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.