Abstract
RECQ5 belongs to the RecQ family of DNA helicases. It is conserved from Drosophila to humans and its deficiency results in genomic instability and cancer susceptibility in mice. Human RECQ5 is known for its ability to regulate homologous recombination by disrupting RAD51 nucleoprotein filaments. It also binds to RNA polymerase II (RNAPII) and negatively regulates transcript elongation by RNAPII. Here, we summarize recent studies implicating RECQ5 in the prevention and resolution of transcription-replication conflicts, a major intrinsic source of genomic instability during cancer development.
Highlights
RECQ5 belongs to the RecQ family of DNA helicases
Chromatin immunoprecipitation experiments have shown that RECQ5 associates with the coding regions of RNA polymerase II (RNAPII)-transcribed genes in a manner dependent on its SRI motif, with RECQ5 density correlating with the density of Ser2-C-terminal-repeat domain (CTD) phosphorylation, suggesting that RECQ5 binds to the RNAPII
This study demonstrated that RECQ5 depletion causes a marked increase in transcript elongation rates genome-wide, which is accompanied by increased frequency of incidents during which the polymerase is paused or arrested in the transcribed region of genes, a phenomenon termed transcription stress [44]
Summary
Helicases are a diverse group of motor proteins that participate in most aspects of DNA and RNA metabolism. RecQ homologues have been found in all organisms examined to date, including bacteria, yeast, plants, Drosophila, amphibians and mammals [2,3,4]. Inherited mutations in the BLM, WRN and RECQ4 genes are linked to Bloom-, Werner- and Rothmund-Thomson syndrome, respectively [7]. These rare autosomal recessive disorders manifest themselves by genomic instability, premature aging, neurodegenerative and developmental defects as well as cancer predisposition [2,3,7,8]. Recent studies, summarized in this review article, suggest that RECQ5 plays major and unique roles in the prevention and resolution of transcription-replication conflicts (TRCs) in human cells
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