Chen L M, Hobbie S, Galán J E
Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY, 11794-5222, USA.
Science. 1996 Dec 20;274(5295):2115-8. doi: 10.1126/science.274.5295.2115.
The bacterial pathogen Salmonella typhimurium triggers host cell signaling pathways that lead to cytoskeletal and nuclear responses required for pathogenesis. Here, the role of the small guanosine triphosphate (GTP)-binding protein CDC42Hs in these responses was examined. Expression of a dominant interfering mutant of CDC42 (CDC42HsN17) prevented S. typhimurium-induced cytoskeletal reorganization and subsequent macropinocytosis and bacterial internalization into host cells. Cells expressing constitutively active CDC42 (CDC42HsV12) internalized an S. typhimurium mutant unable to trigger host cell responses. Furthermore, expression of CDC42HsN17 prevented S. typhimurium-induced JNK kinase activation. These results indicate that CDC42 is required for bacterial invasion and induction of nuclear responses in host cells.
鼠伤寒沙门氏菌这种细菌病原体可触发宿主细胞信号通路，从而引发发病机制所需的细胞骨架和细胞核反应。在此，研究了小GTP结合蛋白CDC42Hs在这些反应中的作用。CDC42显性干扰突变体（CDC42HsN17）的表达可阻止鼠伤寒沙门氏菌诱导的细胞骨架重组以及随后的巨吞饮作用和细菌内化进入宿主细胞。组成型活性CDC42（CDC42HsV12）表达细胞可内化无法触发宿主细胞反应的鼠伤寒沙门氏菌突变体。此外，CDC42HsN17的表达可阻止鼠伤寒沙门氏菌诱导的JNK激酶激活。这些结果表明，CDC42是宿主细胞中细菌入侵和细胞核反应诱导所必需的。
