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Replication arrest is a major threat to growth at low temperature in A ntarctic P seudomonas syringae Lz 4 W
Author(s) -
Sinha Anurag K.,
Pavankumar Theetha L.,
Kamisetty Srinivasulu,
Mittal Pragya,
Ray Malay K.
Publication year - 2013
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/mmi.12315
Subject(s) - recbcd , biology , homologous recombination , pseudomonas syringae , mutant , rad51 , dna replication , dna repair , nuclease , dna , microbiology and biotechnology , holliday junction , dna damage , genetics , gene
Summary Chromosomal damage was detected previously in the recBCD mutants of the A ntarctic bacterium P seudomonas syringae Lz 4 W , which accumulated linear chromosomal DNA leading to cell death and growth inhibition at 4° C . RecBCD protein generally repairs DNA double‐strand breaks by RecA ‐dependent homologous recombination pathway. Here we show that Δ recA mutant of P . syringae is not cold‐sensitive. Significantly, inactivation of additional DNA repair genes ruvAB rescued the cold‐sensitive phenotype of Δ recBCD mutant. The Δ recA and Δ ruvAB mutants were UV ‐sensitive as expected. We propose that, at low temperature DNA replication encounters barriers leading to frequent replication fork ( RF ) arrest and fork reversal. RuvAB binds to the reversed RFs ( RRFs ) having H olliday junction‐like structures and resolves them upon association with RuvC nuclease to cause linearization of the chromosome, a threat to cell survival. RecBCD prevents this by degrading the RRFs , and facilitates replication re‐initiation. This model is consistent with our observation that low temperature‐induced DNA lesions do not evoke SOS response in P . syringae . Additional studies show that two other repair genes, radA (encoding a RecA paralogue) and recF are not involved in providing cold resistance to the A ntarctic bacterium.