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Salmonella enterica Serovar Typhimurium Can Detect Acyl Homoserine Lactone Production by Yersinia enterocolitica in Mice▿

机译:鼠伤寒沙门氏菌鼠伤寒沙门氏菌可以检测鼠小肠结肠炎耶尔森氏菌产生的酰基高丝氨酸内酯

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摘要

LuxR-type transcription factors detect acyl homoserine lactones (AHLs) and are typically used by bacteria to determine the population density of their own species. Escherichia coli and Salmonella enterica serovar Typhimurium cannot synthesize AHLs but can detect the AHLs produced by other bacterial species using the LuxR homolog, SdiA. Previously we determined that S. Typhimurium did not detect AHLs during transit through the gastrointestinal tract of a guinea pig, a rabbit, a cow, 5 mice, 6 pigs, or 12 chickens. However, SdiA was activated during transit through turtles colonized by Aeromonas hydrophila, leading to the hypothesis that SdiA is used for detecting the AHL production of other pathogens. In this report, we determined that SdiA is activated during the transit of S. Typhimurium through mice infected with the AHL-producing pathogen Yersinia enterocolitica. SdiA is not activated during transit through mice infected with a yenI mutant of Y. enterocolitica that cannot synthesize AHLs. However, activation of SdiA did not confer a fitness advantage in Yersinia-infected mice. We hypothesized that this is due to infrequent or short interactions between S. Typhimurium and Y. enterocolitica or that the SdiA regulon members do not function in mice. To test these hypotheses, we constructed an S. Typhimurium strain that synthesizes AHLs to mimic a constant interaction with Y. enterocolitica. In this background, sdiA+ S. Typhimurium rapidly outcompetes the sdiA mutant in mice. All known members of the sdiA regulon are required for this phenotype. Thus, all members of the sdiA regulon are functional in mice.
机译:LuxR型转录因子可检测酰基高丝氨酸内酯(AHL),通常被细菌用于确定其自身物种的种群密度。大肠埃希菌和鼠伤寒沙门氏菌不能合成AHL,但可以使用LuxR同源物SdiA检测其他细菌产生的AHL。以前,我们确定鼠伤寒沙门氏菌在通过豚鼠,兔子,母牛,5只小鼠,6头猪或12只鸡的胃肠道运输过程中未检测到AHL。然而,SdiA在通过嗜水气单胞菌定居的海龟的转运过程中被激活,导致了这样一个假设,即SdiA用于检测其他病原体的AHL产生。在此报告中,我们确定在鼠伤寒沙门氏菌通过感染了AHL的病原性小肠结肠炎耶尔森氏菌感染的小鼠的过程中,SdiA被激活。 SdiA在通过感染不能合成AHL的小肠结肠炎耶尔森氏菌YI突变体感染的小鼠的过程中未激活。但是,SdiA的激活并未在感染耶尔森氏菌的小鼠中赋予健身优势。我们假设这是由于鼠伤寒沙门氏菌和小肠结肠炎耶尔森菌之间很少或短暂的相互作用,或者是SdiA调节子成员在小鼠中不起作用。为了检验这些假设,我们构建了鼠伤寒沙门氏菌菌株,该菌株合成AHL来模拟与小肠结肠炎耶尔森氏菌的持续相互作用。在这种背景下,sdiA +鼠伤寒沙门氏菌在小鼠中迅速胜过sdiA突变体。该表型需要sdiA regulon的所有已知成员。因此,sdiA regulon的所有成员都在小鼠中起作用。

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