Worm Breeder's Gazette 13(4): 36 (October 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.
Dept. of Developmental Biology, Stanford University Medical Center, Stanford CA 91305
An inductive signal from the anchor cell induces vulval precursor cells to divide and thereby generate the vulva. An important issue is whether vulval induction is controlled by a single graded signal (different concentrations of the anchor cell signal could directly cause the expression of either the 1260 or 2260 cell fates) or whether there are two sequential signals (the anchor cell induces P6 .pto express the 1260 cell fate, and P6 .puses another signal(s) to induce both P5 .pand P7 .pto adopt the 2260 cell fate). Previous studies have shown that isolated Pn.p cells can sometimes express the 2260 cell fate. This result supports the graded signal hypothesis by showing that the 2260 cell fate can be expressed in the absence of an adjacent 1260 cell. We have recently obtained evidence supporting the sequential signaling hypothesis using genetic mosaic animals in which some of the precursor cells lack wildtype copies of the let-23 gene, which encodes the receptor for the anchor cell signal. The single graded signal hypothesis predicts that cells that lack let-23 (+)should not express induced (1260 or 2260) cell fates. The sequential signal hypothesis predicts that a given precursor cell should require let-23 (+)in order to express the 1260 cell fate, but should not itself require let-23 (+)in order to express the 2260 cell fate (as long as it was next to a precursor cell that expressed the 1260 fate). Genetic mosaic animals can be generated when an extrachromosomal array is lost at a single cell division during development, yielding a clone of cells that lack the array. The extrachromosomal array expresses let-23 (+)as well as a cell lineage marker, ncl-1 .The ncl-1 marker can be used to distinguish cells that contain the array from those that lack it. First, these studies indicate that let-23 activity is required in order for a precursor cell to express the 1260 cell fate (Figure); P6 .palways adopted a 1260 cell fate if it expressed let-23 (+)(8 cases; rows 4-8) and never adopted the 1260 fate if it lacked the array (4 cases; rows 9-12). Second, as long as P6 .pexpressed the 1260 cell fate, P5 .pand P7 .padopted a 2260 cell fate regardless of whether or not they expressed let-23 (+).This result supports the sequential signal hypothesis in which another signaling pathway, such as the lin-12 signaling pathway, mediates expression of the 2260 cell fate. Third, the lateral signaling pathway mediated by the lin-12 receptor is inductive (induces expression of the 2260 cell fate) rather than inhibitory (inhibits expression of the 1260 cell fate). We observed four animals (rows 9-12) in which P5 .pexpressed the 1260 cell fate and induced P4 .pto express the 2260, rather than the 3260, cell fate . Fourth, in the only animal of this class (row 9), a ncl-1 (+) P7 .pcell did not express the 2260 cell fate if it was not adjacent to a 1260 cell. In this animal, a graded signal from the anchor cell was not sufficient to weakly activate let-23 (+)in P7 .p,and did not result in the expression of the 2260 cell fate. Each of these four points have also been substantiated by analyzing lin-7 mosaic animals (see figures). Our results suggest that the anchor cell signal activates the let-23 receptor on P6 .p,resulting in the expression of the 1260 cell fate. Subsequently, P6 .pmay express a lateral signal(s) that induces the lin-12 signaling pathway in its two neighboring cells (P5.p and P7 .p),causing them to express the 2260 cell fate. Previous observations involving isolated Pn.p cells suggests that a weak signal from the anchor cell may sometimes cause a Pn.p cell to express the lateral signal(s) and adopt the 2260 cell fate in an autocrine fashion. (see figures)
