Greenwald I, Seydoux G
Department of Biology, Princeton University, New Jersey 08540.
Nature. 1990 Jul 12;346(6280):197-9. doi: 10.1038/346197a0.
Certain cell fate decisions are specified by cell-cell interactions during the development of the nematode Caenorhabditis elegans. For example, in a wild-type hermaphrodite gonad, two cells, Z1.ppp and Z4.aaa, have the potential to become the anchor cell (AC). Intercellular communication establishes their fates and ensures that only one cell becomes the AC, while the other becomes a ventral uterine precursor cell (VU). One component of this intercellular communication seems to be the 'AC-to-VU' signal from the presumptive AC that causes the other cell to become a VU. Genetic and developmental studies indicated that the lin-12 gene specifies the fates of Z1.ppp and Z4.aaa. Molecular studies suggest that lin-12 directly participates in their communications, perhaps acting as the receptor for the 'AC-to-VU' signal. Here, we report the molecular lesions associated with lin-12 gain-of-function mutations, cell isolation experiments, and genetic studies of an unusual lin-12 allele. These data suggest that self-association of the putative lin-12-encoded receptor leads to its activation, and that certain gain-of-function mutations result in ligand-independent activation.
在秀丽隐杆线虫的发育过程中，某些细胞命运决定是由细胞间相互作用指定的。例如，在野生型雌雄同体性腺中，两个细胞Z1.ppp和Z4.aaa有潜力成为锚定细胞（AC）。细胞间通讯决定了它们的命运，并确保只有一个细胞成为AC，而另一个成为腹侧子宫前体细胞（VU）。这种细胞间通讯的一个组成部分似乎是来自假定AC的“AC到VU”信号，该信号使另一个细胞成为VU。遗传和发育研究表明，lin-12基因决定了Z1.ppp和Z4.aaa的命运。分子研究表明，lin-12直接参与它们的通讯，可能作为“AC到VU”信号的受体。在这里，我们报告了与lin-12功能获得性突变相关的分子损伤、细胞分离实验以及一个不寻常的lin-12等位基因的遗传研究。这些数据表明，假定的lin-12编码受体的自我缔合导致其激活，并且某些功能获得性突变导致配体非依赖性激活。
