Atypical Role for PhoU in Mutagenic Break Repair under Stress in Escherichia coli

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Atypical Role for PhoU in Mutagenic Break Repair under Stress in Escherichia coli

Mechanisms of mutagenesis activated by stress responses drive pathogen/host adaptation, antibiotic and anti-fungal-drug resistance, and perhaps much of evolution generally. In Escherichia coli, repair of double-strand breaks (DSBs) by homologous recombination is high fidelity in unstressed cells, but switches to a mutagenic mode using error-prone DNA polymerases when the both the SOS and genera...

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The mutagenicity of DNA double-strand break repair in Escherichia coli is controlled by DNA-damage (SOS) and general (RpoS) stress responses, which let error-prone DNA polymerases participate, potentially accelerating evolution during stress. Either base substitutions and indels or genome rearrangements result. Here we discovered that most small basic proteins that compact the genome, nucleoid-...

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Persistent damaged bases in DNA allow mutagenic break repair in Escherichia coli

Bacteria, yeast and human cancer cells possess mechanisms of mutagenesis upregulated by stress responses. Stress-inducible mutagenesis potentially accelerates adaptation, and may provide important models for mutagenesis that drives cancers, host pathogen interactions, antibiotic resistance and possibly much of evolution generally. In Escherichia coli repair of double-strand breaks (DSBs) become...

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ژورنال

عنوان ژورنال: PLOS ONE

سال: 2015

ISSN: 1932-6203

DOI: 10.1371/journal.pone.0123315