Open AccessA1S_2811, a CheA/Y‐like hybrid two‐component regulator from Acinetobacter baumannii ATCC 17978, is involved in surface motility and biofilm formation in this bacterium
Author(s) -
Chen Rong,
Lv Ruichen,
Xiao Lisheng,
Wang Min,
Du Zongmin,
Tan Yafang,
Cui Yujun,
Yan Yanfeng,
Luo Yanping,
Yang Ruifu,
Song Yajun
Publication year - 2017
Publication title -
microbiologyopen
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.881
H-Index - 36
ISSN - 2045-8827
DOI - 10.1002/mbo3.510
Subject(s) - biofilm , two component regulatory system , operon , motility , mutant , pilus , response regulator , chemistry , quorum sensing , histidine kinase , swarming motility , acinetobacter baumannii , regulator , microbiology and biotechnology , bacteria , virulence , gene , biochemistry , biology , pseudomonas aeruginosa , genetics
Two‐component systems in Acinetobacter baumannii are associated with its virulence, drug resistance, motility, biofilm formation, and other characteristics. In this study, we used Rec Ab , a genetic engineering method, to investigate the function of A1S_2811 in A. baumannii strain ATCC 17978. A1S_2811, a hypothetical hybrid sensor histidine kinase/response regulator, has four histidine‐containing phosphotransfer domains, a CheA‐like regulatory domain, and a CheY‐like receiver domain at its C terminus. Compared with the ATCC 17978 strain, both surface motility and biofilm formation at the gas–liquid interface decreased significantly in the A1S_2811 knock‐out strain. The number of pilus‐like structures and the amount of extrapolymeric substances on the cell surface also decreased in the A1S_2811 null strain. Transcription of abaI , which encodes an N ‐acylhomoserine lactone synthase in A. baumannii , decreased significantly in the A1S_2811 null strain, and supplementation with synthetic N ‐(3‐oxodecanoyl) homoserine‐ l ‐lactone rescued the surface motility and biofilm formation phenotype in the null mutant. We speculate that A1S_2811 regulates surface motility and biofilm formation, not by regulating type IV pili‐associated genes expression, but by regulating the chaperone/usher pili‐associated csuA/ ABCDE operon and the AbaI‐dependent quorum‐sensing pathway‐associated A1S_0112‐0119 operon instead.