The C. elegans
let-23 gene is required for induction of the vulva, survival past the L1 stage, hermaphrodite fertility, and for male spicule development. Molecular analysis of its genomic DNA and cDNA revealed that the
let-23 gene encodes a receptor type tyrosine kinase quite similar to the human EGF receptor. Specifically,
let-23 product includes a signal sequence, two cystein-rich extracellular domains, a single transmembrane domain, a tyrosine kinase domain, and a Cterminal tail. Since
let-23 is required for vulval induction and has the structure of a presumptive receptor, we propose that
let-23 acts in the vulval precursor cells (VPCs) to recieve and transduce an inductive signal from the anchor cell. Iet-23 is probably activated by binding the ligand and signals to execute vulval fate through a pathway including
let-60ras. To test this hypothesis and analyze other functions of
let-23, we made a transgenic nematode carrying a chimeric gene which consists of the entire
let-23 gene and lacZ gene inserted within the coding region. X-gal staining of transgenic worms visualized a characteristic expression pattern. In the larvae, many cells along the ventral cord, presumably including VPCs, and several cells in the head and tail were stained, but the anchor cell, the other gonadal cells and
hyp7 were not. These observations support our hypothesis mentioned above. They also suggest other roles of the let- 23 in the ventral cord neurons and the head and tail regions, which may be related to the lethality of a
let-23 mutant. In the adult, the staining pattern is similar to that of the larvae, except that the spermathecal region and ovarian sheath cells stain. The sterile phenotype of
let-23 mutants may result from a defect in a signal acting on the somatic gonad.