Yoon Sara, Liu Zhengchang, Eyobo Yvonne, Orth Kim
Department of Molecular Biology, University of Texas Southwestern Medical School, Dallas 75390-9148, USA.
J Biol Chem. 2003 Jan 24;278(4):2131-5. doi: 10.1074/jbc.M209905200. Epub 2002 Nov 13.
Yersinia effector, YopJ, inhibits the innate immune response by blocking MAP kinase and NFkappaB signaling pathways in mammalian cells. Herein, YopJ is shown to disrupt the MAP kinase signaling pathways in Saccharomyces cerevisiae. Expression of YopJ in yeast blocks the ability of yeast to respond to alpha factor by disrupting activation of the pheromone signaling pathway upstream of the activation of the MAPK Fus3p. YopJ also blocks the high osmolarity growth (HOG) MAP kinase pathway in yeast upstream of the activation of the MAPK Hog1p. YopJ is proposed to block the MAP kinase pathways in yeast in a similar manner to the way it blocks mammalian signaling pathways, implicating that a novel, evolutionarily conserved mechanism of regulation is utilized for signal transduction by these pathways.
耶尔森菌效应蛋白YopJ通过阻断哺乳动物细胞中的丝裂原活化蛋白激酶(MAP激酶)和核因子κB(NFκB)信号通路来抑制先天免疫反应。在此,研究表明YopJ会破坏酿酒酵母中的MAP激酶信号通路。YopJ在酵母中的表达通过破坏丝裂原活化蛋白激酶Fus3p激活上游的信息素信号通路的激活,从而阻断酵母对α因子的反应能力。YopJ还会在丝裂原活化蛋白激酶Hog1p激活上游阻断酵母中的高渗生长(HOG)MAP激酶通路。据推测,YopJ以类似于其阻断哺乳动物信号通路的方式来阻断酵母中的MAP激酶通路,这意味着这些通路利用了一种新的、进化上保守的调节机制进行信号转导。