The regulatory function of LexA is temperature-dependent in the deep-sea bacterium Shewanella piezotolerans WP3
نویسندگان
چکیده
The SOS response addresses DNA lesions and is conserved in the bacterial domain. The response is governed by the DNA binding protein LexA, which has been characterized in model microorganisms such as Escherichia coli. However, our understanding of its roles in deep-sea bacteria is limited. Here, the influence of LexA on the phenotype and gene transcription of Shewanella piezotolerans WP3 (WP3) was investigated by constructing a lexA deletion strain (WP3ΔlexA), which was compared with the wild-type strain. No growth defect was observed for WP3ΔlexA. A total of 481 and 108 genes were differentially expressed at 20 and 4°C, respectively, as demonstrated by comparative whole genome microarray analysis. Furthermore, the swarming motility and dimethylsulfoxide reduction assay demonstrated that the function of LexA was related to temperature. The transcription of the lexA gene was up-regulated during cold acclimatization and after cold shock, indicating that the higher expression level of LexA at low temperatures may be responsible for its temperature-dependent functions. The deep-sea microorganism S. piezotolerans WP3 is the only bacterial species whose SOS regulator has been demonstrated to be significantly influenced by environmental temperatures to date. Our data support the hypothesis that SOS is a formidable strategy used by bacteria against various environmental stresses.
منابع مشابه
Microarray analysis of lexA gene deletion mutant of deep-sea bacterium Shewanella piezotolerans WP3 at low-temperature and high-pressure
Addressing DNA lesion, the SOS response is conserved in bacterial domain and governed by DNA binding protein LexA, which have been well characterized in model microorganism such as Escherichia coli. However, our understanding of the roles of SOS pathway in deep-sea bacteria is limited. To indentify the composition of SOS regulon and function of LexA, we performed whole genome transcriptional pr...
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عنوان ژورنال:
دوره 6 شماره
صفحات -
تاریخ انتشار 2015