LitR, a new transcriptional activator in Vibrio fischeri, regulates luminescence and symbiotic light organ colonization

被引:102
作者
Fidopiastis, PM
Miyamoto, CM
Jobling, MG
Meighen, EA
Ruby, EG
机构
[1] Univ Hawaii Manoa, Pacific Biomed Res Ctr, Honolulu, HI 96813 USA
[2] McGill Univ, Dept Biochem, Montreal, PQ H3G 1Y6, Canada
[3] Univ Colorado, Hlth Sci Ctr, Dept Microbiol, Denver, CO 80262 USA
关键词
D O I
10.1046/j.1365-2958.2002.02996.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Vibrio fischeri is the bacterial symbiont within the light-emitting organ of the sepiolid squid Euprymna scolopes. Upon colonizing juvenile squids, bacterial symbionts grow on host-supplied nutrients, while providing a bioluminescence that the host uses during its nocturnal activities. Mutant bacterial strains that are unable to emit light have been shown to be defective in normal colonization. A 606 bp open reading frame was cloned from V. fischeri that encoded a protein, which we named LitR, that had about 60% identity to four related regulator proteins: Vibrio cholerae HapR, Vibrio harveyi LuxR, Vibrio parahaemolyticus OpaR and Vibrio vulnificus SmcR. When grown in culture, cells of V. fischeri strain PMF8, in which litR was insertionally inactivated, were delayed in the onset of luminescence induction and emitted only about 20% as much light per cell as its parent. Protein-binding studies suggested that LitR enhances quorum sensing by regulating the transcription of the luxR gene. Interestingly, when competed against its parent in mixed inocula, PMF8 became the predominant symbiont present in 83% of light organs. Thus, the litR mutation appears to represent a novel class of mutations in which the loss of a regulatory gene function enhances the bacterium's competence in initiating a benign infection.
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页码:131 / 143
页数:13
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