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The presence of multiple-signaling ligands in LIN-12/GLP-1 signal transduction pathways reveals that the functionality of proteins is mediated by different gene expression. APX-1 can replace LAG-2 during embryonic development. The specificity of different cell fates in GLP-1/LIN-12 depends upon the functioning of ligand and receptor. The APX-1 must react with GLP-1 and LIN-12 to replace LAG-2.

In wild-type Caenorhabditis elegans, the gonad is a complex epithelial tube that consists of long arms composed predominantly of germline tissue as well as somatic structures specialized for particular reproductive functions. In gon-1 mutants, the adult gonad is severely disorganized with essentially no arm extension and no recognizable somatic structure. The developmental defects in gon-1 mutants are limited to the gonad; other cells, tissues, and organs appear to develop normally. Previous work defined the regulatory 'leader' cells as crucial for extension of the gonadal arms (J. F.. Kimble and J. G. White, 1981, Dev. Biol. 81, 208-219). In gon-1 mutants, the leader cells are specified correctly, but they fail to migrate and gonadal arms are not generated. In addition, gon-1 is required for morphogenesis of the gonadal somatic structures. This second role appears to be independent of that required for leader migration. Parallel studies have shown that gon-1 encodes a secreted metalloprotease (R. Blelloch and J. Kimble, 1999, Nature 399, 586-590). We discuss how a metalloprotease may control two aspects of gonadal morphogenesis. [C] 1999 Academic Press Key Words: gon-1; organ shape; gonadogenesis; C. elegans; morphogenesis.