Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA277946 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:H3K9 acetylation was enriched in pluripotency genes in hESCs and in neural genes in neural progenitor cells
2015-03-11 | GSE66778 | GEO
Project description:We report that acetylation of H4K16 is a new marker of active enhancers and that some enhancers are marked by H3K4me1, MOF and H4K16ac but not by acetylated H3K27 or p300, suggesting that they are novel p300-independent regulatory elements. ChIP-seq for H4K16 acetylation in undifferentiated 46c(sox1-gfp) ES cells, and FACS sorted day 5 Neural Progenitor Cells (differentiated with NB27 and Neuro2 medium supplements) , along with MNase digested input for both samples
2013-08-23 | E-GEOD-47761 | 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.
2020-06-01 | PXD018625 | Pride
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.
2020-06-01 | PXD018621 | Pride
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:Using acetylated histone H3 ChIP-seq, we reveal that the histone H3 acetylation level is gradually increased on the neural gene loci while decreased on the neural-inhibitory gene loci during mouse ESC neural differentiation. By overlapping with the targets of HDAC1 ChIP-seq, we identify Nodal as a target gene repressed by histone deacetylation. Thus, our study reveals an intrinsic mechanism that epigenetic histone deacetylation ensures neural fate commitment by restricting Nodal signaling. Examination of HDAC1 in differentiated day 2 cells and acetylated histone H3 in day 2, day 4 and day 6 cells.
2015-02-19 | E-GEOD-66025 | biostudies-arrayexpress
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.
2013-12-24 | GSE46485 | GEO
Project description:The nucleoprotein Geminin (Gmnn) promotes neural cell fate acquisition of embryonic stem cells, while knockdown reduces the efficiency of neural gene activation. This occurs, at least in part, through Geminin’s ability to promote histone hyperacetylation at neural genes, to activate their expression. In mouse models in vivo, Geminin deficiency in the embryonic neural tube between embryonic days 8.5-10.5 also reduces the expression of genes controlling neural specification and/or differentiation, contributing to neural tube defects. To determine where Geminin binding and Gmnn-dependent acetylation occurs throughout the genome, we performed ChIP-chip analysis (these data) and ChIP-seq analysis (GSE77246) to define Geminin-bound chromatin locations in mouse embryonic stem cells (ESCs) and in ESC-derived neuroectoderm. We also performed ChIP-chip analysis of H3K9 acetylation in ESC-derived neuroectoderm, with or without Doxycycline-dependent Gmnn knockdown, to define the requirements for Geminin activity for histone acetylation of promoters during neural fate specification.
2016-12-01 | GSE81450 | GEO
Project description:SAGA member Ada2 is required for the majority of H3K9 acetylation in C. neoformans. To identify specific genomic loci that exhibit Ada2-dependent H3K9 acetylation, we performed ChIP-Seq against H3K9ac in wildtype and ada2Δ cells. ChIP-Seq was performed using antibodies for H3K9ac in KN99 wildtype cells and ada2Δ cells. Input and IPed DNA was collected in triplicate from each strain and sequenced on an Illumnina HiSeq 2000 flow cell producing 84 million reads. Due to the lack of quality scores, raw reads are omitted from the submission.
2012-01-01 | E-GEOD-32075 | biostudies-arrayexpress