6 Interactions found (0.008 seconds)

"We found that simultaneous RNAi depletion of the redundantly functioning paralogs pgl-1 and pgl-3 (Kawasaki et al., 2004) caused msp-3 expansion in 20% of worms (supplementary material Fig. S5; Table 1). This expansion was also observed in 18% of worms only fed pgl-1 RNAi, and in 30% only fed glh-1 RNAi. We also observed an expanded msp-3 domain in 18% of glh-4(gk224) glh-1(ok439) double mutants, in 31% of pgl-1(bn101) single mutants and in 20%of pgl-3(bn104) single mutants. Proximal germlines in pgl-1(bn101); pgl-3(bn104) did not show an expansion of the msp-3 domain, but these double mutants contained very severe germline proliferation defects that might have masked this phenotype."

"We found that simultaneous RNAi depletion of the redundantly functioning paralogs pgl-1 and pgl-3 (Kawasaki et al., 2004) caused msp-3 expansion in 20% of worms (supplementary material Fig. S5; Table 1). This expansion was also observed in 18% of worms only fed pgl-1 RNAi, and in 30% only fed glh-1 RNAi. We also observed an expanded msp-3 domain in 18% of glh-4(gk224) glh-1(ok439) double mutants, in 31% of pgl-1(bn101) single mutants and in 20%of pgl-3(bn104) single mutants. Proximal germlines in pgl-1(bn101); pgl-3(bn104) did not show an expansion of the msp-3 domain, but these double mutants contained very severe germline proliferation defects that might have masked this phenotype."

F08F1.13 : glh-1 : glh-4 : msp-3 : tag-123

"We found that simultaneous RNAi depletion of the redundantly functioning paralogs pgl-1 and pgl-3 (Kawasaki et al., 2004) caused msp-3 expansion in 20% of worms (supplementary material Fig. S5; Table 1). This expansion was also observed in 18% of worms only fed pgl-1 RNAi, and in 30% only fed glh-1 RNAi. We also observed an expanded msp-3 domain in 18% of glh-4(gk224) glh-1(ok439) double mutants, in 31% of pgl-1(bn101) single mutants and in 20%of pgl-3(bn104) single mutants. Proximal germlines in pgl-1(bn101); pgl-3(bn104) did not show an expansion of the msp-3 domain, but these double mutants contained very severe germline proliferation defects that might have masked this phenotype."

"We found that simultaneous RNAi depletion of the redundantly functioning paralogs pgl-1 and pgl-3 (Kawasaki et al., 2004) caused msp-3 expansion in 20% of worms (supplementary material Fig. S5; Table 1). This expansion was also observed in 18% of worms only fed pgl-1 RNAi, and in 30% only fed glh-1 RNAi. We also observed an expanded msp-3 domain in 18% of glh-4(gk224) glh-1(ok439) double mutants, in 31% of pgl-1(bn101) single mutants and in 20%of pgl-3(bn104) single mutants. Proximal germlines in pgl-1(bn101); pgl-3(bn104) did not show an expansion of the msp-3 domain, but these double mutants contained very severe germline proliferation defects that might have masked this phenotype."

"We found that simultaneous RNAi depletion of the redundantly functioning paralogs pgl-1 and pgl-3 (Kawasaki et al., 2004) caused msp-3 expansion in 20% of worms (supplementary material Fig. S5; Table 1). This expansion was also observed in 18% of worms only fed pgl-1 RNAi, and in 30% only fed glh-1 RNAi. We also observed an expanded msp-3 domain in 18% of glh-4(gk224) glh-1(ok439) double mutants, in 31% of pgl-1(bn101) single mutants and in 20%of pgl-3(bn104) single mutants. Proximal germlines in pgl-1(bn101); pgl-3(bn104) did not show an expansion of the msp-3 domain, but these double mutants contained very severe germline proliferation defects that might have masked this phenotype."

"We found that simultaneous RNAi depletion of the redundantly functioning paralogs pgl-1 and pgl-3 (Kawasaki et al., 2004) caused msp-3 expansion in 20% of worms (supplementary material Fig. S5; Table 1). This expansion was also observed in 18% of worms only fed pgl-1 RNAi, and in 30% only fed glh-1 RNAi. We also observed an expanded msp-3 domain in 18% of glh-4(gk224) glh-1(ok439) double mutants, in 31% of pgl-1(bn101) single mutants and in 20%of pgl-3(bn104) single mutants. Proximal germlines in pgl-1(bn101); pgl-3(bn104) did not show an expansion of the msp-3 domain, but these double mutants contained very severe germline proliferation defects that might have masked this phenotype."