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黏质沙雷氏菌的侵袭受编码AHL合酶的sprI基因调控。

Invasion of Serratia proteamaculans is regulated by the sprI gene encoding AHL synthase.

作者信息

Tsaplina Olga, Khmel Inessa, Zaitseva Yulia, Khaitlina Sofia

机构信息

Institute of Cytology, RAS, St Petersburg, Russia.

Institute of Molecular Genetics of National Research Center "Kurchatov Institute", RAS, Moscow, Russia.

出版信息

Microbes Infect. 2021 Nov-Dec;23(9-10):104852. doi: 10.1016/j.micinf.2021.104852. Epub 2021 Jun 29.

DOI:10.1016/j.micinf.2021.104852
PMID:34197907
Abstract

Quorum Sensing (QS) system regulates gene expression in response to a change in the density of the bacterial population. Facultative pathogen Serratia proteamaculans 94 has a LuxI/LuxR type QS system consisting of regulatory protein SprR and AHL synthase SprI. Invasive activity of these bacteria appears at the stationary growth phase corresponding to a maximal density of the bacterial population in vitro. To evaluate the contribution of QS system of S. proteamaculans 94 to the regulation of invasive activity, in this work, S. proteamaculans SprI(-) mutant carrying the inactivated AHL synthase gene was used. Inactivation of the AHL synthase sprI gene resulted in a more than fourfold increase in the invasive activity of S. proteamaculans preceded by the increased adhesion of bacteria to the cell surface. This effect correlated with the increased expression of the outer membrane protein ompX gene and the decrease in the activity of intrabacterial protease protealysin, whose substrate is OmpX. The inverse correlation between activity of protealysin and bacterial invasion was also observed in the model experiments under the iron-limiting culture conditions. These results show that QS system regulates the S. proteamaculans invasion. This regulation can involve changes both in the protealysin activity and in the level of the ompX gene transcription.

摘要

群体感应(QS)系统根据细菌群体密度的变化来调节基因表达。兼性病原菌粘质沙雷氏菌94具有一种LuxI/LuxR型QS系统,由调节蛋白SprR和AHL合酶SprI组成。这些细菌的侵袭活性出现在体外对应于细菌群体最大密度的稳定生长期。为了评估粘质沙雷氏菌94的QS系统对侵袭活性调节的贡献,在本研究中,使用了携带失活AHL合酶基因的粘质沙雷氏菌SprI(-)突变体。AHL合酶sprI基因的失活导致粘质沙雷氏菌的侵袭活性增加了四倍多,之前细菌对细胞表面的粘附也有所增加。这种效应与外膜蛋白ompX基因表达的增加以及细菌内蛋白酶蛋白酶溶素活性的降低相关,蛋白酶溶素的底物是OmpX。在铁限制培养条件下的模型实验中也观察到了蛋白酶溶素活性与细菌侵袭之间的负相关。这些结果表明,QS系统调节粘质沙雷氏菌的侵袭。这种调节可能涉及蛋白酶溶素活性和ompX基因转录水平的变化。

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