ArticleBMC molecular biology2018
Positive cofactor 4 (PC4) contributes to the regulation of replication-dependent canonical histone gene expression.
Article in BMC molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Novel function of U7 snRNA in the repression of HERV1/LTR12s and lincRNAs in human cells.Nucleic acids research · 2024Article
- Modulatory role of RNA helicases in MBNL-dependent alternative splicing regulation.Cellular and molecular life sciences : CMLS · 2023Article
- Molecular Mechanisms of Functional Modulation of Transcriptional Coactivator PC4 via Phosphorylation on Its Intrinsically Disordered Region.ACS omega · 2023Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
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Abstract
backgroundCore canonical histones are required in the S phase of the cell cycle to pack newly synthetized DNA, therefore the expression of their genes is highly activated during DNA replication. In mammalian cells, this increment is achieved by both enhanced transcription and 3' end processing. In this paper, we described positive cofactor 4 (PC4) as a protein that contributes to the regulation of replication-dependent histone gene expression.
resultsWe showed that PC4 influences RNA polymerase II recruitment to histone gene loci in a cell cycle-dependent manner. The most important effect was observed in S phase where PC4 knockdown leads to the elevated level of RNA polymerase II on histone genes, which corresponds to the increased total level of those gene transcripts. The opposite effect was caused by PC4 overexpression. Moreover, we found that PC4 has a negative effect on the unique 3' end processing of histone pre-mRNAs that can be based on the interaction of PC4 with U7 snRNP and CstF64. Interestingly, this effect does not depend on the cell cycle.
conclusionsWe conclude that PC4 might repress RNA polymerase II recruitment and transcription of replication-dependent histone genes in order to maintain the very delicate balance between histone gene expression and DNA synthesis. It guards the cell from excess of histones in S phase. Moreover, PC4 might promote the interaction of cleavage and polyadenylation complex with histone pre-mRNAs, that might impede with the recruitment of histone cleavage complex. This in turn decreases the 3' end processing efficiency of histone gene transcripts.
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