
mechanism. PLoS Genetics. 2014;10(3). doi:10.1371/journal.pgen.1004082
apa: Chen, C., Itakura, E., Weber, K. P., Hegde, R. S., & de Bono, M. (2014).
An ER complex of ODR-4 and ODR-8/Ufm1 specific protease 2 promotes GPCR maturation
by a Ufm1-independent mechanism. PLoS Genetics. Public Library of Science
(PLoS). https://doi.org/10.1371/journal.pgen.1004082
chicago: Chen, Changchun, Eisuke Itakura, Katherine P. Weber, Ramanujan S. Hegde,
and Mario de Bono. “An ER Complex of ODR-4 and ODR-8/Ufm1 Specific Protease 2
Promotes GPCR Maturation by a Ufm1-Independent Mechanism.” PLoS Genetics.
Public Library of Science (PLoS), 2014. https://doi.org/10.1371/journal.pgen.1004082.
ieee: C. Chen, E. Itakura, K. P. Weber, R. S. Hegde, and M. de Bono, “An ER complex
of ODR-4 and ODR-8/Ufm1 specific protease 2 promotes GPCR maturation by a Ufm1-independent
mechanism,” PLoS Genetics, vol. 10, no. 3. Public Library of Science (PLoS),
2014.
ista: Chen C, Itakura E, Weber KP, Hegde RS, de Bono M. 2014. An ER complex of ODR-4
and ODR-8/Ufm1 specific protease 2 promotes GPCR maturation by a Ufm1-independent
mechanism. PLoS Genetics. 10(3), e1004082.
mla: Chen, Changchun, et al. “An ER Complex of ODR-4 and ODR-8/Ufm1 Specific Protease
2 Promotes GPCR Maturation by a Ufm1-Independent Mechanism.” PLoS Genetics,
vol. 10, no. 3, e1004082, Public Library of Science (PLoS), 2014, doi:10.1371/journal.pgen.1004082.
short: C. Chen, E. Itakura, K.P. Weber, R.S. Hegde, M. de Bono, PLoS Genetics 10
(2014).
date_created: 2019-03-19T14:45:56Z
date_published: 2014-03-06T00:00:00Z
date_updated: 2021-01-12T08:06:14Z
day: '06'
ddc:
- '570'
doi: 10.1371/journal.pgen.1004082
extern: '1'
external_id:
pmid:
- '24603482'
file:
- access_level: open_access
checksum: ac19941089a4262bb5bd74434a08b003
content_type: application/pdf
creator: kschuh
date_created: 2019-03-19T14:50:07Z
date_updated: 2020-07-14T12:47:20Z
file_id: '6125'
file_name: 2014_PLOS_Chen.PDF
file_size: 8286819
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 10'
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science (PLoS)
quality_controlled: '1'
status: public
title: An ER complex of ODR-4 and ODR-8/Ufm1 specific protease 2 promotes GPCR maturation
by a Ufm1-independent mechanism
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2014'
...
---
_id: '11086'
abstract:
- lang: eng
text: Faithful execution of developmental gene expression programs occurs at multiple
levels and involves many different components such as transcription factors, histone-modification
enzymes, and mRNA processing proteins. Recent evidence suggests that nucleoporins,
well known components that control nucleo-cytoplasmic trafficking, have wide-ranging
functions in developmental gene regulation that potentially extend beyond their
role in nuclear transport. Whether the unexpected role of nuclear pore proteins
in transcription regulation, which initially has been described in fungi and flies,
also applies to human cells is unknown. Here we show at a genome-wide level that
the nuclear pore protein NUP98 associates with developmentally regulated genes
active during human embryonic stem cell differentiation. Overexpression of a dominant
negative fragment of NUP98 levels decreases expression levels of NUP98-bound genes.
