The autoinducer synthase LqsA and putative sensor kinase LqsS regulate phagocyte interactions, extracellular filaments and a genomic island of Legionella pneumophila.
The autoinducer synthase LqsA and putative sensor kinase LqsS regulate phagocyte interactions, extracellular filaments and a genomic island of Legionella pneumophila.
复制标题
自诱导剂合酶 LqsA 和假定的传感器激酶 LqsS 调节吞噬细胞相互作用、细胞外丝和嗜肺军团菌的基因组岛。
DOI：
10.1111/j.1462-2920.2010.02167.x
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发表时间：
2010
影响因子：
5.1
通讯作者：
Hilbi,Hubert
中科院分区：
文献类型：
--
作者：
Tiaden,André;Spirig,Thomas;Sahr,Tobias;Wälti,MartinA;Boucke,Karin;Buchrieser,Carmen;Hilbi,Hubert
The amoebae‐resistant opportunistic pathogenLegionella pneumophilaemploys a biphasic life cycle to replicate in host cells and spread to new niches. Upon entering the stationary growth phase, the bacteria switch to a transmissive (virulent) state, which involves a complex regulatory network including thelqsgene cluster (lqsA‐lqsR‐hdeD‐lqsS). LqsR is a putative response regulator that promotes host–pathogen interactions and represses replication. The autoinducer synthase LqsA catalyses the production of the diffusible signalling molecule 3‐hydroxypentadecan‐4‐one (LAI‐1) that is presumably recognized by the sensor kinase LqsS. Here, we analysedL. pneumophilastrains lackinglqsAorlqsS. Compared with wild‐typeL. pneumophila, the ΔlqsSstrain was more salt‐resistant and impaired for the Icm/Dot type IV secretion system‐dependent uptake by phagocytes.Legionella pneumophilastrains lackinglqsS,lqsRor the alternative sigma factorrpoSsedimented more slowly and produced extracellular filaments. Deletion oflqsAmoderately reduced the uptake ofL. pneumophilaby phagocytes, and the defect was complemented by expressinglqsA in trans. Unexpectedly, the overexpression oflqsAalso restored the virulence defect and reduced filament production ofL. pneumophilamutant strains lackinglqsSorlqsR, but not the phenotypes of strains lackingrpoSoricmT. These results suggest that LqsA products also signal through sensors not encoded by thelqsgene cluster. A transcriptome analysis of the ΔlqsAand ΔlqsSmutant strains revealed that under the conditions tested,lqsAregulated only few genes, whereaslqsSupregulated the expression of 93 genes at least twofold. These include 52 genes clustered in a 133 kb high plasticity genomic island, which is flanked by putative DNA‐mobilizing genes and encodes multiple metal ion efflux pumps. Upon overexpression oflqsA, a cluster of 19 genes in the genomic island was also upregulated, suggesting that LqsA and LqsS participate in the same regulatory circuit.
