- page settings
- showhide sidebar
- showhide empty fields
- layout
- (too narrow)
- open all
- close all
- Page Content
- Overview
- External Links
- History
- Referenced
- Tools
- Tree Display
- My WormBase
- My Favorites
- My Library
- Recent Activity
- Comments (0)
history logging is off
Tree Display
My Favorites
My Library
Comments on Madhura Kulkarni et al. (2005) International Worm Meeting "Phenotypic characterization of spe-32" (0)
Overview
Madhura Kulkarni, & Harold Smith (2005). Phenotypic characterization of spe-32 presented in International Worm Meeting. Unpublished information; cite only with author permission.
spe-32 was initially identified as a temperature-sensitive, spermatogenesis-defective mutation. Mutant hermaphrodites exhibit sperm-specific sterility (Spe phenotype) when larvae are shifted to the restrictive temperature of 250C before L4. In addition, spe-32 is required for early development. Mutant hermaphrodites produce dead embryos when shifted to 250C as adults, and larval lethality is observed when eggs are shifted to 250C. The embryonic and larval lethality, but not the Spe phenotype, is maternally rescued. Homozygous spe-32 progeny from heterozygous spe-32/+ mother reared at 250C develop normally to adulthood but still exhibit sperm-specific sterility. spe-32 males manifest other phenotypes in addition to sterility and larval lethality. Development of the male tail is aberrant at the restrictive temperature. The tip of the tail is remarkably reduced in length compared to wild type and the fan is smaller. Unlike all the other phenotypes, which are recessive, this male tail effect is semi-dominant. The majority of males grown at restrictive temperature also show progressive paralysis. The movement defect begins at the tail and pregresses anteriorly as the animal ages, leading to total paralysis and premature death. Even at the permissive temperature, spe-32 males show reduced mating efficiency and some proportion of males have constitutively protracted spicules. All of these phenotypes suggest additional male-specific roles for the spe-32 gene in Caenorhabditis elegans.Currently, we are trying to clone the spe-32 gene by cosmid rescue. Prior work mapped spe-32 to LGIV and linked the mutation to dpy-20. We have used snip-SNP mapping technique to narrow down the genomic interval for spe-32 between 4.35cM to 4.55cM. Microinjection of cosmids in this interval is underway. Our other efforts are directed toward characterization of specific defect in spermatogenesis that results in sterility.
Affiliations:
- Center for Advanced Research In Biotechnology, UMBI, Rockville, MD
- Department of Cell and Molecular Genetics, University of Maryland, College Park, MD