In addition, we identify two modes of developmental gene regulation by NUP98 that
are differentiated by the spatial localization of NUP98 target genes. Genes in
the initial stage of developmental induction can associate with NUP98 that is
embedded in the nuclear pores at the nuclear periphery. Alternatively, genes that
are highly induced can interact with NUP98 in the nuclear interior, away from
the nuclear pores. This work demonstrates for the first time that NUP98 dynamically
associates with the human genome during differentiation, revealing a role of a
nuclear pore protein in regulating developmental gene expression programs.
article_number: e1003308
article_processing_charge: No
article_type: original
author:
- first_name: Yun
full_name: Liang, Yun
last_name: Liang
- first_name: Tobias M.
full_name: Franks, Tobias M.
last_name: Franks
- first_name: Maria C.
full_name: Marchetto, Maria C.
last_name: Marchetto
- 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: Liang Y, Franks TM, Marchetto MC, Gage FH, Hetzer M. Dynamic association of
NUP98 with the human genome. PLoS Genetics. 2013;9(2). doi:10.1371/journal.pgen.1003308
apa: Liang, Y., Franks, T. M., Marchetto, M. C., Gage, F. H., & Hetzer, M. (2013).
Dynamic association of NUP98 with the human genome. PLoS Genetics. Public
Library of Science. https://doi.org/10.1371/journal.pgen.1003308
chicago: Liang, Yun, Tobias M. Franks, Maria C. Marchetto, Fred H. Gage, and Martin
Hetzer. “Dynamic Association of NUP98 with the Human Genome.” PLoS Genetics.
Public Library of Science, 2013. https://doi.org/10.1371/journal.pgen.1003308.
ieee: Y. Liang, T. M. Franks, M. C. Marchetto, F. H. Gage, and M. Hetzer, “Dynamic
association of NUP98 with the human genome,” PLoS Genetics, vol. 9, no.
2. Public Library of Science, 2013.
ista: Liang Y, Franks TM, Marchetto MC, Gage FH, Hetzer M. 2013. Dynamic association
of NUP98 with the human genome. PLoS Genetics. 9(2), e1003308.
mla: Liang, Yun, et al. “Dynamic Association of NUP98 with the Human Genome.” PLoS
Genetics, vol. 9, no. 2, e1003308, Public Library of Science, 2013, doi:10.1371/journal.pgen.1003308.
short: Y. Liang, T.M. Franks, M.C. Marchetto, F.H. Gage, M. Hetzer, PLoS Genetics
9 (2013).
date_created: 2022-04-07T07:50:59Z
date_published: 2013-02-28T00:00:00Z
date_updated: 2022-07-18T08:45:58Z
day: '28'
doi: 10.1371/journal.pgen.1003308
extern: '1'
external_id:
pmid:
- '23468646'
intvolume: ' 9'
issue: '2'
keyword:
- Cancer Research
- Genetics (clinical)
- Genetics
- Molecular Biology
- Ecology
- Evolution
- Behavior and Systematics
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1371/journal.pgen.1003308
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dynamic association of NUP98 with the human genome
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 9
year: '2013'
...
---
_id: '6128'
abstract:
- lang: eng
text: Different interoceptive systems must be integrated to ensure that multiple
homeostatic insults evoke appropriate behavioral and physiological responses.
Little is known about how this is achieved. Using C. elegans, we dissect cross-modulation
between systems that monitor temperature, O2 and CO2. CO2 is less aversive to
animals acclimated to 15°C than those grown at 22°C. This difference requires
the AFD neurons, which respond to both temperature and CO2 changes. CO2 evokes
distinct AFD Ca2+ responses in animals acclimated at 15°C or 22°C. Mutants defective
in synaptic transmission can reprogram AFD CO2 responses according to temperature
experience, suggesting reprogramming occurs cell autonomously. AFD is exquisitely
sensitive to CO2. Surprisingly, gradients of 0.01% CO2/second evoke very different
Ca2+ responses from gradients of 0.04% CO2/second. Ambient O2 provides further
contextual modulation of CO2 avoidance. At 21% O2 tonic signalling from the O2-sensing
neuron URX inhibits CO2 avoidance. This inhibition can be graded according to
O2 levels. In a natural wild isolate, a switch from 21% to 19% O2 is sufficient
to convert CO2 from a neutral to an aversive cue. This sharp tuning is conferred
partly by the neuroglobin GLB-5. The modulatory effects of O2 on CO2 avoidance
involve the RIA interneurons, which are post-synaptic to URX and exhibit CO2-evoked
Ca2+ responses. Ambient O2 and acclimation temperature act combinatorially to
modulate CO2 responsiveness. Our work highlights the integrated architecture of
homeostatic responses in C. elegans.
