Replication mutations differentially enhance RecA-dependent and RecA-independent recombination between tandem repeats in Bacillus subtilis

• Published in: Molecular microbiology Vol. 39; no. 5; pp. 1248 - 1258
• Main Authors: Bruand, C, Bidnenko, V, Ehrlich, S D
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.03.2001; Wiley
• Subjects: Bacillus subtilis; Bacillus subtilis - drug effects; Bacillus subtilis - genetics; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; DNA Replication - genetics; DnaB protein; DnaG protein; DnaN protein; Gene Deletion; Gene Expression Regulation, Bacterial; Kanamycin Resistance - genetics; Life Sciences; Microbiology and Parasitology; Mutation; Rec A Recombinases - genetics; Rec A Recombinases - metabolism; Recombination, Genetic - genetics; Tandem Repeat Sequences - genetics; ADN POLYMERASE
• ISSN: 0950-382X; 1365-2958
• DOI: 10.1046/j.1365-2958.2001.02312.x

We have studied DNA recombination between 513 bp tandem direct repeats present in a kanamycin resistance gene inserted in the Bacillus subtilis chromosome. Tandem repeat deletion was not significantly affected by a recA mutation. However, recombination was stimulated by mutations in genes encoding replication proteins, including the primosomal proteins DnaB, DnaD and the DnaG primase, the putative DNA polymerase III subunits PolC, DnaN and DnaX, as well as the DNA polymerase DnaE. Hyper-recombination was found to be dependent on RecA in the dnaE, dnaN and dnaX mutants, whereas the dnaG and dnaD mutants stimulated recombination independently of RecA. Altogether, these data show that both RecA-dependent and RecA-independent mechanisms contribute to recombination between tandem repeats in B. subtilis and that both types of recombination are stimulated by replication mutations.