Disease relevance of spe-26

• Six independent mutations in the Caenorhabditis elegans spe-26 gene cause sterility in males and hermaphrodites by disrupting spermatogenesis [1].

High impact information on spe-26

• The functional importance of these repeat motifs is shown by the fact that five of the spe-26 mutations are in the tandem repeats, and one of the most severe mutations is a substitution in a highly conserved glycine [1].
• The spe-26 gene is expressed throughout the testis in both spermatogonial cells and spermatocytes [1].
• These results suggest that spe-26 encodes a cytoskeletal protein, perhaps actin binding, which is necessary to segregate the cellular components that form haploid spermatids [1].
• Long-lived spe-26 and daf-2 mutants also exhibit Itt [2].
• The mutations in daf-16 did not alter the reduced fertility of spe-26 and interestingly a daf-16 mutant is more fertile than wild type [3].

Biological context of spe-26

• In contrast, a spe-26 mutant had a tenfold lower mortality until approximately 2 weeks of age but ultimately achieved a higher mortality, whereas clk-1 mutants show slightly higher mortality than wild type during the fertile period, early in life, but ultimately level off at lower mortality [4].

References