Worm Breeder's Gazette 13(1): 67 (October 1, 1993)
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.
During male development the anterior daughter of B divides to produce eight progeny: the ventral (aa) and dorsal (pp) pairs, and two identical lateral (ap/pa) pairs. Within each pair there is a distinct anterior and a distinct posterior fate. Cell ablation experiments have identified several cell interactions that promote the normal pattern of fates (Chamberlin and Sternberg, 1993, Development 118, 297-323). In particular, F and U promote anterior fate in each pair.
We had previously found that reduction-of-function mutations in genes of the lin-3 / let-23 signaling pathway result in a disruption of the fates of the anterior cell, but not the posterior cell, in each pair (e.g., WBG 11.2 p. 103; data summarized below). In many cases the anterior cells produce the lineages normally associated with their posterior neighbors. This phenotype mimics the defect observed when F and U are ablated with a laser microbeam. However, F and U lineages are normal in mutant animals (2/2 lin-3 and 2/2 lin-45 lineages followed), and the linker cell in the gonad is killed with the same timing as in wild type animals (10/10 lin-3 and 8/8 lin-45 ).Thus the genes in the lin-3 / let-23 signaling pathway are necessary to promote anterior fates, and likely mediate the signal from F and U.
In order to further test the role of this pathway in the B lineage, we used transgenic constructs made by Russell Hill that include the EGF domain of lin-3 under control of the heat-inducible hsp-16 promoter. These transgenes should express LIN-3 protein in a tissue general manner. Heat shock treatment of transgenic males results in a disruption of the fates of the posterior cells in the B lineage. Posterior cells can produce the lineages normally associated with their anterior neighbors. Ectopic lin-3 can promote anterior fates in the absence of F and U. Thus activation of the lin-3 / let-23 pathway is sufficient to promote anterior fates.