ANALYSIS OF GAIN-OF-FUNCTION MUTATIONS OF THE LIN-12 GENE OF CAENORHABDITIS-ELEGANS
ANALYSIS OF GAIN-OF-FUNCTION MUTATIONS OF THE LIN-12 GENE OF CAENORHABDITIS-ELEGANS
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DOI：
10.1038/346197a0
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发表时间：
1990-07-12
期刊：
影响因子：
64.8
通讯作者：
SEYDOUX, G
中科院分区：
文献类型：
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作者：
GREENWALD, I;SEYDOUX, G
在线虫发育过程中，某些细胞命运决定是由细胞间相互作用决定的。例如，在野生型雌雄同体性腺中，两个细胞 Z1.ppp 和 Z4.aaa 有可能成为锚细胞 (AC)1。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，而另一个细胞成为腹侧子宫前体细胞 (VU)2,3。这种细胞间通信的一个组成部分似乎是来自假定 AC 的“AC 到 VU”信号，该信号导致另一个细胞变成 VU3。遗传和发育研究3,4表明thelin-12基因决定Z1.ppp和Z4.aaa的命运。分子研究5,6表明lin-12直接参与它们的通讯，可能充当“AC-to-VU”信号3的受体。在这里，我们报告了与 lin-12 功能获得突变相关的分子损伤、细胞分离实验以及异常 lin-12 等位基因的遗传学研究。这些数据表明推定lin-12编码受体的自缔合导致其激活，并且某些功能获得性突变导致配体依赖性激活。
CERTAIN cell fate decisions are specified by cell–cell interactions during the development of the nematodeCaenorhabditis 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)1. Intercellular communication establishes their fates and ensures that only one cell becomes the AC, while the other becomes a ventral uterine precursor cell (VU)2,3. 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 VU3. Genetic and developmental studies3,4indicate that thelin-12gene specifies the fates of Z1.ppp and Z4.aaa. Molecular studies5,6suggest thatlin-12directly participates in their communications, perhaps acting as the receptor for the 'AC-to-VU' signal3. Here, we report the molecular lesions associated withlin-12gain-of-function mutations, cell isolation experiments, and genetic studies of an unusuallin-12allele. These data suggest that self-association of the putativelin-12-encoded receptor leads to its activation, and that certain gain-of-function mutations result in ligand-independent activation.