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In vivo T-box Transcription Factor Profiling Reveals Joint Regulation of Embryonic Neuro-mesodermal Bipotency

ABSTRACT: Brachyury (Xbra/Xbra3) knock-down embryos of the frog Xenopus tropicalis were profiled to quantify neuro-mesodermal cell fate switches at a transcriptional level.

ORGANISM(S): Xenopus tropicalis

PROVIDER: GSE48663 | GEO | 2013/09/19

SECONDARY ACCESSION(S): PRJNA210967

REPOSITORIES: GEO

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In vivo T-box Transcription Factor Profiling Reveals Joint Regulation of Embryonic Neuro-mesodermal Bipotency

Project description:Brachyury (Xbra/Xbra3) knock-down embryos of the frog Xenopus tropicalis were profiled to quantify neuro-mesodermal cell fate switches at a transcriptional level. Transcriptional profiling of Xbra/Xbra3 double morphants at early tadpole stage (RNA-Seq) in biological triplicates.

2013-09-19 | E-GEOD-48663 | biostudies-arrayexpress

In vivo T-box Transcription Factor Profiling Reveals Joint Regulation of Embryonic Neuro-mesodermal Bipotency.

Project description:We defined genome-wide regulatory inputs of the T-box transcription factors Brachyury (Xbra), Eomesodermin (Eomes) and VegT that maintain neuro-mesodermal stem cells and determine their bipotential fates in the Xenopus tropicalis frog embryo. Binding profiles for Xbra, Eomes and VegT in X. tropicalis embryos (ChIP-Seq)

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In vivo T-box Transcription Factor Profiling Reveals Joint Regulation of Embryonic Neuro-mesodermal Bipotency.

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Antagonistic activities of Sox2 and Brachyury control the fate choice of neuro-mesodermal progenitors

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Project description:We report on the implications of genetic KO versus MO-mediated KD of the mesoderm-specifying Brachyury paralogues in the Western clawed frog Xenopus tropicalis. While both KO and KD embryos fail to activate the same core gene regulatory network, resulting in virtually identical morphological defects, embryos injected with control or target MOs also show a systemic GC content dependent immune response and many off-target splicing defects.

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Project description:The p.R482W hotspot mutation in A-type nuclear lamins causes familial partial lipodystrophy of Dunnigantype (FPLD2), a lipodystrophic syndrome complicated by early-onset atherosclerosis. Molecular mechanisms underlying endothelial cell dysfunction conferred by the lamin A mutation remain elusive. However, lamin A regulates epigenetic developmental pathways and mutations could perturb these functions. Here, we demonstrate that lamin A R482W elicits endothelial differentiation defects in a developmental model of FPLD2. Genome modeling in fibroblasts from patients with FPLD2 caused by the lamin A R482W mutation reveals repositioning of the mesodermal regulator T/Brachyury locus towards the nuclear center relative to normal fibroblasts, suggesting enhanced activation propensity of the locus in a developmental model of FPLD2. Addressing this issue, we report phenotypic and transcriptional alterations in mesodermal and endothelial differentiation of induced pluripotent stem cells we generated from a patient with R482Wassociated FPLD2. Correction of the LMNA mutation ameliorates R482W-associated phenotypes and gene expression. Transcriptomics links endothelial differentiation defects to decreased Polycomb-mediated repression of the T/Brachyury locus and over-activation of T target genes. Binding of the Polycomb repressor complex PRC2 to T/Brachyury is impaired by the mutated lamin A network, which is unable to properly associate with the locus. This leads to a deregulation of vascular gene expression over time. By connecting a lipodystrophic hotspot lamin A mutation to a disruption of early mesodermal gene expression and defective endothelial differentiation, we propose that the mutation rewires the fate of several lineages, resulting in multitissue pathogenic phenotypes.

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A mesodermal factor, T (Brachyury), specifies mouse germ cell fate by directly activating germline determinants

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Mus musculus

Project description:Antagonistic activities of Sox2 and Brachyury control the fate choice of neuro-mesodermal progenitors

| PRJNA360989 | ENA

A mesodermal factor, T (Brachyury), specifies mouse germ cell fate by directly activating germline determinants

2013-12-11 | GSE50394 | GEO