Rampioni Giordano, Bertani Iris, Zennaro Elisabetta, Polticelli Fabio, Venturi Vittorio, Leoni Livia
Department of Biology, University Roma Tre, Viale G. Marconi 446, 00146, Rome, Italy.
J Bacteriol. 2006 Jan;188(2):815-9. doi: 10.1128/JB.188.2.815-819.2006.
A mutation in the rsaL gene of Pseudomonas aeruginosa produces dramatically higher amounts of N-acyl homoserine lactone with respect to the wild type, highlighting the key role of this negative regulator in controlling quorum sensing (QS) in this opportunistic pathogen. The DNA binding site of the RsaL protein on the rsaL-lasI bidirectional promoter partially overlaps the binding site of the LasR protein, consistent with the hypothesis that RsaL and LasR could be in binding competition on this promoter. This is the first direct demonstration that RsaL acts as a QS negative regulator by binding to the lasI promoter.
铜绿假单胞菌rsaL基因的突变相对于野生型产生了显著更多的N-酰基高丝氨酸内酯,突出了这种负调控因子在控制这种机会致病菌群体感应(QS)中的关键作用。RsaL蛋白在rsaL-lasI双向启动子上的DNA结合位点与LasR蛋白的结合位点部分重叠,这与RsaL和LasR可能在该启动子上存在结合竞争的假设一致。这是首次直接证明RsaL通过与lasI启动子结合而作为QS负调控因子发挥作用。