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

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

PROVIDER: PRJNA633383 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11804647_1.fastq.gz	Fastqsanger.gz
	SRR11804647_2.fastq.gz	Fastqsanger.gz
	SRR11804648_1.fastq.gz	Fastqsanger.gz
	SRR11804648_2.fastq.gz	Fastqsanger.gz
	SRR11804649_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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.

2022-01-21 | GSE150721 | GEO

Genomic Integrity Safeguards Self-Renewal in Embryonic Stem Cells.

Project description:A multitude of signals are coordinated to maintain self-renewal in embryonic stem cells (ESCs). To unravel the essential internal and external signals required for sustaining the ESC state, we expand upon a set of ESC pluripotency-associated phosphoregulators (PRs) identified previously by short hairpin RNA (shRNA) screening. In addition to the previously described Aurka, we identify 4 additional PRs (Bub1b, Chek1, Ppm1g, and Ppp2r1b) whose depletion compromises self-renewal and leads to consequent differentiation. Global gene expression profiling and computational analyses reveal that knockdown of the 5 PRs leads to DNA damage/genome instability, activating p53 and culminating in ESC differentiation. Similarly, depletion of genome integrity-associated genes involved in DNA replication and checkpoint, mRNA processing, and Charcot-Marie-Tooth disease lead to compromise of ESC self-renewal via an increase in p53 activity. Our studies demonstrate an essential link between genomic integrity and developmental cell fate regulation in ESCs.

| S-EPMC6708277 | biostudies-literature

Genomic integrity safeguards pluripotency in embryonic stem cells

Project description:Genomic integrity safeguards pluripotency in embryonic stem cells

| PRJNA438830 | ENA

JAK2-CHK2 signaling safeguards the integrity of the mitotic spindle assembly checkpoint and genome stability

Project description:This dataset consists of 1 raw MS file and associated peak list and result file, acquired on an Orbitrap Elite mass spectrometer operated in Data Dependent Acquisition mode. The files are associated with a manuscript submitted for publication. Publication title: "JAK2-CHK2 signaling safeguards the integrity of the mitotic spindle assembly checkpoint and genome stability"

2021-03-31 | MSV000087138 | MassIVE

HMCES counterbalances the transcriptional regulation of nodal/activin and BMP signaling in mESCs (ChIP-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 | GSE186222 | GEO

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

2022-09-14 | GSE186223 | GEO

Transcriptional repressor FOXD3 safeguards genome integrity in embryonic stem cells

Project description:Transcriptional repressor FOXD3 safeguards genome integrity in embryonic stem cells

| PRJNA760536 | ENA

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.

2019-01-17 | GSE121515 | GEO

circular RNA Kat6b-e2 expression safeguards self-renewal and lineage differentiation of mouse embryonic stem cells

Project description:circular RNA Kat6b-e2 expression safeguards self-renewal and lineage differentiation of mouse embryonic stem cells

| PRJNA874300 | ENA

HMCES safeguards replication from oxidative stress and ensures error-free repair.

Project description:Replication across oxidative DNA lesions can give rise to mutations that pose a threat to genome integrity. How such lesions, which escape base excision repair, get removed without error during replication remains unknown. Our PCNA-based screen to uncover changes in replisome composition under different replication stress conditions had revealed a previously unknown PCNA-interacting protein, HMCES/C3orf37. Here, we show that HMCES is a critical component of the replication stress response, mainly upon base misincorporation. We further demonstrate that the absence of HMCES imparts resistance to pemetrexed treatment due to error-prone bypass of oxidative damage. Furthermore, based on genetic screening, we show that homologous recombination repair proteins, such as CtIP, BRCA2, BRCA1, and PALB2, are indispensable for the survival of HMCES KO cells. Hence, HMCES, which is the sole member of the SRAP superfamily in higher eukaryotes known so far, acts as a proofreader on replication forks, facilitates resolution of oxidative base damage, and therefore ensures faithful DNA replication.

| S-EPMC7271331 | biostudies-literature

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