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ChIP-seq data of prefoldin subunit PFDN5 in HCT116 human colon carcinoma cells

ABSTRACT: ChIP-seq data of prefoldin subunit PFDN5 in HCT116 human colon carcinoma cells

PROVIDER: PRJNA719741 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14142355_1.fastq.gz	Fastqsanger.gz
	SRR14142355_2.fastq.gz	Fastqsanger.gz
	SRR14142356_1.fastq.gz	Fastqsanger.gz
	SRR14142356_2.fastq.gz	Fastqsanger.gz
	SRR14142357_1.fastq.gz	Fastqsanger.gz

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RNA-seq data of prefoldin subunits PFDN2 and PFDN5 knockdowns in HCT116 human colon carcinoma cells

Project description:We report gene expression data from total RNA-seq of HCT116 human colon carcinoma cells treated with siRNA against PFDN2 and PFDN5 (both part of a complex known as prefoldin). Cells were independently treated with one of the previously mentioned siRNAs or with an exogenous control siRNA (luciferase GL2). All cells were treated with the different siRNAs for 24 hours, then serum-starved them for 48 hours, and finally stimulated by adding serum for 90 minutes. Samples were taken before and after serum stimulation. Prefoldin depletion provoked transcriptional alterations across the genome of human cells. Severe pre-mRNA splicing defects were also detected, particularly under serum stimulation conditions. We found a significant impairment of co-transcriptional splicing during transcription elongation.

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ChIP-seq data of prefoldin subunit PFDN5 in HCT116 human colon carcinoma cells

Project description:Prefoldin is a heterohexameric complex conserved from archaea to humans that plays a cochaperone role during the co-translational folding of actin and tubulin monomers. Additional functions of prefoldin in the cell nucleus have been described, including a positive contribution to transcription elongation and chromatin dynamics in yeast. Here we show that prefoldin perturbations provoked transcriptional alterations across the genome of human cells. We detected genome-wide prefoldin binding to transcribed genes and found that this binding negatively correlate with the impact of prefoldin depletion on gene expression. Moreover, lack of prefoldin caused significant global decrease in the levels of Ser2 and Ser5 phosphorylation of the RNA polymerase II carboxy-terminal domain (CTD). Altogether the reported results indicate that human prefoldin is able to act locally on the genome to modulate gene expression by influencing phosphorylation of elongating RNA polymerase II, and thereby regulating co-transcriptional splicing.

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