Sw. Lhernault et al., GENETIC AND MOLECULAR CHARACTERIZATION OF THE CAENORHABDITIS-ELEGANS SPERMATOGENESIS-DEFECTIVE GENE SPE-17, Genetics, 134(3), 1993, pp. 769-780
Two self-sterile mutations that define the spermatogenesis-defective g
ene spe-1 7 have been analyzed. These mutations affect unc-22 and fail
to complement each other for both Unc-22 and spermatogenesis defects.
Both of these mutations are deficiencies (hcDf1 and hDf13) that affec
t more than one transcription unit. Genomic DNA adjacent to and includ
ing the region deleted by the smaller deficiency (hcDf1) has been sequ
enced and four mRNAs (including unc-22) have been localized to this se
quenced region. The three non unc-22 mRNAs are shown to be sex-specifi
c: a 1.2-kb mRNA that can be detected in sperm-free hermaphrodites and
1.2- and 0.56-kb mRNAs found in males. hDf13 deletes at least 55 kb o
f chromosome IV, including all of unc-22, both male-specific mRNAs and
at least part of the female-specific mRNA. hcDf1, which is approximat
ely 15.6 kb, deletes only the 5' end of unc-22 and the gene that encod
es the 0.56-kb male-specific mRNA. The common defect that apparently a
ccounts for the defective sperm in hcDf1 and hDf13 homozygotes is dele
tion of the spe-17 gene, which encodes the 0. 56-kb mRNA. Strains carr
ying two copies of either deletion are self-fertile when they are tran
sgenic for any of four extrachromosomal array that include spe-17. We
have sequenced two spe-17 cDNAs, and the deduced 142 amino acid protei
n sequence is highly charged and rich in serine and threonine, but sho
ws no significant homology to any previously determined protein sequen
ce.