TABLE 2

Tests for suppression of meiotic entry defects by atx-2(RNAi)

Genotype% suppressed
 germlinesn
gld-2(q497) gld-1(q485) 0a
gld-2(q497) gld-1(q485); atx-2(RNAi)b9555
gld-2(q497) gld-1(q485); glp-1(q175) 0a
gld-2(q497) gld-1(q485); glp-1(q175)
   atx-2(RNAi)b6853
gld-2(q497); nos-3(oz231); glp-1(q175) 0a
gld-2(q497); nos-3(oz231); glp-1(q175)
   atx-2(RNAi)c1770
  • a Defined here as zero, on the basis of criteria in Hansen et al. (2004b), Table 1.

  • b Experiments were done by feeding at 25°.

  • c Experiments were done by injection; animals were raised at 20°.

  • Consistent results were obtained in independent RNAi experiments; 100% of gld-2 gld-1 and gld-2; nos-3 double mutants have a meiotic entry defect (tumorous phenotype) that, surprisingly, is partially enhanced by glp-1 null mutations, e.g., glp-1(q175) null (Hansen et al. 2004b). Although all three genotypes cause a severe meiotic entry defect, they can be ranked with respect to the proportion of meiotic nuclei, as follows: gld-2; nos-3; glp-1 > gld-2 gld-1 > gld-2 gld-1; glp-1 (Hansen et al. 2004b). n, number of gonad arms examined; % suppressed germlines, the percentage of germlines with a decrease in the proportion of proliferating nuclei (REC-8 positive, HIM-3 negative), a corresponding increase in the proportion of meiotic nuclei (REC-8 negative, HIM-3 positive; see Hansen et al. 2004b), and the presence of pachytene nuclei, which are never observed in gld-2 gld-1, gld-2 gld-1; glp-1 or gld-2; nos-3; glp-1 synthetic tumorous mutants.