We are interested in understanding the mechanism by which antero- posterior differences in body pattern arise after hatching. A striking example of antero-posterior patterning takes place among the V cells, which lie along the lateral margin of the animal. Initially these cells appear uniform, but subsequently anterior V cells generate seam cells that make alae, while posterior V cells instead produce neuroblasts that make sensory rays. Two genes are known to influence the 'ray/alae' decision.
mab-5 null mutations cause all V cells to generate lineages characteristic of V(1-4) and to produce alae but no rays. Recessive
lin-22 mutations (Horvitz, et al., CSHSQB 43:453) cause certain cells produced by V(2-4) , and sometimes V1, to generate rays instead of the alae they would normally produce. Thus, in a
lin-22 mutant, alae is located near the head and the body is lined with ray papillae. The phenotypes of these mutants indicate that in wild type males,
mab-5 + is required for ray production by V cells, and
lin-22 is required to produce alae (at least as far anteriorly as V2). We have found that Bill Fixsen's
lin-22 allele
n372 is temperature sensitive for ray production. This suggested that either the
n372 product is thermolabile, or else that this mutation reveals an intrinsic temperature dependence of the ray/alae decision. In our efforts to define the Lin-22 null phenotype, we have isolated two new alleles,
mu2 and
mu5. Like
n372, both are temperature sensitive.
n372 and
mu2 have similar phenotypes, while
mu5 appears to be a weaker allele because it results in the formation of approximately twice as much alae as
n372 and
mu2 at 16 C, 20 C and 25 C. The fact that all alleles are temperature sensitive supports the notion of an intrinsic temperature-dependence of the ray/alae decision such that ray production is favored at high temperature. The transformation of V cells is variable in all three alleles, so there are often patches of alae interspersed with ray cells. However, in general, alae appear to be made preferentially in the anterior, and are progressively lost from posterior regions as the temperature is increased from 16 C to 25 C. In other words, changes in temperature have the effect of shifting the ray/alae boundary along the body axis, as if there is a graded anterior-posterior difference in the response of these cells to temperature. Previously, we showed that as the
mab-5+ gene dosage is increased in a
lin-22 mutant, cells located progressively more anteriorly will produce rays (Kenyon, Cell 46:477). Thus,
mab-5 activity may play a role in the important process of determining the position of the ray/alae boundary. To test whether
lin-22 activity could also be involved in positioning the boundary, we lowered
lin-22 dosage in a
mab-5 mutant. At 20 C, 0/50
mab-5 (
e1239 n372 1+;
e1490 males produced extra rays. However, we had determined that the formation of rays is favored at high temperature, so we examined the animals at 25 C. At this temperature an extra ray was present in the fan of 13/50 animals (one side scored) and 1/50 animals had two extra rays ( 0/64
e1239;
e1490 males had extra rays at 25 C). Thus, like
mab-5, can also influence the position of the ray/alae boundary. The fact that
lin-22 and
mab-5 activities shift the boundary in opposite directions suggests that in the wild type the boundary may be positioned by the
lin-22/mab-5 ratio.