Induction of the uterine P. fate by the anchor cell results in lin-ll-lacZ expression and requires
egl-29. Anna P. Newman and Paul W. Sternberg, Division of Biology, 156-29, Caltech, Pasadena, CA The cells of the ventral portion of the hermaphrodite uterus arise from intermediate precursors that can have one of two fates, P. or p.. P. and p. cells differ in the morphology of their progeny and the number of descendants generated. Furthermore, as initially observed by Gwen Freyd and Bob Horvitz and confirmed by us, a lin-ll-lacZ fusion protein is specifically expressed in the P. cells and their progeny during L3 lethargus/ early IA. A signal from the anchor cell is required to induce the P. fate; ablation of the anchor cell at a time when replacement regulation can no longer occur leads to a p. --> p cell fate transformation and to an absence of lin-ll-lacZ expression in the uterus. Induction of P. fates by the anchor cell is temporally and genetically distinct from anchor cell induction of the vulva and requires
lin-12 activity (WBG 12(5) p.52). Ablation of the P. cells leads to an egg-laying defect. Therefore, we screened the Class A Egl mutants of Trent, Tsung & Horvitz in order to identify additional genes required to produce P. cells. We found that
egl-29(
n482) has a defect in n fate specification. However, other
lin-12- dependent events such as the AC vs. W decision and specification of the vulval 2 fate are wild type. Thus, egl- 29 may interact with
lin-12 in a tissue-specific manner to specify the P. fate.
egl-29 mutants have little uterine lin- ll-lacZ staining; staining in occasional animals probably reflects the leakiness of the allele used. An
egl-29(
n482);
lin-12(d) double mutant has excess P. cells like a
lin-12(d) mutant, suggesting that
egl-29 functions upstream of
lin-12. Analysis of the
egl-29 null phenotype and cloning of
egl-29 are in progress.