Replication arrest is a major threat to growth at low temperature in A ntarctic P seudomonas syringae   Lz 4 W

• Published in: Molecular microbiology 2013-08, Vol.89 (4), p.792-810
• Main Authors: Sinha, Anurag K., Pavankumar, Theetha L., Kamisetty, Srinivasulu, Mittal, Pragya, Ray, Malay K.
• Format: Article
• Language: English
• ISSN: 0950-382X; 1365-2958
• DOI: 10.1111/mmi.12315

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.