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LitR是费氏弧菌中的一种新型转录激活因子,可调节发光和共生光器官定殖。

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

作者信息

Fidopiastis Pat M, Miyamoto Carol M, Jobling Michael G, Meighen Edward A, Ruby Edward G

机构信息

Pacific Biomedical Research Center, University of Hawai'i, Honolulu, 96813, USA.

出版信息

Mol Microbiol. 2002 Jul;45(1):131-43. doi: 10.1046/j.1365-2958.2002.02996.x.

Abstract

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.

摘要

费氏弧菌是乌贼(Euprymna scolopes)发光器官内的细菌共生体。在定殖于幼年乌贼后,细菌共生体利用宿主提供的营养物质生长,同时提供生物发光,宿主在夜间活动时会利用这种生物发光。已证明无法发光的突变细菌菌株在正常定殖方面存在缺陷。从费氏弧菌中克隆出一个606 bp的开放阅读框,它编码一种蛋白质,我们将其命名为LitR,该蛋白质与四种相关调节蛋白:霍乱弧菌HapR、哈氏弧菌LuxR、副溶血性弧菌OpaR和创伤弧菌SmcR具有约60%的同一性。在培养过程中,litR被插入失活的费氏弧菌菌株PMF8的细胞在发光诱导开始时延迟,并且每个细胞发出的光仅为其亲本的约20%。蛋白质结合研究表明,LitR通过调节luxR基因的转录来增强群体感应。有趣的是,当在混合接种物中与其亲本竞争时,PMF8成为83%的发光器官中存在的主要共生体。因此,litR突变似乎代表了一类新的突变,其中调节基因功能的丧失增强了细菌引发良性感染的能力。

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