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RNA-seq data of mouse cerebral cortex in control and UTX conditional knockout groups

ABSTRACT: We demonstrate that UTX deficiency increases neural progenitor cells (NPCs) proliferation, decreases terminal mitosis and neuronal differentiation. Furthermore, we discover that impairment of cortex development caused by lack of UTX is less significant in males than in females. And further knockdown of UTY in male UTX-deficient cortex makes the phenotype consistent with the female’s. In order to understand the amount of gene expression, gene expression differences, as well as differences in gene patterns and functional clustering and other aspects of the situation after UTX conditional knockout in cortex, we conducted RNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE110392 | GEO | 2018/02/10

REPOSITORIES: GEO

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UTX-mediated enhancer and chromatin remodeling suppresses myeloid leukemogenesis through noncatalytic inverse regulation of ETS and GATA programs

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UTX-mediated enhancer and chromatin remodeling suppresses myeloid leukemogenesis through noncatalytic inverse regulation of ETS and GATA programs

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2012-08-01 | E-GEOD-39472 | biostudies-arrayexpress

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2012-07-31 | E-GEOD-39473 | biostudies-arrayexpress

RNA-seq data of mouse cerebral cortex in control and UTX conditional knockout groups

Project description:RNA-seq data of mouse cerebral cortex in control and UTX conditional knockout groups

| PRJNA433664 | ENA

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2016-03-22 | E-GEOD-69968 | biostudies-arrayexpress

X-linked H3K27me3 demethylase Utx is required for embryonic development in a sex-specific manner [ChIP-Seq data]

Project description:Embryogenesis requires the timely and coordinated activation of developmental regulators. It has been suggested that the recently discovered class of histone demethylases (UTX and JMJD3) that specifically target the repressive H3K27me3 modification play an important role in the activation of “bivalent” genes in response to specific developmental cues. To determine the requirements for UTX in pluripotency and development, we have generated Utx null ES cells and mutant mice. The loss of UTX had a profound effect during embryogenesis. Utx null embryos had reduced somite counts, neural tube closure defects and heart malformation which presented between E9.5 and E13.5. Unexpectedly, homozygous mutant female embryos were more severely affected than hemizygous mutant male embryos. In fact, we observed the survival of a subset of UTX-deficient males which were smaller in size and had reduced life-span. Interestingly, these animals were fertile with normal spermatogenesis. Consistent with a mid-gestation lethality, UTX null male and female ES cells gave rise to all three germ layers in teratoma assays although sex-specific differences could be observed in the activation of developmental regulators in embryoid body assays. Lastly, ChIP-seq analysis revealed an increase in H3K27me3 in Utx null male ES cells. In summary, our data demonstrate sex-specific requirements for this X-linked gene while suggesting a role for UTY during development.

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