PuSH - Publication Server of Helmholtz Zentrum München: Rad53 regulates RNase H1, which promotes DNA replication through sites of transcription-replication conflict.

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Wagner, C.B.* ; Longaretti, M.* ; Sergi, S.G.* ; Singh, N.* ; Tsirkas, I. ; Bento, F.* ; Wong, R.P.* ; Wilkens, M.* ; Hamperl, S. ; Butter, F.* ; Aharoni, A.* ; Ulrich, H.D.* ; Luke, B.*

Rad53 regulates RNase H1, which promotes DNA replication through sites of transcription-replication conflict.

Cell Rep. 44:116565 (2025)

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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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