Goebel W, Leimeister-Wächter M, Kuhn M, Domann E, Chakraborty T, Köhler S, Bubert A, Wuenscher M, Sokolovic Z
Theodor-Boveri-Institut für Biowissenschaften (Biozentrum), Lehrstuhl für Mikrobiologie, Universität Würzburg, Germany.
Zentralbl Bakteriol. 1993 Apr;278(2-3):334-47. doi: 10.1016/s0934-8840(11)80850-9.
Virulence of Listeria monocytogenes is determined by a cluster of five genes in the order plcA, hly, mpl, actA and plcB, which are coordinately regulated by a transcriptional activator, termed PrfA. The gene for PrfA is located in front of plcA. Mutations within each of these genes reduce the virulence considerably and render the mutants unable to properly multiply and/or spread within the infected host cells. Under growth-limiting conditions PrfA-dependent proteins are preferentially synthesised. These studies indicate the existence of additional PrfA-regulated proteins in L. monocytogenes. The synthesis of catalase, superoxide dismutase, LmaA and p60 is not under the control of PrfA. These proteins seem to be also associated with virulence of L. monocytogenes. P60-related proteins are found as major extracellular proteins in all Listeria species but only p60 of L. monocytogenes is able to restore the failure of R-mutants (exhibiting a drastically reduced synthesis of p60) to adhere to 3T6 mouse fibroblasts. Adherence of L. monocytogenes to the epithelial Caco-2 cells seem to be independent of p60. The p60 protein of L. monocytogenes differs characteristically from the p60-related proteins of the nonvirulent Listeria species.
单核细胞增生李斯特菌的毒力由一组五个基因决定，其顺序为plcA、hly、mpl、actA和plcB，这些基因由一种称为PrfA的转录激活因子协同调控。PrfA基因位于plcA之前。这些基因中的每一个发生突变都会显著降低毒力，并使突变体无法在受感染的宿主细胞内正常繁殖和/或扩散。在生长受限条件下，优先合成PrfA依赖性蛋白。这些研究表明，单核细胞增生李斯特菌中存在其他受PrfA调控的蛋白。过氧化氢酶、超氧化物歧化酶、LmaA和p60的合成不受PrfA的控制。这些蛋白似乎也与单核细胞增生李斯特菌的毒力有关。在所有李斯特菌属物种中，P60相关蛋白都是主要的细胞外蛋白，但只有单核细胞增生李斯特菌的p60能够恢复R突变体（p60合成大幅减少）黏附3T6小鼠成纤维细胞失败的情况。单核细胞增生李斯特菌对上皮Caco-2细胞的黏附似乎与p60无关。单核细胞增生李斯特菌的p60蛋白与无毒李斯特菌物种的p60相关蛋白在特性上有所不同。