article_number: e1004011
author:
- first_name: Eiji
full_name: Kodama-Namba, Eiji
last_name: Kodama-Namba
- first_name: Lorenz A.
full_name: Fenk, Lorenz A.
last_name: Fenk
- first_name: Andrew J.
full_name: Bretscher, Andrew J.
last_name: Bretscher
- first_name: Einav
full_name: Gross, Einav
last_name: Gross
- first_name: K. Emanuel
full_name: Busch, K. Emanuel
last_name: Busch
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: Kodama-Namba E, Fenk LA, Bretscher AJ, Gross E, Busch KE, de Bono M. Cross-modulation
of homeostatic responses to temperature, oxygen and carbon dioxide in C. elegans.
PLoS Genetics. 2013;9(12). doi:10.1371/journal.pgen.1004011
apa: Kodama-Namba, E., Fenk, L. A., Bretscher, A. J., Gross, E., Busch, K. E., &
de Bono, M. (2013). Cross-modulation of homeostatic responses to temperature,
oxygen and carbon dioxide in C. elegans. PLoS Genetics. Public Library
of Science (PLoS). https://doi.org/10.1371/journal.pgen.1004011
chicago: Kodama-Namba, Eiji, Lorenz A. Fenk, Andrew J. Bretscher, Einav Gross, K.
Emanuel Busch, and Mario de Bono. “Cross-Modulation of Homeostatic Responses to
Temperature, Oxygen and Carbon Dioxide in C. Elegans.” PLoS Genetics. Public
Library of Science (PLoS), 2013. https://doi.org/10.1371/journal.pgen.1004011.
ieee: E. Kodama-Namba, L. A. Fenk, A. J. Bretscher, E. Gross, K. E. Busch, and M.
de Bono, “Cross-modulation of homeostatic responses to temperature, oxygen and
carbon dioxide in C. elegans,” PLoS Genetics, vol. 9, no. 12. Public Library
of Science (PLoS), 2013.
ista: Kodama-Namba E, Fenk LA, Bretscher AJ, Gross E, Busch KE, de Bono M. 2013.
Cross-modulation of homeostatic responses to temperature, oxygen and carbon dioxide
in C. elegans. PLoS Genetics. 9(12), e1004011.
mla: Kodama-Namba, Eiji, et al. “Cross-Modulation of Homeostatic Responses to Temperature,
Oxygen and Carbon Dioxide in C. Elegans.” PLoS Genetics, vol. 9, no. 12,
e1004011, Public Library of Science (PLoS), 2013, doi:10.1371/journal.pgen.1004011.
short: E. Kodama-Namba, L.A. Fenk, A.J. Bretscher, E. Gross, K.E. Busch, M. de Bono,
PLoS Genetics 9 (2013).
date_created: 2019-03-19T14:58:51Z
date_published: 2013-12-19T00:00:00Z
date_updated: 2021-01-12T08:06:15Z
day: '19'
ddc:
- '570'
doi: 10.1371/journal.pgen.1004011
extern: '1'
external_id:
pmid:
- '24385919'
file:
- access_level: open_access
checksum: 299b6321be79931c7c17c5db6e69c711
content_type: application/pdf
creator: kschuh
date_created: 2019-03-19T15:14:51Z
date_updated: 2020-07-14T12:47:20Z
file_id: '6129'
file_name: 2013_PLOS_Kodama-Namba.PDF
file_size: 4499039
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science (PLoS)
quality_controlled: '1'
status: public
title: Cross-modulation of homeostatic responses to temperature, oxygen and carbon
dioxide in C. elegans
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2013'
...
