Hopper N A, Lee J, Sternberg P W
MRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
Mol Cell. 2000 Jul;6(1):65-75.
A screen for synthetic enhancers of sli-1 identified ark-1 (forAck-related tyrosine kinase), a novel inhibitor of let-23 EGFR signaling in C. elegans. An ark-1 mutation synergizes with mutations in other negative regulators of let-23, resulting in increased RAS signaling. Genetic analysis suggests that ARK-1 acts upstream of RAS and is dependent upon SEM-5. ARK-1 inhibits LET-23-mediated ovulation, a RAS-independent function. ARK-1 physically interacts with SEM-5 in the yeast two-hybrid assay. We find that sem-5 also has a negative function in let-23-mediated ovulation and suggest that this negative function is mediated by the recruitment of inhibitors such as ARK-1.
一项针对sli-1合成增强子的筛选鉴定出ark-1(Ack相关酪氨酸激酶),它是秀丽隐杆线虫中let-23表皮生长因子受体(EGFR)信号传导的一种新型抑制剂。ark-1突变与let-23其他负调控因子的突变协同作用,导致RAS信号增强。遗传学分析表明,ARK-1在RAS上游起作用,且依赖于SEM-5。ARK-1抑制LET-23介导的排卵,这是一种不依赖RAS的功能。在酵母双杂交试验中,ARK-1与SEM-5发生物理相互作用。我们发现,sem-5在let-23介导的排卵中也具有负功能,并表明这种负功能是由招募诸如ARK-1等抑制剂介导的。