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ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion.

ABSTRACT: ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion.

PROVIDER: PRJNA874443 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21284900_1.fastq.gz	Fastqsanger.gz
	SRR21284900_2.fastq.gz	Fastqsanger.gz
	SRR21284901_1.fastq.gz	Fastqsanger.gz
	SRR21284901_2.fastq.gz	Fastqsanger.gz
	SRR21284902_1.fastq.gz	Fastqsanger.gz

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ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [HTGTS]

Project description:The ATR kinase, which coordinates cellular responses to DNA replication stress, is also essential for the proliferation of normal unstressed cells. Although its role in the replication stress response is well defined, the mechanisms by which ATR supports normal cell proliferation remain elusive. Here, we show that Atr is dispensable for the viability of G0-arrested naïve B cells. However, upon cytokine-induced proliferation, Atr-deficient B cells initiate DNA replication efficiently in early S phase, but by mid-S phase they display dNTP depletion, fork stalling, and replication failure. Nonetheless, productive DNA replication can be restored in Atr-deficient cells by pathways that suppress origin firing, such as downregulation of CDC7 and CDK1 kinase activities. Together, these findings indicate that ATR supports the proliferation of normal unstressed cells by tempering the pace of origin firing during the early S phase to avoid exhaustion of dNTPs and other replication factors.

2022-12-31 | GSE212195 | GEO

ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [HTGTS]

Project description:ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [HTGTS]

| PRJNA874445 | ENA

ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [RNA-seq]

2022-12-31 | GSE212194 | GEO

ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [RNA-seq]

Project description:ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [RNA-seq]

| PRJNA874444 | ENA

ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [CRISPR-Cas9 gRNA screen]

2022-12-31 | GSE214643 | GEO

ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [CRISPR-Cas9 gRNA screen]

Project description:ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion [CRISPR-Cas9 gRNA screen]

| PRJNA886447 | ENA

ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion.

Project description:The ATR kinase, which coordinates cellular responses to DNA replication stress, is also essential for the proliferation of normal unstressed cells. Although its role in the replication stress response is well defined, the mechanisms by which ATR supports normal cell proliferation remain elusive. Here, we show that ATR is dispensable for the viability of G0-arrested naïve B cells. However, upon cytokine-induced proliferation, Atr-deficient B cells initiate DNA replication efficiently, but by mid-S phase they display dNTP depletion, fork stalling, and replication failure. Nonetheless, productive DNA replication and dNTP levels can be restored in Atr-deficient cells by suppressing origin firing, such as partial inhibition of CDC7 and CDK1 kinase activities. Together, these findings indicate that ATR supports the proliferation of normal unstressed cells by tempering the pace of origin firing during the early S phase to avoid exhaustion of dNTPs and importantly also other replication factors.

| S-EPMC10279696 | biostudies-literature

ATR kinase supports normal proliferation in the early S phase by preventing replication resource exhaustion.

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

2022-12-31 | GSE212196 | GEO

5-HT6R-ATR-Primary Cilia Network Supports Memory Extinction

Project description:5-HT6R-ATR-Primary Cilia Network Supports Memory Extinction

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5-HT6R-ATR-Primary Cilia Network Supports Memory Extinction

Project description:Drug addiction represents a pathological form of learning and memory with profound implications for individuals and society. The serotonin receptor 5-HT6R, uniquely expressed on primary cilia, is associated with neurological development, cognitive impairments, emotional disorders, and reward memory for cocaine and nicotine. However, its role in morphine-related reward memory remains unclear. This study demonstrated that 5-HT6R expression was downregulated during the early stage of morphine-induced conditioned place preference (CPP) extinction but returned to baseline levels later, with no significant changes observed during CPP establishment or reinstatement. Knocking down 5-HT6R accelerated CPP extinction, while overexpression prolonged the process. Furthermore, primary cilia defects within the mPFC were noted during the early stage of CPP extinction, and the removal of primary cilia expedited this process. Finally, ATR was identified as a novel target molecule of 5-HT6R, and the 5-HT6R-ATR-primary cilia network was found to regulate morphine-induced CPP extinction, offering new insights for opioid addiction therapy.

2025-09-03 | GSE273842 | GEO

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