Kornfeld K, Hom D B, Horvitz H R
Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
Cell. 1995 Dec 15;83(6):903-13. doi: 10.1016/0092-8674(95)90206-6.
By screening for mutations that suppress the vulval defects caused by a constitutively active let-60 ras gene, we identified six loss-of-function alleles of ksr-1, a novel C. elegans gene. Our genetic analysis showed ksr-1 positively mediates Ras signaling and functions downstream of or in parallel to let-60. In the absence of ksr-1 function, normal Ras signaling is impaired only slightly, suggesting ksr-1 may act to modulate, or in a branch that diverges from, the main signaling pathway. The predicted KSR-1 protein has a protein kinase domain and is most similar to a recently identified Drosophila protein involved in Ras signaling. We propose that the function of ksr-1 is evolutionarily conserved.
通过筛选抑制组成型激活的let-60 ras基因所导致的外阴缺陷的突变,我们鉴定出了ksr-1基因的六个功能丧失型等位基因,ksr-1是一种新的秀丽隐杆线虫基因。我们的遗传分析表明,ksr-1正向介导Ras信号传导,并且在let-60的下游或与其平行发挥作用。在缺乏ksr-1功能的情况下,正常的Ras信号传导仅受到轻微损害,这表明ksr-1可能起到调节作用,或者在与主要信号通路不同的分支中发挥作用。预测的KSR-1蛋白具有一个蛋白激酶结构域,并且与最近鉴定出的参与Ras信号传导的果蝇蛋白最为相似。我们提出ksr-1的功能在进化上是保守的。