Two mutations in pab-1 encoding poly(A)-binding protein show similar defects in germline stem cell proliferation but different longevity in C. elegans.

Abstract

Four new alleles, bn116, bn117, bn118, and bn119, on LG I were isolated in C. elegans with defects in germline stem cell proliferation. Using genetic mapping and snip-SNP mapping, bn116, bn117, bn118, and bn119 were located 5.0 cM, 1.3 cM, 2.3 cM, and 5.0 cM, respectively, to the right of dpy-5 on LG I. Further, bn116 and bn119 were grouped into the same complementation group by a complementation test. They are loss-of-function recessive alleles that produce homozygous sterile worms whose germ cells do not proliferate during larval development. However, the worms contained normal somatic gonadal structures including distal tip cells and gonadal sheath cells, suggesting that the defect in germline proliferation was not caused by the absence of somatic signaling. Although DAF-16 was localized to the nucleus in all four mutants, the life span was extended only in the three mutants except bn116. These results suggest that the defect in germline stem cell proliferation, the presence of normal somatic gonadal tissues, and DAF-16 nuclear translocation were sufficient for extending the lifespan of the bn117, bn118, and bn119 mutants, but not the bn116 mutant. Intriguingly, bn116 and bn119 were identified as two different mutations on the same gene, pab-1, which encodes a poly(A)-binding protein. Therefore, although the bn116 and bn119 mutations cause similar defects in germ cell proliferation, their effects on life span are different.