Worm Breeder's Gazette 10(3): 112
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.
We are trying to understand the mechanisms that specify V cell lineages in the C. elegans male. In studying the gene pal-1 we have found that V cell fates are specified, at least in part, by a mechanism that involves local cell interactions. In the newly hatched male, six V cells and one T cell are aligned along each side of the animal. V1-V4 each generate identical lineages and each produce two seam cells that will produce alae. V6 undergoes additional cell divisions that lead to the production of five ray sensilla. V5 produces one ray one seam cell and also the postdeirid. The T cell, which undergoes a lineage rather different from the V cells, produces three rays. Sulston and White(1) first demonstrated that these cells are able to respond to environmental cues. When V6 is ablated, V5 gradually moves back into the position of V6 and generates a lineage similar to or identical to the wild type V6 lineage. When V5 and V6 are ablated, V4 moves back and produces rays. These ablations have no effect on T. Likewise, the ablation of T has no effect on the V rays. As we reported at the C. elegans meeting last year, mutations in pal-1 cause V6 to generate a lineage identical to those of V1-V4, and so to produce seam cells instead of rays. V5 and T are unaffected in these animals. Further evidence that V6 is transformed into a V1-V4 like cell by pal-1 mutations is provided by the pal-1; utant. lin-22 mutations cause V1-V4 but not V6 to adopt a V5 like fate(2), and so to produce postdeirids in both sexes and rays in males. In pal-1; 6 also produces a postdeirid and rays, as V1-V4 do in a lin-22 background. ( V6 produces a postdeirid in pal-1; odites.) When V6 is ablated in pal-1 animals, V5 produces additional rays, as it does when V6 is ablated in the wild type. Similarly, when V5 and V6 are ablated in pal-1 animals, V4 can produce rays. We were puzzled by these results. If V6 is transformed to a V4 like cell, and V4 makes rays when it moves into the position of V6 following the ablations, why does V6 not make rays? We were led (some of us kicking and screaming) to the idea that a cell produces extra rays in response to the ablations because it senses the absence of its posterior neighbor not simply because it moves into a region containing different positional information. We predicted that if we ablated the posterior neighbor of V6 in a pal-1 animal, V6 would undergo a wild type lineage. Therefore we ablated T. We had reason to think that ablation of T would have no effect on V6. First, in the wild type, V cells are unaffected by the ablation of T and vice-versa. Second, T rays are unaffected by mutations in mab-5 and mab-3, two mutations that affect all the V rays. Thus it seemed that T might be quite different from the V cells and that there might be no interaction between them. To our surprise and delight, when T was ablated in pal- 1 animals, V6 produced rays, (13/13 animals) and in most cases behaved as it would in the wild type, producing five rays (8/13). This has been seen with both pal-1 alleles, e2091 and mu13. V6 does not move into the position of T following these ablations. This suggests that the inhibition of ray formation that T asserts on V6 in the pal-1 mutant is due to direct cell signals, and not simply a consequence of a change in V cell position. It appears that the function of pal-1 is to inhibit or override these signals. The production of rays by V6 following T ablation in pal-1 animals closely resembles the production of rays by V5 in response to the ablation of V6. We suggest that V6 inhibits ray formation by V5 in the wild type by the same mechanism that T inhibits ray formation by V6 in a pal-1 mutant. In other words, it seems that each V and T cell sends signals to its anterior neighbors which inhibit the formation of rays (or promote the formation of seam cells), and that these signals are selectively inhibited or overridden in V6 by the action of pal-1. We predict that there is an analogous activity that overrides these signals in V5 to allow the production of the V5 ray. We do not know whether or not our pal-1 alleles are null alleles, thus it is possible that residual pal-1 activity in our pal-1 mutants could provide such an function. We believe that these cell signals and pal-1 olling the activity of the genes mab-5 and lin-22. The inhibition of V6 rays in the pal-1 mutant is dependent on lin-22 activity (V6 produces rays in the pal-1; utant). Thus pal-1 behaves as a negative regulator of lin-22. When T is ablated in mab-5 animals V6 does not make rays. The same is true in a pal-1; mab- 5 activity is therefore required for the production of rays even in the absence of signals from T. This suggests that the function of pal- 1 is to promote the activity of mab-5 in V6. pal-1 could act by interfering with the transmission or reception of the signal from T, or by simply overriding the signal by more directly controlling the activity of mab-5 and/or lin-22 . Although local cell interactions appear to specify V cell fates, there is also evidence of a separate control system that biases anterior V cells toward the production of seam cells and posterior V cells toward the production of rays. For example, Sulston and White found that the further anteriorly a cell is located, the less likely it is to produce rays following the ablation of its posterior neighbors. In fact, their results suggest that if local cell interactions were blocked completely, a variable pattern of rays and seam cells would develop, in which the density of rays would increase gradually toward the posterior of the animal. It may be the case that the function of local cell signalling mechanism is to convert a variable, coarse pattern of seam cells and rays into a highly reproducible pattern with sharp boundaries between cell types.