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LATEST PUBLICATIONS
2014
Samarut, Eric; Gaudin, Cyril; Hughes, Sandrine; Gillet, Benjamin; Bernard, Simon; Jouve, Pierre-Emmanuel; Buffat, Laurent; Allot, Alexis; Lecompte, Odile; Berekelya, Liubov; Rochette-Egly, Cécile; Laudet, Vincent
Retinoic acid receptor subtype-specific transcriptotypes in the early zebrafish embryo Journal Article
In: Mol. Endocrinol., vol. 28, no. 2, pp. 260–272, 2014.
@article{Samarut2014-my,
title = {Retinoic acid receptor subtype-specific transcriptotypes in the early zebrafish embryo},
author = {Eric Samarut and Cyril Gaudin and Sandrine Hughes and Benjamin Gillet and Simon Bernard and Pierre-Emmanuel Jouve and Laurent Buffat and Alexis Allot and Odile Lecompte and Liubov Berekelya and Cécile Rochette-Egly and Vincent Laudet},
doi = {10.1210/me.2013-1358},
year = {2014},
date = {2014-02-01},
urldate = {2014-02-01},
journal = {Mol. Endocrinol.},
volume = {28},
number = {2},
pages = {260--272},
publisher = {The Endocrine Society},
abstract = {Retinoic acid (RA) controls many aspects of embryonic
development by binding to specific receptors (retinoic acid
receptors [RARs]) that regulate complex transcriptional
networks. Three different RAR subtypes are present in
vertebrates and play both common and specific roles in
transducing RA signaling. Specific activities of each receptor
subtype can be correlated with its exclusive expression pattern,
whereas shared activities between different subtypes are
generally assimilated to functional redundancy. However, the
question remains whether some subtype-specific activity still
exists in regions or organs coexpressing multiple RAR subtypes.
We tackled this issue at the transcriptional level using early
zebrafish embryo as a model. Using morpholino knockdown, we
specifically invalidated the zebrafish endogenous RAR subtypes
in an in vivo context. After building up a list of RA-responsive
genes in the zebrafish gastrula through a whole-transcriptome
analysis, we compared this panel of genes with those that still
respond to RA in embryos lacking one or another RAR subtype. Our
work reveals that RAR subtypes do not have fully redundant
functions at the transcriptional level but can transduce RA
signal in a subtype-specific fashion. As a result, we define RAR
subtype-specific transcriptotypes that correspond to repertoires
of genes activated by different RAR subtypes. Finally, we found
genes of the RA pathway (cyp26a1, raraa) the regulation of which
by RA is highly robust and can even resist the knockdown of all
RARs. This suggests that RA-responsive genes are differentially
sensitive to alterations in the RA pathway and, in particular,
cyp26a1 and raraa are under a high pressure to maintain
signaling integrity.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Retinoic acid (RA) controls many aspects of embryonic
development by binding to specific receptors (retinoic acid
receptors [RARs]) that regulate complex transcriptional
networks. Three different RAR subtypes are present in
vertebrates and play both common and specific roles in
transducing RA signaling. Specific activities of each receptor
subtype can be correlated with its exclusive expression pattern,
whereas shared activities between different subtypes are
generally assimilated to functional redundancy. However, the
question remains whether some subtype-specific activity still
exists in regions or organs coexpressing multiple RAR subtypes.
We tackled this issue at the transcriptional level using early
zebrafish embryo as a model. Using morpholino knockdown, we
specifically invalidated the zebrafish endogenous RAR subtypes
in an in vivo context. After building up a list of RA-responsive
genes in the zebrafish gastrula through a whole-transcriptome
analysis, we compared this panel of genes with those that still
respond to RA in embryos lacking one or another RAR subtype. Our
work reveals that RAR subtypes do not have fully redundant
functions at the transcriptional level but can transduce RA
signal in a subtype-specific fashion. As a result, we define RAR
subtype-specific transcriptotypes that correspond to repertoires
of genes activated by different RAR subtypes. Finally, we found
genes of the RA pathway (cyp26a1, raraa) the regulation of which
by RA is highly robust and can even resist the knockdown of all
RARs. This suggests that RA-responsive genes are differentially
sensitive to alterations in the RA pathway and, in particular,
cyp26a1 and raraa are under a high pressure to maintain
signaling integrity.
development by binding to specific receptors (retinoic acid
receptors [RARs]) that regulate complex transcriptional
networks. Three different RAR subtypes are present in
vertebrates and play both common and specific roles in
transducing RA signaling. Specific activities of each receptor
subtype can be correlated with its exclusive expression pattern,
whereas shared activities between different subtypes are
generally assimilated to functional redundancy. However, the
question remains whether some subtype-specific activity still
exists in regions or organs coexpressing multiple RAR subtypes.
