TY - JOUR
T1 - Analysis of gain-of-function mutations of the lin-12 gene of Caenorhabditis elegans
AU - Greenwald, Iva
AU - Seydoux, Geraldine
PY - 1990
Y1 - 1990
N2 - 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)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 studies3,4 indicate that the lin-12 gene specifies the fates of Z1.ppp and Z4.aaa. Molecular studies5,6 suggest that lin-12 directly participates in their communications, perhaps acting as the receptor for the 'AC-to-VU' signal3. 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.
AB - 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)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 studies3,4 indicate that the lin-12 gene specifies the fates of Z1.ppp and Z4.aaa. Molecular studies5,6 suggest that lin-12 directly participates in their communications, perhaps acting as the receptor for the 'AC-to-VU' signal3. 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.
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U2 - 10.1038/346197a0
DO - 10.1038/346197a0
M3 - Article
C2 - 2164160
AN - SCOPUS:0025316499
SN - 0028-0836
VL - 346
SP - 197
EP - 199
JO - Nature
JF - Nature
IS - 6280
ER -