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RNA sequencing to determine gene expression changes in HMCES knockout cells

ABSTRACT: RNA sequencing to determine gene expression changes in HMCES knockout cells

PROVIDER: PRJNA497524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8079602_1.fastq.gz	Fastqsanger.gz
	SRR8079602_2.fastq.gz	Fastqsanger.gz
	SRR8079603_1.fastq.gz	Fastqsanger.gz
	SRR8079603_2.fastq.gz	Fastqsanger.gz
	SRR8079604_1.fastq.gz	Fastqsanger.gz

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RNA sequencing to determine gene expression changes in HMCES knockout cells

Project description:The purpose of this study was to deteremine gene expression changes in when HMCES is inactivated. We found very few changes.

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HMCES counterbalances the transcriptional regulation of nodal/activin and BMP signaling in mESCs (RNA-Seq)

Project description:Despite the fundamental roles to cell fates determination in all metazoans, the mechanism by which the TGF-β family signaling is interpreted into spatial and temporal manner and multiple cell fates is still elusive. The cell context dependent function of TGF-β signaling largely relies on the transcriptional regulation centered by SMAD proteins. Here, we discovered that the DNA-repair related protein, HMCES contributes to early development by maintaining the nodal/activin or BMP signaling related transcriptome homeostasis. HMCES is a R-SMAD proteins binding partner that co-localizes with R-SMADs at active histone marks. However, HMCES chromatin occupancy is independent of nodal/activin or BMP signaling. Mechanically, HMCES exerts its transcriptional regulation role by counteracting R-SMAD proteins association with chromatin. In Xenopus embryo, hmces-KD causes dramatic development defects with altered left-right axis asymmetry along with increasing expression of lefty1. In sum, we disclosed the novel transcriptional regulatory function of HMCES integrated in TGF-β family signaling.

2022-09-14 | GSE186223 | GEO

HMCES counterbalances the transcriptional regulation of nodal/activin and BMP signaling in mESCs (ChIP-Seq)

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HMCES safeguards genome integrity and long-term self-renewal of hematopoietic stem cells during stress responses

Project description:Hematopoietic stress drives quiescent hematopoietic stem cells (HSCs) to proliferate, generating reactive oxygen species and oxidative DNA damage including abasic sites. The coupling between abasic site generation and DNA replication during HSC stress responses, however, presents a challenge to accurately repair these abasic sites in the single-stranded DNA (ssDNA) generated during replication, leading to strand breaks and mutations. Here, we show in mice that HMCES, an evolutionarily conserved sensor and shield of ssDNA abasic sites, plays a pivotal role in overcoming this challenge. Hmces-deficient HSCs exhibited compromised long-term self-renewal capacity and elevated DNA damage in vivo in response to various hematopoietic stress, as well as broad attenuation of DNA damage response and repair pathways. Loss of HMCES also rendered HSCs hypersensitive to alcohol-derived acetaldehyde and might associate with increased susceptibility of leukemia. Collectively, our findings highlighted HMCES as a novel protector of HSCs and shed light on its physiological roles in regeneration and tumorigenesis.

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