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DNA polymerase I acts in translesion synthesis mediated by the Y‐polymerases in Bacillus subtilis
Author(s) -
Duigou Stéphane,
Ehrlich S. Dusko,
Noirot Philippe,
NoirotGros MarieFrançoise
Publication year - 2005
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2005.04725.x
Subject(s) - dna polymerase , biology , dna polymerase ii , polymerase , dna polymerase mu , dna polymerase delta , dna clamp , dna replication , processivity , microbiology and biotechnology , genetics , dna , circular bacterial chromosome , polymerase chain reaction , gene , reverse transcriptase
Summary Translesion synthesis (TLS) across damaged DNA bases is most often carried out by the ubiquitous error‐prone DNA polymerases of the Y‐family. Bacillus subtilis encodes two Y‐polymerases, Pol Y1 and Pol Y2, that mediate TLS resulting in spontaneous and ultraviolet light (UV)‐induced mutagenesis respectively. Here we show that TLS is a bipartite dual polymerase process in B. subtilis , involving not only the Y‐polymerases but also the A‐family polymerase, DNA polymerase I (Pol I). Both the spontaneous and the UV‐induced mutagenesis are abolished in Pol I mutants affected solely in the polymerase catalytic site. Physical interactions between Pol I and either of the Pol Y polymerases, as well as formation of a ternary complex between Pol Y1, Pol I and the β‐clamp, were detected by yeast two‐ and three‐hybrid assays, supporting the model of a functional coupling between the A‐ and Y‐family polymerases in TLS. We suggest that the Pol Y carries the synthesis across the lesion, and Pol I takes over to extend the synthesis until the functional replisome resumes replication. This key role of Pol I in TLS uncovers a new function of the A‐family DNA polymerases.