Xiao Gaoping, Déziel Eric, He Jianxin, Lépine François, Lesic Biliana, Castonguay Marie-Hélène, Milot Sylvain, Tampakaki Anastasia P, Stachel Scott E, Rahme Laurence G
Department of Surgery, Harvard Medical School, Massachusetts General Hospital, USA.
Mol Microbiol. 2006 Dec;62(6):1689-99. doi: 10.1111/j.1365-2958.2006.05462.x.
MvfR (PqsR), a Pseudomonas aeruginosa LysR-type transcriptional regulator, plays a critical role in the virulence of this pathogen. MvfR modulates the expression of multiple quorum sensing (QS)-regulated virulence factors; and the expression of the phnAB and pqsA-E genes that encode functions mediating 4-hydroxy-2-alkylquinolines (HAQs) signalling compounds biosynthesis, including 3,4-dihydroxy-2heptylquinoline (PQS) and its precursor 4-hydroxy-2-heptylquinoline (HHQ). PQS enhances the in vitro DNA-binding affinity of MvfR to the pqsA-E promoter, to suggest it might function as the in vivo MvfR ligand. Here we identify a novel MvfR ligand, as we show that HHQ binds to the MvfR ligand-binding-domain and potentiates MvfR binding to the pqsA-E promoter leading to transcriptional activation of pqsA-E genes. We show that HHQ is highly produced in vivo, where it is not fully converted into PQS, and demonstrate that it is required for MvfR-dependent gene expression and pathogenicity; PQS is fully dispensable, as pqsH-mutant cells, which produce HHI but completely lack PQS, display normal MvfR-dependent gene expression and virulence. Conversely, PQS is required for full production of pyocyanin. These results uncover a novel biological role for HHQ; and provide novel insights on MvfR activation that may aid in the development of therapies that prevent or treat P. aeruginosa infections in humans.
MvfR(PqsR)是一种铜绿假单胞菌LysR型转录调节因子,在该病原体的毒力中起关键作用。MvfR调节多种群体感应(QS)调控的毒力因子的表达;以及phnAB和pqsA - E基因的表达,这些基因编码介导4 - 羟基 - 2 - 烷基喹啉(HAQs)信号化合物生物合成的功能,包括3,4 - 二羟基 - 2 - 庚基喹啉(PQS)及其前体4 - 羟基 - 2 - 庚基喹啉(HHQ)。PQS增强了MvfR在体外与pqsA - E启动子的DNA结合亲和力,表明它可能作为体内MvfR配体发挥作用。在这里,我们鉴定出一种新型的MvfR配体,因为我们发现HHQ与MvfR配体结合域结合,并增强MvfR与pqsA - E启动子的结合,导致pqsA - E基因的转录激活。我们表明HHQ在体内大量产生,在体内它不会完全转化为PQS,并证明它是MvfR依赖性基因表达和致病性所必需的;PQS是完全可有可无的,因为产生HHI但完全缺乏PQS的pqsH突变细胞显示出正常的MvfR依赖性基因表达和毒力。相反,PQS是绿脓菌素完全产生所必需的。这些结果揭示了HHQ的一种新的生物学作用;并为MvfR激活提供了新的见解,这可能有助于开发预防或治疗人类铜绿假单胞菌感染的疗法。