We tackled this issue at the transcriptional level using early
zebrafish embryo as a model. Using morpholino knockdown, we
specifically invalidated the zebrafish endogenous RAR subtypes
in an in vivo context. After building up a list of RA-responsive
genes in the zebrafish gastrula through a whole-transcriptome
analysis, we compared this panel of genes with those that still
respond to RA in embryos lacking one or another RAR subtype. Our
work reveals that RAR subtypes do not have fully redundant
functions at the transcriptional level but can transduce RA
signal in a subtype-specific fashion. As a result, we define RAR
subtype-specific transcriptotypes that correspond to repertoires
of genes activated by different RAR subtypes. Finally, we found
genes of the RA pathway (cyp26a1, raraa) the regulation of which
by RA is highly robust and can even resist the knockdown of all
RARs. This suggests that RA-responsive genes are differentially
sensitive to alterations in the RA pathway and, in particular,
cyp26a1 and raraa are under a high pressure to maintain
signaling integrity.
Samarut, Eric; Gaudin, Cyril; Hughes, Sandrine; Gillet, Benjamin; de Bernard, Simon; Jouve, Pierre-Emmanuel; Buffat, Laurent; Allot, Alexis; Lecompte, Odile; Berekelya, Liubov; Rochette-Egly, Cécile; Laudet, Vincent
Retinoic acid receptor subtype-specific transcriptotypes in the early zebrafish embryo Journal Article
In: Mol Endocrinol, vol. 28, no. 2, pp. 260–272, 2014, ISSN: 1944-9917.
@article{pmid24422634,
title = {Retinoic acid receptor subtype-specific transcriptotypes in the early zebrafish embryo},
author = {Eric Samarut and Cyril Gaudin and Sandrine Hughes and Benjamin Gillet and Simon de Bernard and Pierre-Emmanuel Jouve and Laurent Buffat and Alexis Allot and Odile Lecompte and Liubov Berekelya and Cécile Rochette-Egly and Vincent Laudet},
doi = {10.1210/me.2013-1358},
issn = {1944-9917},
year = {2014},
date = {2014-02-01},
urldate = {2014-02-01},
journal = {Mol Endocrinol},
volume = {28},
number = {2},
pages = {260--272},
abstract = {Retinoic acid (RA) controls many aspects of embryonic development by binding to specific receptors (retinoic acid receptors [RARs]) that regulate complex transcriptional networks. Three different RAR subtypes are present in vertebrates and play both common and specific roles in transducing RA signaling. Specific activities of each receptor subtype can be correlated with its exclusive expression pattern, whereas shared activities between different subtypes are generally assimilated to functional redundancy. However, the question remains whether some subtype-specific activity still exists in regions or organs coexpressing multiple RAR subtypes. We tackled this issue at the transcriptional level using early zebrafish embryo as a model. Using morpholino knockdown, we specifically invalidated the zebrafish endogenous RAR subtypes in an in vivo context. After building up a list of RA-responsive genes in the zebrafish gastrula through a whole-transcriptome analysis, we compared this panel of genes with those that still respond to RA in embryos lacking one or another RAR subtype. Our work reveals that RAR subtypes do not have fully redundant functions at the transcriptional level but can transduce RA signal in a subtype-specific fashion. As a result, we define RAR subtype-specific transcriptotypes that correspond to repertoires of genes activated by different RAR subtypes. Finally, we found genes of the RA pathway (cyp26a1, raraa) the regulation of which by RA is highly robust and can even resist the knockdown of all RARs. This suggests that RA-responsive genes are differentially sensitive to alterations in the RA pathway and, in particular, cyp26a1 and raraa are under a high pressure to maintain signaling integrity.