As a basis for investigating the evolution of form in the nematode male tail, we are characterizing the cellular basis of male tail morphological diversity in Rhabditida and are isolating genes required for C. elegans male tail morphogenesis (and eventually orthologous genes from related species). By characterizing process and pattern in the ontogeny of the male tail in C. elegans mutants and related species, we aim to identify genetic changes responsible for the evolution of morphological diversity of this structure. To visualize the changes in cell shape and position that accompany male tail morphogenesis, we have used MH27 (an antibody, kindly provided by R. Waterston, that recognizes belt junctions surrounding cells), for the immunofluorescent staining of different developmental stages of C. elegans and other Rhabditidae. In C. elegans L4s, the formation of both the SET syncytium and another syncytium in the tail tip are revealed by degradation of the MH27 staining at the cell boundaries between the fusing cells. Retraction of the tail tip anteriorly occurs immediately after these fusions. Because these cell fusion events are specific to L4 males, they serve as good markers for the male-specific and L4 stage-specific fates of these cells. Two mutations isolated in our laboratory,
bx37 and
bx42, both alleles of the lep-l gene (LG I), cause failure of the tail tip to retract to the same extent as in wild type, thus leaving the tip of the tail protruding beyond the posterior edge of the fan (i.e., forming a 'leptoderan' tail). MH27 antibody staining of both lep-l mutants and 'leptoderan' species, such as Rhabditis terricola, show that failure of tail tip retraction in leptoderan tails is accompanied by a failure in the fusion of only the most posterior cells until after retraction of the anterior cells has already occurred. We speculate that heterochronic changes in lep-l may have led to one aspect of the morphological diversity of nematode male tails, i.e. the difference between 'leptoderan' and 'peloderan' tails. The gene,
lep-2(
bx73), also appears to encode products required for retraction specifically of the tail tip syncytium. Conversely, several mutations affecting fan morphogenesis (e.g.,
bx49) do not result in leptoderan tail tips. Thus, wild type products from lep-l and
lep-2 are not required for the retraction involved in morphogenesis of the fan and rays, indicating that tail tip and fan retraction are independent processes. Additional mutations indicate that stabilization of morphogenesis must occur before the L4 cuticle is shed in the last larval molt. At least one gene,
mab-17(
e2167)I, that appears to be involved in this stabilization process has been defined by a mutation that results in the formation of a bulged or 'clubbed' tail after the L4 molt. Prior to the molt, this mutation shows wild- type morphogenesis.