
Significance DNA polymerases frequently incorporate ribonucleotides in place of deoxyribonucleotides during genome replication. RNase HII is responsible for initiating the removal of ribonucleotide errors across all three domains of life. Ribonucleotides that persist in genomic DNA due to defects in RNase HII result in strand breaks, mutagenesis, and neurodevelopmental disease in humans. Here, we define the proteins important for ribonucleotide excision repair in Bacillus subtilis and use genome-wide mutational profiling to determine the mutagenic cost of ribonucleotides in RNase HII-deficient cells. We show that the absence of RNase HII yields error-prone ribonucleotide correction via a pathway that relies on an essential DNA polymerase. We further demonstrate that error-prone ribonucleotide removal causes sequence context-dependent GC → AT transitions on the lagging strand.
DNA, Bacterial, Bacterial Proteins, Base Sequence, Mutagenesis, Mutation, Ribonuclease H, Gene Expression Regulation, Bacterial, Biological Sciences, Ribonucleotides, DNA Polymerase I, Models, Biological, Gene Expression Regulation, Enzymologic, Bacillus subtilis
DNA, Bacterial, Bacterial Proteins, Base Sequence, Mutagenesis, Mutation, Ribonuclease H, Gene Expression Regulation, Bacterial, Biological Sciences, Ribonucleotides, DNA Polymerase I, Models, Biological, Gene Expression Regulation, Enzymologic, Bacillus subtilis
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