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Retinoic acid (RA) controls many aspects of embryonic development by binding to specific receptors (retinoic acid receptors [RARs]) that regulate complex transcriptional networks. Three different RAR subtypes are present in vertebrates and play both common and specific roles in transducing RA signaling. Specific activities of each receptor subtype can be correlated with its exclusive expression pattern, whereas shared activities between different subtypes are generally assimilated to functional redundancy. However, the question remains whether some subtype-specific activity still exists in regions or organs coexpressing multiple RAR subtypes. We tackled this issue at the transcriptional level using early zebrafish embryo as a model. Using morpholino knockdown, we specifically invalidated the zebrafish endogenous RAR subtypes in an in vivo context. After building up a list of RA-responsive genes in the zebrafish gastrula through a whole-transcriptome analysis, we compared this panel of genes with those that still respond to RA in embryos lacking one or another RAR subtype. Our work reveals that RAR subtypes do not have fully redundant functions at the transcriptional level but can transduce RA signal in a subtype-specific fashion. As a result, we define RAR subtype-specific transcriptotypes that correspond to repertoires of genes activated by different RAR subtypes. Finally, we found genes of the RA pathway (cyp26a1, raraa) the regulation of which by RA is highly robust and can even resist the knockdown of all RARs. This suggests that RA-responsive genes are differentially sensitive to alterations in the RA pathway and, in particular, cyp26a1 and raraa are under a high pressure to maintain signaling integrity.
Faugaret, Delphine; Amara, Amira Ben; Alingrin, Julie; Daumas, Aurélie; Delaby, Amélie; Lépolard, Catherine; Raoult, Didier; Textoris, Julien; Mège, Jean-Louis
Granulomatous response to Coxiella burnetii, the agent of Q fever: the lessons from gene expression analysis Journal Article
In: Front Cell Infect Microbiol, vol. 4, pp. 172, 2014, ISSN: 2235-2988.
@article{pmid25566510,
title = {Granulomatous response to Coxiella burnetii, the agent of Q fever: the lessons from gene expression analysis},
author = {Delphine Faugaret and Amira Ben Amara and Julie Alingrin and Aurélie Daumas and Amélie Delaby and Catherine Lépolard and Didier Raoult and Julien Textoris and Jean-Louis Mège},
doi = {10.3389/fcimb.2014.00172},
issn = {2235-2988},
year = {2014},
date = {2014-01-01},
urldate = {2014-01-01},
journal = {Front Cell Infect Microbiol},
volume = {4},
pages = {172},
abstract = {The formation of granulomas is associated with the resolution of Q fever, a zoonosis due to Coxiella burnetii; however the molecular mechanisms of granuloma formation remain poorly understood. We generated human granulomas with peripheral blood mononuclear cells (PBMCs) and beads coated with C. burnetii, using BCG extracts as controls. A microarray analysis showed dramatic changes in gene expression in granuloma cells of which more than 50% were commonly modulated genes in response to C. burnetii and BCG. They included M1-related genes and genes related to chemotaxis. The inhibition of the chemokines, CCL2 and CCL5, directly interfered with granuloma formation. C. burnetii granulomas also expressed a specific transcriptional profile that was essentially enriched in genes associated with type I interferon response. Our results showed that granuloma formation is associated with a core of transcriptional response based on inflammatory genes. The specific granulomatous response to C. burnetii is characterized by the activation of type 1 interferon pathway.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The formation of granulomas is associated with the resolution of Q fever, a zoonosis due to Coxiella burnetii; however the molecular mechanisms of granuloma formation remain poorly understood. We generated human granulomas with peripheral blood mononuclear cells (PBMCs) and beads coated with C. burnetii, using BCG extracts as controls. A microarray analysis showed dramatic changes in gene expression in granuloma cells of which more than 50% were commonly modulated genes in response to C. burnetii and BCG. They included M1-related genes and genes related to chemotaxis. The inhibition of the chemokines, CCL2 and CCL5, directly interfered with granuloma formation. C. burnetii granulomas also expressed a specific transcriptional profile that was essentially enriched in genes associated with type I interferon response. Our results showed that granuloma formation is associated with a core of transcriptional response based on inflammatory genes. The specific granulomatous response to C. burnetii is characterized by the activation of type 1 interferon pathway.