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LATEST PUBLICATIONS
2014
Daussy, Cécile; Faure, Fabrice; Mayol, Katia; Viel, Sébastien; Gasteiger, Georg; Charrier, Emily; Bienvenu, Jacques; Henry, Thomas; Debien, Emilie; Hasan, Uzma A; Marvel, Jacqueline; Yoh, Keigyou; Takahashi, Satoru; Prinz, Immo; de Bernard, Simon; Buffat, Laurent; Walzer, Thierry
T-bet and Eomes instruct the development of two distinct natural killer cell lineages in the liver and in the bone marrow Journal Article
In: J Exp Med, vol. 211, no. 3, pp. 563–577, 2014, ISSN: 1540-9538.
@article{pmid24516120,
title = {T-bet and Eomes instruct the development of two distinct natural killer cell lineages in the liver and in the bone marrow},
author = {Cécile Daussy and Fabrice Faure and Katia Mayol and Sébastien Viel and Georg Gasteiger and Emily Charrier and Jacques Bienvenu and Thomas Henry and Emilie Debien and Uzma A Hasan and Jacqueline Marvel and Keigyou Yoh and Satoru Takahashi and Immo Prinz and Simon de Bernard and Laurent Buffat and Thierry Walzer},
doi = {10.1084/jem.20131560},
issn = {1540-9538},
year = {2014},
date = {2014-03-01},
urldate = {2014-03-01},
journal = {J Exp Med},
volume = {211},
number = {3},
pages = {563--577},
abstract = {Trail(+)DX5(-)Eomes(-) natural killer (NK) cells arise in the mouse fetal liver and persist in the adult liver. Their relationships with Trail(-)DX5(+) NK cells remain controversial. We generated a novel Eomes-GFP reporter murine model to address this question. We found that Eomes(-) NK cells are not precursors of classical Eomes(+) NK cells but rather constitute a distinct lineage of innate lymphoid cells. Eomes(-) NK cells are strictly dependent on both T-bet and IL-15, similarly to NKT cells. We observed that, in the liver, expression of T-bet in progenitors represses Eomes expression and the development of Eomes(+) NK cells. Reciprocally, the bone marrow (BM) microenvironment restricts T-bet expression in developing NK cells. Ectopic expression of T-bet forces the development of Eomes(-) NK cells, demonstrating that repression of T-bet is essential for the development of Eomes(+) NK cells. Gene profile analyses show that Eomes(-) NK cells share part of their transcriptional program with NKT cells, including genes involved in liver homing and NK cell receptors. Moreover, Eomes(-) NK cells produce a broad range of cytokines, including IL-2 and TNF in vitro and in vivo, during immune responses against vaccinia virus. Thus, mutually exclusive expression of T-bet and Eomes drives the development of different NK cell lineages with complementary functions.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Trail(+)DX5(-)Eomes(-) natural killer (NK) cells arise in the mouse fetal liver and persist in the adult liver. Their relationships with Trail(-)DX5(+) NK cells remain controversial. We generated a novel Eomes-GFP reporter murine model to address this question. We found that Eomes(-) NK cells are not precursors of classical Eomes(+) NK cells but rather constitute a distinct lineage of innate lymphoid cells. Eomes(-) NK cells are strictly dependent on both T-bet and IL-15, similarly to NKT cells. We observed that, in the liver, expression of T-bet in progenitors represses Eomes expression and the development of Eomes(+) NK cells. Reciprocally, the bone marrow (BM) microenvironment restricts T-bet expression in developing NK cells. Ectopic expression of T-bet forces the development of Eomes(-) NK cells, demonstrating that repression of T-bet is essential for the development of Eomes(+) NK cells. Gene profile analyses show that Eomes(-) NK cells share part of their transcriptional program with NKT cells, including genes involved in liver homing and NK cell receptors. Moreover, Eomes(-) NK cells produce a broad range of cytokines, including IL-2 and TNF in vitro and in vivo, during immune responses against vaccinia virus. Thus, mutually exclusive expression of T-bet and Eomes drives the development of different NK cell lineages with complementary functions.
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.