Casanueva Ana I, Paul Lynthia, Patrick Sheila, Abratt Valerie R
FEMS Microbiol Lett. 2008 Jan;278(2):249-56. doi: 10.1111/j.1574-6968.2007.01004.x.
A putative transcriptional regulator of the AraC/XylS family was identified in a genomic genebank of Bacteroides fragilis Bf-1, which partially relieved the sensitivity of Escherichia coli DNA repair mutants to the DNA-damaging agents, metronidazole and mitomycin C. A homologue of this gene with the same phenotype was identified as BF638R3281 in B. fragilis 638R. Transcription of BF638R3281 was constitutive with respect to exposure to sublethal doses of metronidazole. BF638R3281 was interrupted by single cross-over gene-specific insertion mutation, and the gene disruption was confirmed by PCR and DNA-sequencing analysis. The mutant grew more slowly than the wild type, and the mutation rendered B. fragilis more sensitive to metronidazole and mitomycin C. This indicates that the BF638R3281 gene product plays a role in the survival of B. fragilis following DNA damage by these agents.
在脆弱拟杆菌Bf-1的基因组文库中鉴定出一种推定的AraC/XylS家族转录调节因子,该调节因子可部分缓解大肠杆菌DNA修复突变体对DNA损伤剂甲硝唑和丝裂霉素C的敏感性。在脆弱拟杆菌638R中,具有相同表型的该基因的同源物被鉴定为BF638R3281。BF638R3281的转录对于亚致死剂量甲硝唑的暴露是组成型的。通过单交换基因特异性插入突变中断了BF638R3281,并通过PCR和DNA测序分析证实了基因破坏。该突变体的生长比野生型慢,并且该突变使脆弱拟杆菌对甲硝唑和丝裂霉素C更敏感。这表明BF638R3281基因产物在这些试剂造成DNA损伤后脆弱拟杆菌的存活中起作用。