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

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

PROVIDER: PRJNA874444 | 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.

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

| PRJNA874443 | ENA

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 [RNA-seq]

2022-12-31 | GSE212194 | 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 [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:This SuperSeries is composed of the SubSeries listed below.

2022-12-31 | GSE212196 | GEO

Transcription profiling of shoot apices from Arabidopsis wild type, teb, atr, and teb atr mutant plants

Project description:Global gene expression patterns were compared among wild-type Col-0, teb, atr, teb atr of A. thaliana using shoot apices.

2008-04-01 | E-MEXP-1329 | biostudies-arrayexpress

RNA processing proteins regulate Mec1/ATR activation by promoting generation of RPA-coated ssDNA.

Project description:Eukaryotic cells respond to DNA double-strand breaks (DSBs) by activating a checkpoint that depends on the protein kinases Tel1/ATM and Mec1/ATR. Mec1/ATR is activated by RPA-coated single-stranded DNA (ssDNA), which arises upon nucleolytic degradation (resection) of the DSB. Emerging evidences indicate that RNA processing factors play critical, yet poorly understood, roles in genomic stability. Here, we provide evidence that the Saccharomyces cerevisiae RNA decay factors Xrn1, Rrp6 and Trf4 regulate Mec1/ATR activation by promoting generation of RPA-coated ssDNA. The lack of Xrn1 inhibits ssDNA generation at the DSB by preventing the loading of the MRX complex. By contrast, DSB resection is not affected in the absence of Rrp6 or Trf4, but their lack impairs the recruitment of RPA, and therefore of Mec1, to the DSB. Rrp6 and Trf4 inactivation affects neither Rad51/Rad52 association nor DSB repair by HR, suggesting that full Mec1 activation requires higher amount of RPA-coated ssDNA than HR-mediated repair. Noteworthy, deep transcriptome analyses do not identify common misregulated gene expression that could explain the observed phenotypes. Our results provide a novel link between RNA processing and genome stability. Strand-specific transcriptome analysis of biological replicates of WT cells (JKM139 strain) at T0, or 60 and 240 minutes after HO induction, and of xrn1∆, rrp6∆ and trf4∆ cells at T0.

2014-11-20 | E-GEOD-63444 | biostudies-arrayexpress

Atr maintains chromosomal integrity during postnatal cerebellar neurogenesis [Affymetrix]

Project description:Microcephaly and medulloblastoma result from mutations that compromise genomic stability. We report that Atr, which is mutated in the microcephalic disorder Seckel syndrome, is required to maintain chromosomal integrity during postnatal cerebellar neurogenesis. Atr deletion in cerebellar granule neuron progenitors (CGNPs) induced proliferation-associated DNA damage, p53 activation, apoptosis, and cerebellar hypoplasia. Co-deletions of either Bax and Bak or p53 prevented apoptosis in Atr-deleted CGNPs, but failed to fully rescue cerebellar growth. Atr-deficient CGNPs showed impaired cell cycle checkpoint function and continued to proliferate, accumulating chromosomal abnormalities. RNA-Seq demonstrated that the transcriptional response to Atr-deficient proliferation was p53-driven. Acute Atr inhibition in vivo by nanoparticle-formulated VE-822 reproduced the disruptions seen with Atr deletion. Our data show that p53-driven apoptosis and senescence, and non-apoptotic cell death redundantly limit growth in Atr-deficient progenitors. These overlapping mechanisms that suppress growth in Atr-disrupted CGNPs may be exploited for treatment of CGNP-derived medulloblastoma using Atr inhibition.

2016-09-01 | GSE85393 | GEO

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