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Rad53 regulates RNase H1, which promotes DNA replication through sites of transcription-replication conflict.
Cell Rep. 44:116565 (2025)
RNA-DNA hybrids and R-loops can lead to extensive DNA damage and loss of genomic integrity if not regulated in a timely manner. Although RNase H1 overexpression is frequently used as a tool to resolve R-loops, the regulation of RNase H1, overexpressed or endogenous, remains poorly characterized. We reveal that in yeast, overexpressed RNase H1 (RNH1) has no effect on gene expression, cell growth, or RNA-DNA hybrid resolution in wild-type cells. Overexpressed RNase H1 does, however, remove RNA-DNA hybrids in mutants where hybrids have become dysregulated. Endogenous RNase H1 becomes up-regulated and chromatin-associated in the absence of Sen1 in a DNA replication checkpoint-dependent manner. Rnh1 gets recruited to genomic loci where RNA-DNA hybrids accumulate following the loss of Sen1. Rnh1, together with Sen1, promotes DNA replication at sites of transcription-replication conflict. Hence, RNase H1, overexpressed or endogenous, responds to unscheduled, stress-inducing RNA-DNA hybrids.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Cp: Molecular Biology ; R-loop ; Rna-dna Hybrid ; Rnase H1 ; Rnh1 ; Sen1 ; Senataxin
ISSN (print) / ISBN
2211-1247
e-ISSN
2211-1247
Journal
Cell Reports
Quellenangaben
Volume: 44,
Issue: 11,
Article Number: 116565
Publisher
Cell Press
Reviewing status
Peer reviewed
Institute(s)
Institute of Epigenetics and Stem Cells (IES)