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Role of PARP-1 in transcriptional regulation during development (ChIP-seq)

ABSTRACT: Role of PARP-1 in transcriptional regulation during development (ChIP-seq)

PROVIDER: PRJNA900233 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22255922_1.fastq.gz	Fastqsanger.gz
	SRR22255922_2.fastq.gz	Fastqsanger.gz
	SRR22255923_1.fastq.gz	Fastqsanger.gz
	SRR22255923_2.fastq.gz	Fastqsanger.gz
	SRR22255924_1.fastq.gz	Fastqsanger.gz

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Role of PARP-1 in transcriptional regulation during development (ChIP-seq)

Project description:We interrogated the role of PARP-1 in developmental gene regulation in Drosophila via ChIP-seq in third-instar larvae.

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Role of PARP-1 in transcriptional regulation during development

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The role of PARP-1 in estrogen-dependent transcription [ChIP-seq]

Project description:Poly (ADP-ribose) polymerase-1 (PARP-1), a multifunctional chromatin-modulating protein, has gained considerable attention as a target for therapeutic inhibitors in breast cancers. Accumulating evidence suggests a pathological role for PARP-1 in breast cancer through its effects on the transcription of tumor-related genes. Here we report the role of PARP-1 in estrogen-dependent transcription in estrogen receptor alpha (ERα)-positive breast cancers. Global nuclear run-on and sequencing (GRO-seq) analyses suggest that PARP-1 controls the expression of estrogen-regulated genes in ER-positive (ER+) MCF-7 breast cancer cells. Further, ChIP-seq analyses revealed that PARP-1 directly regulates the ligand-dependent binding of ERa and FoxA1 to a subset of its genomic binding sites. Finally, we uncovered that the expression levels of the PARP-1 and estrogen coregulated gene set are enriched in luminal molecular-subtype of breast tumors and high PARP-1 expression in ER+ cases correlates with poor survival. Additionally, treatment with PARP-1 selective inhibitors showed attenuated estrogen-dependent growth of ER+ breast cancer cells. Taken together, the current study suggests that PARP-1 regulates critical molecular pathways that underlie proliferation of ER+ breast cancer cells.

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Role of PARP-1 in transcriptional regulation during development

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

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The role of Dichaete in transcriptional regulation during Drosophila embryonic development

Project description:The role of Dichaete in transcriptional regulation during Drosophila embryonic development

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CDK2-dependent activation of PARP-1 is required for hormonal gene regulation in breast cancer cells.

Project description:Eukaryotic gene regulation implies that transcription factors gain access to genomic information via poorly understood processes involving activation and targeting of kinases, histone-modifying enzymes, and chromatin remodelers to chromatin. Here we report that progestin gene regulation in breast cancer cells requires a rapid and transient increase in poly-(ADP)-ribose (PAR), accompanied by a dramatic decrease of cellular NAD that could have broad implications in cell physiology. This rapid increase in nuclear PARylation is mediated by activation of PAR polymerase PARP-1 as a result of phosphorylation by cyclin-dependent kinase CDK2. Hormone-dependent phosphorylation of PARP-1 by CDK2, within the catalytic domain, enhances its enzymatic capabilities. Activated PARP-1 contributes to the displacement of histone H1 and is essential for regulation of the majority of hormone-responsive genes and for the effect of progestins on cell cycle progression. Both global chromatin immunoprecipitation (ChIP) coupled with deep sequencing (ChIP-seq) and gene expression analysis show a strong overlap between PARP-1 and CDK2. Thus, progestin gene regulation involves a novel signaling pathway that connects CDK2-dependent activation of PARP-1 with histone H1 displacement. Given the multiplicity of PARP targets, this new pathway could be used for the pharmacological management of breast cancer. PARP-1 activation mechanism by CDK2 in response of progestin in breast cancer cells

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Project description:To address the global impact of PARP-1 on alternative splicing, we isolated total RNA in two biological replicates from control (non-treated), PARP-1 siRNA- and PJ-34-treated cells. Sequencing of these RNAs on an Illumina HiSeq 2500, yielded >56 million 100-bp paired-end RNA-seq reads. First we tested if PARP-1 KD was effective at the RNA-seq level. Read aligning to the entire gene body of PARP-1 shown a reduction in PARP-1 expression of about 1.5-fold (P-value < 0.0003), confirming that indeed PARP-1 was depleted after PARP-1 siRNA treatment. We next used these RNA-seq data sets (control, PARP-1 KD and PARylation inhibited) to assess whether these treatments resulted in changes in i) gene expression and ii) alternative splicing.

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