von Bodman S B, Majerczak D R, Coplin D L
Department of Biology, University of Puerto Rico, San Juan, Puerto Rico 00931-3360.
Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7687-92. doi: 10.1073/pnas.95.13.7687.
Classical quorum-sensing (autoinduction) regulation, as exemplified by the lux system of Vibrio fischeri, requires N-acyl homoserine lactone (AHL) signals to stimulate cognate transcriptional activators for the cell density-dependent expression of specific target gene systems. For Pantoea stewartii subsp. stewartii, a bacterial pathogen of sweet corn and maize, the extracellular polysaccharide (EPS) stewartan is a major virulence factor, and its production is controlled by quorum sensing in a population density-dependent manner. Two genes, esaI and esaR, encode essential regulatory proteins for quorum sensing. EsaI is the AHL signal synthase, and EsaR is the cognate gene regulator. esaI, DeltaesaR, and DeltaesaI-esaR mutations were constructed to establish the regulatory role of EsaR. We report here that strains containing an esaR mutation produce high levels of EPS independently of cell density and in the absence of the AHL signal. Our data indicate that quorum-sensing regulation in P. s. subsp. stewartii, in contrast to most other described systems, uses EsaR to repress EPS synthesis at low cell density, and that derepression requires micromolar amounts of AHL. In addition, derepressed esaR strains, which synthesize EPS constitutively at low cell densities, were significantly less virulent than the wild-type parent. This finding suggests that quorum sensing in P. s. subsp. stewartii may be a mechanism to delay the expression of EPS during the early stages of infection so that it does not interfere with other mechanisms of pathogenesis.
经典的群体感应（自诱导）调节，如费氏弧菌的lux系统所示，需要N-酰基高丝氨酸内酯（AHL）信号来刺激同源转录激活因子，以实现特定靶基因系统的细胞密度依赖性表达。对于甜玉米和玉米的细菌病原体斯氏泛菌亚种斯氏泛菌来说，细胞外多糖（EPS）斯图沃特聚糖是一种主要的毒力因子，其产生受到群体感应的群体密度依赖性控制。两个基因，esaI和esaR，编码群体感应所需的必需调节蛋白。EsaI是AHL信号合成酶，EsaR是同源基因调节因子。构建了esaI、ΔesaR和ΔesaI-esaR突变体以确定EsaR的调节作用。我们在此报告，含有esaR突变的菌株在细胞密度无关且无AHL信号的情况下产生高水平的EPS。我们的数据表明，与大多数其他已描述的系统相比，斯氏泛菌亚种斯氏泛菌中的群体感应调节利用EsaR在低细胞密度下抑制EPS合成，而去抑制需要微摩尔量的AHL。此外，在低细胞密度下组成型合成EPS的去抑制esaR菌株的毒力明显低于野生型亲本。这一发现表明，斯氏泛菌亚种斯氏泛菌中的群体感应可能是一种在感染早期延迟EPS表达的机制，从而使其不会干扰其他致病机制。
