Worm Breeder's Gazette 13(3): 100 (June 1, 1994)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
The cells of the ventral portion of the hermaphrodite uterus arise from intermediate precursors that can have one of two fates, ¹ or rho. ¹ and rho 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-11 -lacZfusion protein is specifically expressed in the ¹ cells and their progeny during L3 lethargus/early L4 .
A signal from the anchor cell is required to induce the ¹ fate; ablation of the anchor cell at a time when replacement regulation can no longer occur leads to a ¹ --> rho cell fate transformation and to an absence of lin-11 -lacZexpression in the uterus. Induction of ¹ 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 ¹ 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 ¹ cells. We found that egl-29 ( n482 )has a defect in ¹ fate specification. However, other lin-12 -dependentevents such as the AC vs. VU 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 ¹ fate. egl-29 mutants have little uterine lin-11 -lacZstaining; staining in occasional animals probably reflects the leakiness of the allele used.
An egl-29 ( n482 ); lin-12 (d)double mutant has excess ¹ 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.