Baharoglu Zeynep, Mazel Didier
Institut Pasteur, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, 25 rue du docteur Roux, 75015 Paris, France; CNRS, UMR3525, Paris, France.
Institut Pasteur, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, 25 rue du docteur Roux, 75015 Paris, France; CNRS, UMR3525, Paris, France.
Res Microbiol. 2014 Jul-Aug;165(6):476-80. doi: 10.1016/j.resmic.2014.05.039. Epub 2014 Jun 16.
Low concentrations of aminoglycosides induce the SOS response in Vibrio cholerae but not in Escherichia coli. In order to determine whether a specific factor present in E. coli prevents this induction, we developed a genetic screen where only SOS inducing mutants are viable. We identified the vsr gene coding for the Vsr protein of the very short patch mismatch repair (VSPR) pathway. The effect of mismatch repair (MMR) mutants was also studied. We propose that lesions formed upon aminoglycoside treatment are preferentially repaired by VSPR without SOS induction in E. coli and by MMR when VSPR is impaired.
低浓度的氨基糖苷类药物可诱导霍乱弧菌的SOS反应，但不能诱导大肠杆菌的SOS反应。为了确定大肠杆菌中存在的特定因子是否能阻止这种诱导，我们开发了一种遗传筛选方法，只有SOS诱导突变体才能存活。我们鉴定出了编码极短补丁错配修复（VSPR）途径中Vsr蛋白的vsr基因。我们还研究了错配修复（MMR）突变体的作用。我们提出，氨基糖苷类药物处理后形成的损伤在大肠杆菌中优先由VSPR修复而不诱导SOS反应，而当VSPR受损时则由MMR修复。
