SOS involvement in stress-inducible biofilm formation.
SOS involvement in stress-inducible biofilm formation.
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DOI：
10.1080/08927014.2010.501895
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发表时间：
2010-07-01
期刊：
影响因子：
2.7
通讯作者：
Weitao, T
中科院分区：
文献类型：
--
作者：
Gotoh, H;Kasaraneni, N;Weitao, T
抗菌剂和DNA损伤剂可以诱导细菌生物膜的形成。这些试剂触发SOS反应，其中SOS传感器RecA刺激阻遏物莱克萨的自动切割。这些观察结果导致一个假设的压力诱导的生物膜形成和RecA-LexA相互作用之间的连接。为了检验这一假设，进行了三种生物膜测定，即标准96孔测定、共聚焦激光扫描显微镜和新开发的生物膜纸测定。结果发现，由DNA复制抑制剂羟基脲的生物膜刺激依赖于RecA，并且似乎被铜绿假单胞菌的不可切割的莱克萨抑制。令人惊讶的是，缺失莱克萨导致正常和应激诱导的生物膜形成减少，表明野生型莱克萨有助于生物膜形成。这种下降不是突变体生长不良的结果。这些结果表明SOS参与了羟基脲诱导的生物膜形成。此外，通过纸生物膜测定，发现DNA酶I对生物膜基质DNA的降解似乎使生物膜对复制抑制剂敏感。令人困惑的问题有关的作用莱克萨在DNA释放的生物膜的背景下进行了讨论。
Bacterial biofilm formation can be induced by antimicrobial and DNA damage agents. These agents trigger the SOS response, in which SOS sensor RecA stimulates auto-cleavage of repressor LexA. These observations lead to a hypothesis of a connection between stress-inducible biofilm formation and the RecA-LexA interplay. To test this hypothesis, three biofilm assays were conducted, viz. the standard 96-well assay, confocal laser scanning microscopy, and the newly developed biofilm-on-paper assay. It was found that biofilm stimulation by the DNA replication inhibitor hydroxyurea was dependent on RecA and appeared repressed by the non-cleavable LexA of Pseudomonas aeruginosa. Surprisingly, deletion of lexA led to reduction of both normal and stress-inducible biofilm formation, suggesting that the wild-type LexA contributes to biofilm formation. The decreases was not the result of poor growth of the mutants. These results suggest SOS involvement in hydroxyurea-inducible biofilm formation. In addition, with the paper biofilm assay, it was found that degradation of the biofilm matrix DNA by DNase I appeared to render the biofilms susceptible to the replication inhibitor. The puzzling questions concerning the roles of LexA in DNA release in the biofilm context are discussed.