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ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

ABSTRACT: ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

PROVIDER: PRJNA900286 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22258052_1.fastq.gz	Fastqsanger.gz
	SRR22258052_2.fastq.gz	Fastqsanger.gz
	SRR22258053_1.fastq.gz	Fastqsanger.gz
	SRR22258053_2.fastq.gz	Fastqsanger.gz
	SRR22258054_1.fastq.gz	Fastqsanger.gz

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ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

Project description:ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

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ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

Project description:ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

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ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

Project description:In this study, we found that the ARF tumor suppressor directly binds the PAF1 subunit to block the assembly of PAF1 complex (PAF1c) and its interaction with RNAPII, thereby dampening PAF1c-dependent transcription in vitro and in cells. To investigate whether ARF regulates RNAPII and PAF1c occupancy at putative target genes identified through RNA-seq, we performed ChIP-seq (RNAPII, PAF1, and CTR9) in ARF (shARF) vs. control (shNT) knockdown MEFs. Our data show that loss of ARF increases RNAPII, PAF1, and CTR9 occupancy on upregulated genes, consistent with ARF-mediated gene-specific repression. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for RNA polymerase subunit RPB3 and PAF1 complex subunits PAF1 and CTR9 in mouse embryonic fibroblasts.

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ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

Project description:In this study, we found that the ARF tumor suppressor directly binds the PAF1 subunit to block the assembly of PAF1 complex (PAF1c) and its interaction with RNAPII, thereby dampening PAF1c-dependent transcription in vitro and in cells. Using RNA-seq of control (shNT) and ARF knockdown (shARF) mouse embryonic fibroblasts (MEFs) we first define transcriptome changes upon ARF loss. Through downstream mechanistic analysis we then validate direct ARF-mediated inactivation of PAF1c-dependent RNAPII transcription and their cellular consequences.

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ARF alters PAF1 complex integrity to selectively repress oncogenic transcription programs upon p53 loss

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ARF alters PAF1 complex integrity to selectively restrain a pro-growth transcriptional program to tune cell proliferation

Project description:Sample 1, LUM2_920735: GFP:FLAG, as negative control Sample 2, LUM2_920736: ARF:FLAG (untreated) Sample 3, LUM2_920737: ARF:FLAG (with DNase treatment) Sample 4, LUM2_920738: ARF:FLAG (with RNase treatment)

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ARF alters PAF1 complex integrity to selectively restrain a pro-growth transcriptional program to tune cell proliferation

Project description:Sample 1: LUM2_875391: IgG, as negative control Sample 2: LUM2_875392: ARF IP

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Transcription profiling of S. cerevisiae paf1 and ctr9 mutants to identify direct targets of the Paf1/RNA polymerase II complex

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