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Transcriptome of TNF-a-treated and untreated HeLa cells before and after TFIIB knockdown

ABSTRACT: Transcriptome of TNF-a-treated and untreated HeLa cells before and after TFIIB knockdown

PROVIDER: PRJNA414971 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6189790.fastq.gz	Fastqsanger.gz
	SRR6189781.fastq.gz	Fastqsanger.gz
	SRR6189791.fastq.gz	Fastqsanger.gz
	SRR6189782.fastq.gz	Fastqsanger.gz
	SRR6189792.fastq.gz	Fastqsanger.gz

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Transcriptome of TNF-a-treated and untreated HeLa cells before and after TFIIB knockdown

Project description:The goal of this study was to compare transcriptome of HeLa cells with or without TFIIB knockdown for gene expression changes in steady state or after TNF-a treatment. Although a broad effect on gene expression would be anticipated, TFIIB depletion led only to an altered expression of a limited number of genes.

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Project description:Experimental and bioinformatic studies of transcription initiation by RNA polymerase II (RNAP2) have revealed a mechanism of RNAP2 transcription initiation less uniform across gene promoters than initially thought. However, the general transcription factor TFIIB is presumed to be universally required for RNAP2 transcription initiation. Based on bioinformatic analysis of data, TFIIB knockdown in primary and transformed cell lines, and in vitro transcription experiments, we report that TFIIB is dispensable for transcription of most human promoters, but is essential for HSV-1 gene transcription and replication. We report a novel cell cycle TFIIB regulation and involvement of the acetylated TFIIB variant in chromosomal condensation. Taken together, these results establish a new paradigm for TFIIB functionality as a determinant of the human transcriptome, which when downregulated has potent anti-viral effects.

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Protein interaction network revealed by quantitative proteomic analysis elucidates TFIIB role in multiple aspects of the transcription cycle

Project description:Although TFIIB is widely regarded as an initiation factor, recent reports have implicated it in multiple aspects of eukaryotic transcription. To investigate the broader role of TFIIB in transcription, we performed quantitative proteomic analysis of yeast TFIIB. We purified two different populations of TFIIB; one form soluble cell lysate, which is not engaged in transcription, and the other from chromatin fraction which yields the transcriptionally active form of the protein. TFIIB purified from the chromatin exhibits several interactions that explain its non-canonical roles in transcription. RNAPII, TFIIF and TFIIH were the only components of preinitiation complex with a significant presence in chromatin TFIIB. A notable feature was the substantial enrichment of all 3’ end processing-termination factors; CF1, CPF and Rat1 in chromatin-TFIIB preparation. These results corroborate the role of TFIIB in termination of transcription. Presence of the Lsm complex as well as TREX complex subunit Sub2 in chromatin-TFIIB opens the possibility of novel roles of TFIIB in synthesis-decay coupling and nucleocytoplasmic transport of mRNA. This multiplicity of functions may contribute to the preferential targeting of TFIIB during viral pathogenesis

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