Worm Breeder's Gazette 12(5): 52 (February 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.
The cells of the ventral portion of the C. elegans hermaphrodite uterus arise from division of three precursors VU1 , VU2 ,and VU3 (Kimble and Hirsh, Dev. Biol. 70: 396 479; 1979). Each VU cell generates 4 intermediate precursors. These precursors are either ¹ (proximal to the anchor cell), p(medial) or {sigma} (distal; see figure). One intermediate precursor, ¹ (which we previously referred to as d/v) produces two descendants, while p and {sigma} each produce four descendants. The three VU lineages differ in the number of ¹'s they produce(VU1, 2 and 3 produce one, two, and three ¹'s respectively, see figure). We have previously reported that the anchor cell is necessary for the ¹ fate (WBG 12(4) p.52); when the anchor cell is ablated during L2 lethargus/ early L3 ,all three VU cells follow a "VU0" lineage in which no ¹'s are produced (i.e. all cells produce four descendants). Experiments with highly penetrant vulvaless mutants of let-23 and lin-3 suggest that these genes are not required for the corresponding signaling process.
We were interested in identifying additional signaling molecules, and therefore followed the VU lineages in several lin-12 mutants. lin-12 is required for a number of cell fate decisions in C. elegans (Greenwald et. al, Cell 34: 435-444; 1983). lin-12 is required for the AC vs. VU decision; in lin-12 loss-of-function mutants [ lin-12 (0)],from one to three of the VU precursors are transformed into anchor cells. We have determined the VU lineages in eight lin-12 (0)animals ( n676 n909 or n137 n720 )which had either one or two VU precursors. All VU lineages were VU0 ,i.e., produced no ¹'s. (This cannot be an indirect consequence of the defect in the AC vs. VU decision since, if anything, the presence of extra anchor cells in and of itself might be expected to lead to extra ¹'s). Thus, lin-12 appears to be required for induction of the ¹ fate by the anchor cell Dominant alleles of lin-12 [ lin-12 (d)]lead to the opposite transformation from the loss-of-function phenotype. We have followed the VU lineages in a lin-12 (d)strain ( n137 )which has four VU precursors and no anchor cell. All were either VU3 , VU31 /2,or VU4 (5 animals). That is, most intermediate precursors were ¹'s (i.e. produced only two descendants). Thus, excluding the cells at the very ends of the uterus, one could consider this as a gain-of-function phenotype with respect to the their fate. Regarding the VU progeny at the very ends, they may be different in fate from their immediate neighbors because of intercellular signaling. This difference would not be evident (in terms of cell divisions) in a wild type background, but would be uncovered in a lin-12 (d)background. We're currently performing ablations in a lin-12 (d)background in order to test the hypothesis that intercellular signaling is occurring at the distal ends of the uterus.
Summary and interpretation:
1) Ablation of the anchor cell during L2 lethargus/ early L3 leads all UV precursors to follow the UV0 fate in which no ¹'s are produced. lin-12 (0)mutants have the same phenotype. Thus, the anchor cell and lin-12 appear to be required for the ¹ fate.
2) lin-12 has been shown to act in the AC vs. VU decision in a process that is complete by the end of L2 .Our results indicate that lin-12 is required for a decision in which the anchor cell signals the progeny of the VU precursors during L3 (See WBG 12(4) p.52 for timing). In this later process, lin-12 could be acting directly as a receptor for a signal from the anchor cell to the VU progeny. Alternatively the anchor cell could signal the VU progeny by a lin-12 -independentmechanism, you would require that these VU progeny laterally excite one another via lin-12 in order for the ¹ fate to be specified. In either case, this represents a novel role for lin-12 during C. elegans development induction or lateral excitation.
[See Figure]