Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ERCC6L2 mitigates replication stress and promotes centromere stability

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE226155 | GEO | 2023/04/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ERCC6L2 mitigates replication stress and promotes centromere stability [Nascent_DNA_seq]

Project description:Structurally complex genomic regions, such as centromeres, are inherently difficult to duplicate. The mechanism that underlies centromere inheritance is not well understood, and one of the key questions relates to the reassembly of centromeric chromatin following DNA replication. Here we define the SNF2 ATPase ERCC6L2 as a key regulator of this process. ERCC6L2 accumulates at centromeres and promotes efficient deposition of core centromeric factors. Our genomic analyses show that ERCC6L2 deficiency erodes centromeric chromatin, leading to unrestrained replication of centromeric DNA. We also establish that, beyond centromeres, ERCC6L2 facilitates replication at genomic repeats and non-canonical DNA structures. Notably, ERCC6L2 interacts with the major DNA replication factor PCNA through an atypical peptide, presented here as a co-crystal structure. Finally, we examine ERCC6L2 activities at DNA breaks, and show that it acts to restrict end resection independently of the 53BP1-REV7-Shieldin complex. Our observations allow us to propose a mechanistic model of ERCC6L2 activity, which reconciles its seemingly distinct functions in DNA repair and DNA replication. Together, these findings provide a new molecular context for studies linking ERCC6L2 to human disease.

2023-04-10 | GSE226154 | GEO

ERCC6L2 mitigates replication stress and promotes centromere stability [ChIP-seq]

2023-04-10 | GSE226152 | GEO

ERCC6L2 mitigates replication stress and promotes centromere stability

Project description:ERCC6L2 mitigates replication stress and promotes centromere stability

| PRJNA939098 | ENA

ERCC6L2 mitigates replication stress and promotes centromere stability [Nascent_DNA_seq]

Project description:ERCC6L2 mitigates replication stress and promotes centromere stability [Nascent_DNA_seq]

| PRJNA939103 | ENA

ERCC6L2 mitigates replication stress and promotes centromere stability [ChIP-seq]

Project description:ERCC6L2 mitigates replication stress and promotes centromere stability [ChIP-seq]

| PRJNA939100 | ENA

Nucleotide depletion promotes cell fate transitions by inducing DNA replication stress

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-04 | GSE172335 | GEO

Taz1-Shelterin promotes facultative heterochromatin assembly at chromosome-internal sites containing late replication origins

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-09 | E-GEOD-78823 | biostudies-arrayexpress

ZEB1 expression prevents DNA replication stress in cancer stem cells and delays chromosomal instability

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-31 | E-GEOD-56031 | biostudies-arrayexpress

Haploinsufficiency of an RB-E2F1-Condensin II complex causes replication stress and contributes to mesenchymal cancers

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-19 | E-GEOD-55041 | biostudies-arrayexpress

Human CDK18 promotes replication stress signaling and genome stability.

Project description:Cyclin-dependent kinases (CDKs) coordinate cell cycle checkpoints with DNA repair mechanisms that together maintain genome stability. However, the myriad mechanisms that can give rise to genome instability are still to be fully elucidated. Here, we identify CDK18 (PCTAIRE 3) as a novel regulator of genome stability, and show that depletion of CDK18 causes an increase in endogenous DNA damage and chromosomal abnormalities. CDK18-depleted cells accumulate in early S-phase, exhibiting retarded replication fork kinetics and reduced ATR kinase signaling in response to replication stress. Mechanistically, CDK18 interacts with RAD9, RAD17 and TOPBP1, and CDK18-deficiency results in a decrease in both RAD17 and RAD9 chromatin retention in response to replication stress. Importantly, we demonstrate that these phenotypes are rescued by exogenous CDK18 in a kinase-dependent manner. Collectively, these data reveal a rate-limiting role for CDK18 in replication stress signalling and establish it as a novel regulator of genome integrity.

| S-EPMC5062979 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data