---
_id: '6140'
abstract:
- lang: eng
text: 'Genome sequence comparisons have highlighted many novel gene families that
are conserved across animal phyla but whose biological function is unknown. Here,
we functionally characterize a member of one such family, the macoilins. Macoilins
are characterized by several highly conserved predicted transmembrane domains
towards the N-terminus and by coiled-coil regions C-terminally. They are found
throughout Eumetazoa but not in other organisms. Mutants for the single Caenorhabditis
elegans macoilin, maco-1, exhibit a constellation of behavioral phenotypes, including
defects in aggregation, O2 responses, and swimming. MACO-1 protein is expressed
broadly and specifically in the nervous system and localizes to the rough endoplasmic
reticulum; it is excluded from dendrites and axons. Apart from subtle synapse
defects, nervous system development appears wild-type in maco-1 mutants. However,
maco-1 animals are resistant to the cholinesterase inhibitor aldicarb and sensitive
to levamisole, suggesting pre-synaptic defects. Using in vivo imaging, we show
that macoilin is required to evoke Ca2+ transients, at least in some neurons:
in maco-1 mutants the O2-sensing neuron PQR is unable to generate a Ca2+ response
to a rise in O2. By genetically disrupting neurotransmission, we show that pre-synaptic
input is not necessary for PQR to respond to O2, indicating that the response
is mediated by cell-intrinsic sensory transduction and amplification. Disrupting
the sodium leak channels NCA-1/NCA-2, or the N-,P/Q,R-type voltage-gated Ca2+
channels, also fails to disrupt Ca2+ responses in the PQR cell body to O2 stimuli.
By contrast, mutations in egl-19, which encodes the only Caenorhabditis elegans
L-type voltage-gated Ca2+ channel α1 subunit, recapitulate the Ca2+ response defect
we see in maco-1 mutants, although we do not see defects in localization of EGL-19.
Together, our data suggest that macoilin acts in the ER to regulate assembly or
traffic of ion channels or ion channel regulators.'
article_number: e1001341
author:
- first_name: Fausto
full_name: Arellano-Carbajal, Fausto
last_name: Arellano-Carbajal
- first_name: Luis
full_name: Briseño-Roa, Luis
last_name: Briseño-Roa
- first_name: Africa
full_name: Couto, Africa
last_name: Couto
- first_name: Benny H. H.
full_name: Cheung, Benny H. H.
last_name: Cheung
- first_name: Michel
full_name: Labouesse, Michel
last_name: Labouesse
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: Arellano-Carbajal F, Briseño-Roa L, Couto A, Cheung BHH, Labouesse M, de Bono
M. Macoilin, a conserved nervous system–specific ER membrane protein that regulates
neuronal excitability. PLoS Genetics. 2011;7(3). doi:10.1371/journal.pgen.1001341
apa: Arellano-Carbajal, F., Briseño-Roa, L., Couto, A., Cheung, B. H. H., Labouesse,
M., & de Bono, M. (2011). Macoilin, a conserved nervous system–specific ER
membrane protein that regulates neuronal excitability. PLoS Genetics. Public
Library of Science. https://doi.org/10.1371/journal.pgen.1001341
chicago: Arellano-Carbajal, Fausto, Luis Briseño-Roa, Africa Couto, Benny H. H.
Cheung, Michel Labouesse, and Mario de Bono. “Macoilin, a Conserved Nervous System–Specific
ER Membrane Protein That Regulates Neuronal Excitability.” PLoS Genetics.
Public Library of Science, 2011. https://doi.org/10.1371/journal.pgen.1001341.
ieee: F. Arellano-Carbajal, L. Briseño-Roa, A. Couto, B. H. H. Cheung, M. Labouesse,
and M. de Bono, “Macoilin, a conserved nervous system–specific ER membrane protein
that regulates neuronal excitability,” PLoS Genetics, vol. 7, no. 3. Public
Library of Science, 2011.
ista: Arellano-Carbajal F, Briseño-Roa L, Couto A, Cheung BHH, Labouesse M, de Bono
M. 2011. Macoilin, a conserved nervous system–specific ER membrane protein that
regulates neuronal excitability. PLoS Genetics. 7(3), e1001341.
mla: Arellano-Carbajal, Fausto, et al. “Macoilin, a Conserved Nervous System–Specific
ER Membrane Protein That Regulates Neuronal Excitability.” PLoS Genetics,
vol. 7, no. 3, e1001341, Public Library of Science, 2011, doi:10.1371/journal.pgen.1001341.
short: F. Arellano-Carbajal, L. Briseño-Roa, A. Couto, B.H.H. Cheung, M. Labouesse,
M. de Bono, PLoS Genetics 7 (2011).
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title: Macoilin, a conserved nervous system–specific ER membrane protein that regulates
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