Department of Microbiology, Ohio State University, 484 West 12th Ave., 376 Biological Sciences Building, Columbus, OH 43210, USA.
J Bacteriol. 2010 Jan;192(1):29-37. doi: 10.1128/JB.01139-09.
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.
LuxR 型转录因子可检测酰基高丝氨酸内酯 (AHL)，通常用于细菌来判断自身物种的种群密度。大肠杆菌和肠炎沙门氏菌不能合成 AHL，但可以通过 LuxR 同源物 SdiA 来检测其他细菌物种产生的 AHL。以前我们确定，鼠伤寒沙门氏菌在通过豚鼠、兔、牛、5 只老鼠、6 只猪或 12 只鸡的胃肠道转运时不会检测到 AHL。然而，SdiA 在通过定植于嗜水气单胞菌的龟类的肠道转运时被激活，这导致了一个假设，即 SdiA 用于检测其他病原体的 AHL 产生。在本报告中，我们确定 SdiA 在鼠伤寒沙门氏菌通过产生 AHL 的病原体耶尔森氏菌感染的老鼠体内转运时被激活。SdiA 在通过无法合成 AHL 的耶尔森氏菌 yenI 突变体感染的老鼠体内转运时不会被激活。然而，SdiA 的激活并没有赋予沙门氏菌在感染耶尔森氏菌的老鼠中更好的适应性。我们假设这是由于鼠伤寒沙门氏菌和耶尔森氏菌之间的相互作用很少或很短，或者 SdiA 调控基因成员在老鼠中不起作用。为了验证这些假设，我们构建了一个合成 AHL 的鼠伤寒沙门氏菌菌株，以模拟与耶尔森氏菌的持续相互作用。在这种背景下，sdiA(+)鼠伤寒沙门氏菌在老鼠中迅速取代 sdiA 突变体。sdiA 调控基因座的所有已知成员都需要这种表型。因此，sdiA 调控基因座的所有成员在老鼠中都具有功能。
