Lackner M R, Kim S K
Department of Developmental Biology, Stanford University School of Medicine, Stanford, California 94305-5329, USA.
Genetics. 1998 Sep;150(1):103-17. doi: 10.1093/genetics/150.1.103.
The Caenorhabditis elegans mpk-1 gene encodes a MAP kinase protein that plays an important role in Ras-mediated induction of vulval cell fates. We show that mutations that eliminate mpk-1 activity result in a highly penetrant, vulvaless phenotype. A double mutant containing a gain-of-function mpk-1 mutation and a gain-of-function mek mutation (MEK phosphorylates and activates MPK-1) exhibits a multivulva phenotype. These results suggest that mpk-1 may transduce most or all of the anchor cell signal. Epistasis analysis suggests that mpk-1 acts downstream of mek-2 (encodes a MEK homolog) and upstream of lin-1 (encodes an Ets transcription factor) in the anchor cell signaling pathway. Finally, mpk-1 may act together with let-60 ras in multiple developmental processes, as mpk-1 mutants exhibit nearly the same range of developmental phenotypes as let-60 ras mutants.
秀丽隐杆线虫的mpk-1基因编码一种MAP激酶蛋白，该蛋白在Ras介导的外阴细胞命运诱导中起重要作用。我们发现，消除mpk-1活性的突变会导致高度显性的无外阴表型。一个包含功能获得性mpk-1突变和功能获得性mek突变（MEK磷酸化并激活MPK-1）的双突变体表现出多外阴表型。这些结果表明，mpk-1可能转导大部分或所有锚定细胞信号。上位性分析表明，在锚定细胞信号通路中，mpk-1在mek-2（编码一种MEK同源物）的下游和lin-1（编码一种Ets转录因子）的上游起作用。最后，mpk-1可能在多个发育过程中与let-60 ras共同起作用，因为mpk-1突变体表现出与let-60 ras突变体几乎相同范围的发育表型。
