Selective Lineage Specification by mab-19 During Caenorhabditis elegans Male Peripheral Sense Organ Development

• Published in: Genetics (Austin) Vol. 138; no. 3; pp. 675 - 688
• Main Authors: Sutherlin, M. E, Emmons, S. W
• Format: Journal Article
• Language: English
• Published: United States Genetics Soc America 01.11.1994; Genetics Society of America
• Subjects: Alleles; Animals; Biochemistry; Caenorhabditis elegans; Caenorhabditis elegans - embryology; Caenorhabditis elegans - genetics; Female; Genes; Genes, Helminth; Heterozygote; Hot Temperature; Investigations; Larva; Male; Metals; Morphogenesis; Mutation; Pedigree; Sense Organs - embryology; Worms
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1093/genetics/138.3.675

The action of the gene mab-19 is required for specification of a subset of Caenorhabditis elegans male peripheral sense organ (ray) lineages. Two mab-19 alleles, isolated in screens for ray developmental mutations, resulted in males that lacked the three most posterior rays. Cell lineage alterations of male-specific divisions of the most posterior lateral hypodermal (seam) blast cell, T, resulted in the ray loss phenotype in mab-19 mutant animals. Postembryonic seam lineage defects were limited to male-specific T descendent cell divisions. Embryonic lethality resulted when either mab-19 mutation was placed over a chromosomal deficiency encompassing the mab-19 locus. The earliest detectable defect was aberrant hypodermal cell movements during morphogenesis. From these data, it is inferred that both mab-19 alleles described are hypomorphs, and further reduction of mab-19 function results in embryos that are unable to complete morphogenesis. Thus, mab-19 may play a larger role in developmental regulation of hypodermal cell fate, including sensory ray development in males. Body morphology mutations, passage through the dauer stage, and heat or CdCl2 treatment suppressed mab-19 male phenotypes. A model is presented in which all three types of suppression result in a physiological stress response, which in turn leads to correction of the mab-19 defect.