Worm Breeder's Gazette 13(5): 71 (February 1, 1995)
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.
Division of Biology and HHMI, Caltech, Pasadena, CA, 91125 IMBB, Simon Fraser University, Burnaby, BC, V5A 1S6 We identified sy238, the first allele of lin-49, in a screen for mutations that result in cell lineage defects during male tail development. Adult sy238 homozygous males have abnormally short and crumpled spicules, and sy238 is recessive for this defect. Cell lineage analysis of sy238 males indicates that the F and U cells produce variably abnormal lineages, and in some cases one or the other of the cells appears to be missing. F and U are embryonic sister cells that make up one "ring" of the rectal epithelium (Sulston, et al., Dev. Biol. 100: 64-119 (1983)). In addition, F and U, or their progeny, produce a signal that is required for normal development of the male spicules (Chamberlin and Sternberg, Devt. 118: 297-323 (1993)). Consistent with this function, sy238 males also exhibit B cell lineage defects that are similar to those seen in wild type animals in which F and U have been ablated. The lineage results suggest that lin-49 may play an important role in the specification or development of the F and U cells. lin-49 maps to LG IV, between unc-24 and mec-3, and inside of eDf18. Although sy238/sy238 animals are generally viable and hermaphrodites are fertile, sy238/Df animals arrest at mid-larval stages. They are severely constipated, and exhibit heavy "scarring" at the intestinal/rectal juncture. Genetically, this observation suggests that (1) sy238 does not represent a null mutation in the lin-49 gene, and (2) we would not be able to recover null alleles in a standard non-complementation mutagenesis screen for additional alleles. To recover additional alleles of lin-49, we have tested a panel of previously isolated lethal mutations that roughly map to the lin-49 region. We focused on a set of mutations linked to unc-22 that map outside of sDf2 but to the right of unc-24 (D. Clark, D. Riddle, pers. comm.). Of these, five exhibited arrest points earlier than L4 larval stage (J. Schein, pers. comm.). We found that two of the five were uncovered by eDf18. These two mutations complement each other, but one, s1198, fails to complement sy238. sy238/s1198 animals can also exhibit the mid-larval arrest and rectal scarring phenotypes associated with sy238/Df animals. We are currently investigating the cellular phenotype of s1198 homozygotes.