Beitel G J, Tuck S, Greenwald I, Horvitz H R
Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.
Genes Dev. 1995 Dec 15;9(24):3149-62. doi: 10.1101/gad.9.24.3149.
The Caenorhabditis elegans gene lin-1 appears to act after the Ras-Raf-MEK-MAPK signaling cascade that mediates vulval induction. We show that lin-1 is a negative regulator of vulval cell fates and encodes an ETS-domain putative transcription factor containing potential MAPK phosphorylation sites. In lin-1 null mutants, the vulval precursor cells (VPCs) still respond to signaling from the gonadal anchor cell, indicating that lin-1 defines a branch of the inductive signaling pathway. We also provide evidence that the inductive and lateral signaling pathways are integrated to control the 1 degree and 2 degrees vulval cell fates after the point at which lin-1 acts in the inductive pathway and that VPCs can assess the relative rather than absolute levels of inductive and lateral signaling in determining whether to express the 1 degree or 2 degrees vulval cell fates.
秀丽隐杆线虫基因lin-1似乎在介导外阴诱导的Ras-Raf-MEK-MAPK信号级联反应之后发挥作用。我们发现lin-1是外阴细胞命运的负调节因子，编码一种含有潜在MAPK磷酸化位点的ETS结构域假定转录因子。在lin-1基因缺失突变体中，外阴前体细胞（VPCs）仍然对性腺锚定细胞的信号作出反应，这表明lin-1定义了诱导信号通路的一个分支。我们还提供了证据，表明诱导信号通路和侧向信号通路在lin-1在诱导通路中发挥作用的点之后整合，以控制1°和2°外阴细胞命运，并且VPCs在决定表达1°还是2°外阴细胞命运时可以评估诱导信号和侧向信号的相对而非绝对水平。
