Camilli A, Tilney L G, Portnoy D A
Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia 19104-6076.
Mol Microbiol. 1993 Apr;8(1):143-57. doi: 10.1111/j.1365-2958.1993.tb01211.x.
The plcA gene of Listeria monocytogenes encodes a secreted phosphatidylinositol-specific phospholipase C (Pl-PLC). Recent studies have established that transposon mutations within plcA result in avirulence for mice and pleiotropic effects when examined in tissue-culture models of infection. Genetic analysis reveals that many of the effects of the transposon insertions are due to loss of readthrough transcription from plcA into the downstream gene prfA, which encodes an essential transcription factor of numerous L. monocytogenes virulence genes. Construction of an in-frame deletion within plcA had no effect on expression of prfA thus allowing direct assignment of a role of the Pl-PLC in pathogenesis. Pl-PLC was shown to play a significant role in mediating escape of L. monocytogenes from phagosomes of primary murine macrophages. Interestingly, this defect manifested itself in vivo in the liver but not in the spleen of infected mice.
单核细胞增生李斯特菌的plcA基因编码一种分泌型磷脂酰肌醇特异性磷脂酶C（Pl-PLC）。最近的研究表明，plcA内的转座子突变在小鼠体内导致无毒性，并且在感染的组织培养模型中检测时具有多效性。遗传分析表明，转座子插入的许多效应是由于plcA到下游基因prfA的通读转录缺失，prfA编码众多单核细胞增生李斯特菌毒力基因的必需转录因子。在plcA内构建框内缺失对prfA的表达没有影响，从而可以直接确定Pl-PLC在发病机制中的作用。结果表明，Pl-PLC在介导单核细胞增生李斯特菌从原代小鼠巨噬细胞的吞噬体中逃逸方面发挥着重要作用。有趣的是，这种缺陷在感染小鼠的肝脏中而非脾脏中在体内表现出来。
