ChIP-seq analysis of H3K9 acetylation enrichment in hESCs and day 8 neural progenitor cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE66778 | GEO | 2015/03/11
SECONDARY ACCESSION(S): PRJNA277946
REPOSITORIES: GEO
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Project description:H3K9 acetylation was enriched in pluripotency genes in hESCs and in neural genes in neural progenitor cells Examination of H3K9 acetylation distributions in hESCs and neural progenitor cells
2015-03-11 | E-GEOD-66778 | biostudies-arrayexpress
Project description:Histones modulate gene expression by chromatin compaction, regulating numerous processes such as differentiation. However, the mechanisms underlying histone degradation remain elusive. When compared with their differentiated counterparts, immortal human embryonic stem cells (hESCs) have a unique chromatin architecture and low levels of trimethylated histone H3 at lysine 9 (H3K9me3), a heterochromatin-associated modification. Here we assess a link between the intrinsic epigenetic landscape and ubiquitin-proteasome system of hESCs. We find that hESCs exhibit high expression of UBE2K, a ubiquitin-conjugating enzyme. Loss of UBE2K increases the levels of H3K9 trimethyltransferase SETDB1, resulting in H3K9 trimethylation and repression of neurogenic genes during differentiation. Concomitantly, loss of UBE2K impairs the ability of hESCs to differentiate into neural progenitors with neurogenic properties. Besides H3K9 trimethylation, we find that UBE2K binds histone H3 to induce its polyubiquitination and degradation by the proteasome. Notably, ubc-20, the worm orthologue of UBE2K, also regulates both histone H3 levels and H3K9 trimethylation in C. elegans germline. Thus, our results indicate that UBE2K crosses evolutionary boundaries to promote histone H3 degradation and reduce H3K9me3 repressive marks in immortal cells.
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Project description:Mutations in STAMBP have been well-established to cause congenital human microcephaly-capillary malformation (MIC-CAP) syndrome, a rare genetic disorder characterized by global developmental delay, severe microcephaly, capillary malformations, etc.We report here that STAMBP is dispensable for the pluripotency maintenance or neural differentiation of hESCs. However, neural progenitor cells (NPCs) derived from STAMBP-deficient hESCs fail to be long-term maintained/expanded in vitro. We identified the anti-apoptotic protein CFLAR is down-regulated in those affected NPCs and ectopic expression of CFLAR rescues NPC defects induced by STMABP-deficiency.
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Project description:To compare transcriptomic profiles between UCSF4 hESCs and their neural derivatives, neural precursor cells (NPCs), we performed microarray analysis using the Affymetrix Human Gene 2.0 ST array platform. Six biological samples, three biological replicates for each developmental cell stage (in vitro)
2016-03-01 | E-GEOD-74378 | biostudies-arrayexpress
Project description:Histones modulate gene expression by chromatin compaction, regulating numerous processes such as differentiation. However, the mechanisms underlying histone degradation remain elusive. When compared with their differentiated counterparts, immortal human embryonic stem cells (hESCs) have a unique chromatin architecture and low levels of trimethylated histone H3 at lysine 9 (H3K9me3), a heterochromatin-associated modification. Here we assess a link between the intrinsic epigenetic landscape and ubiquitin-proteasome system of hESCs. We find that hESCs exhibit high expression of UBE2K, a ubiquitin-conjugating enzyme. Loss of UBE2K increases the levels of H3K9 trimethyltransferase SETDB1, resulting in H3K9 trimethylation and repression of neurogenic genes during differentiation. Concomitantly, loss of UBE2K impairs the ability of hESCs to differentiate into neural progenitors with neurogenic properties. Besides H3K9 trimethylation, we find that UBE2K binds histone H3 to induce its polyubiquitination and degradation by the proteasome. Notably, ubc-20, the worm orthologue of UBE2K, also regulates both histone H3 levels and H3K9 trimethylation in C. elegans germline. Thus, our results indicate that UBE2K crosses evolutionary boundaries to promote histone H3 degradation and reduce H3K9me3 repressive marks in immortal cells.
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Project description:It has been recently reported that the pluripotency factor OCT4, the early neural inducing factor NR2F2, and the pluripotency-associated miRNA miR-302 are linked in a regulatory circuitry that critically regulate both pluripotency and neural differentiation of human embryonic stem cells (hESCs). We show here that JMJD1C, a H3K9 demethylase expressed in undifferentiated hESCs, plays a key role in the regulatory circuitry. hESCs with JMJD1C knockdown (KD) retain the state of self-renewal and pluripotency, but express lower miR-302c than control hESCs. JMJD1C directly binds to the miR-302 promoter in hESCs and reduces H3K9 methylation on the promoter. Upon withdrawal of bFGF (an inhibitor of neural initiation) from a defined culture medium, the KD, but not control, hESCs differentiate into neural progenitors within three days – the fastest ever reported, accompanied by rapid increase of NR2F2 expression. A miR-302c analogue or an inhibitor of H3K9 methylation reduces neural induction from the KD hESCs, whereas a miR-302c inhibitor promotes hESC differentiation. Together, our findings suggest that JMJD1C plays a central role in control of neural differentiation from hESCs, which involves sustained miR-302c expression, and that inhibition of JMJD1C is sufficient to rapidly induce neural progenitors from hESCs in the defined medium depleted of bFGF. This is also the first evidence, to our knowledge, for epigenetic modification of miR-302 in hESCs. 6 human ES cell lines were used in this microarray assay. Each line has two replicates.
2013-12-24 | E-GEOD-46485 | biostudies-arrayexpress
Project description:STAMBP is required for long-term maintenance of neural progenitor cells derived from hESCs
| PRJNA1029579 | ENA
Project description:It has been recently reported that the pluripotency factor OCT4, the early neural inducing factor NR2F2, and the pluripotency-associated miRNA miR-302 are linked in a regulatory circuitry that critically regulate both pluripotency and neural differentiation of human embryonic stem cells (hESCs). We show here that JMJD1C, a H3K9 demethylase expressed in undifferentiated hESCs, plays a key role in the regulatory circuitry. hESCs with JMJD1C knockdown (KD) retain the state of self-renewal and pluripotency, but express lower miR-302c than control hESCs. JMJD1C directly binds to the miR-302 promoter in hESCs and reduces H3K9 methylation on the promoter. Upon withdrawal of bFGF (an inhibitor of neural initiation) from a defined culture medium, the KD, but not control, hESCs differentiate into neural progenitors within three days – the fastest ever reported, accompanied by rapid increase of NR2F2 expression. A miR-302c analogue or an inhibitor of H3K9 methylation reduces neural induction from the KD hESCs, whereas a miR-302c inhibitor promotes hESC differentiation. Together, our findings suggest that JMJD1C plays a central role in control of neural differentiation from hESCs, which involves sustained miR-302c expression, and that inhibition of JMJD1C is sufficient to rapidly induce neural progenitors from hESCs in the defined medium depleted of bFGF. This is also the first evidence, to our knowledge, for epigenetic modification of miR-302 in hESCs.
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