Genetic and molecular studies of Caenorhabditis elegans male tail development

Abstract

The Caenorhabditis elegans male tail sensory organs provide a simple model system in which to study the role of genetic specification and organization of the peripheral nervous system. Mutations resulting in male tail defects were isolated in order to identify genes that are required for sense organ development. Of the mutations identified, those that mapped to two previously unidentified genes, mab-19 and mab-22, have been studied in greater detail.;mab-19 is required for specification of a subset of sensory ray cell lineages. Two mab-19 alleles, bx38 and bx83, were identified; both result in cell lineage defects leading to loss of the last three pairs of sensory rays in the male tail, derived from a single lateral hypodermal blast cell. Further genetic analysis revealed that the two mab-19 alleles were hypomorphic, and the putative null phenotype was embryonic arrest at the twofold stage. The mutant phenotypes were consistent with a model that mab-19 is required for hypodermal cell specification.;Both mab-19 alleles were suppressed by agents that induce physiological stress. Suppression data are consistent with the hypothesis that mab-19 mutant phenotypes are the result of an unstable protein product.;Preliminary research toward cloning the gene has been conducted. The mutant alleles were mapped to a narrow interval on the X chromosome (less than 250 Kbp) by sequence tagged site mapping. Cosmid DNA of this region from ordered genomic libraries has been prepared for transformation rescue experiments.;mab-22 was identified by isolation of a conditional allele, bx59ts, that resulted in males that were missing most or all rays at the nonpermissive temperature of 25{dollar}\sp\circ{dollar} but are normal at 16{dollar}\sp\circ{dollar}. The temperature-sensitive period was during ray morphogenesis. Cell lineage patterns were unaffected by bx59ts, and cell movements during early morphogenesis appeared to be normal. Neuronal morphology was normal in electron micrographs of serially-sectioned mutant rays. The observations support a model in which mab-22 is required during ray assembly, perhaps at the level of neuronal-structural cell interactions or structural cell differentiation.