Fig. 7. Synergism of ptp-3 with vab-1 and vab-2 and lack of synergism with ina-1 or clr-1. (A) Lethality was quantitated as described in Materials and Methods; error bars show s.e.m. Strains were raised at 20°C unless indicated. Data for vab-1 are from George et al. (George et al., 1998). Strains doubly mutant for ptp-3(op147) and weaker vab-1 kinase alleles (the missense alleles e2 and ju63) showed partially penetrant synergistic lethality yet were viable as homozygotes; strains containing stronger kinase alleles were completely inviable as double mutants with op147 (not shown). (B) Synergism of ptp-3 with efn mutations. Data for efn-1 from Chin-Sang et al. (Chin-Sang et al., 1999). Only efn-1 displays synergistic lethality with ptp-3. Over 90% of the lethality in vab-1(kinase) ptp-3 double mutants occurred during embryogenesis, whereas vab-1(e699) and efn-1 double mutants displayed approx. 60% embryonic lethality and approx. 30% larval lethality. (C) Synergism of the RPTP clr-1 with vab-1 or ptp-3 was tested using the temperature-sensitive clr-1(e1745), which is fully viable at 15°C and 20°C and is a fully penetrant late larval lethal at 25°C. vab-1 clr-1 homozygotes were viable at 20°C; clr-1 ptp-3 strains were viable at 15°C but not at 20°C, possibly suggestive of a mild enhancement of the Clr-1 phenotype. Embryonic lethality was quantitated using balanced strains of genotype clr-1/mIn1 mIs14, vab-1 clr-1/mIn1 mIs14, and clr-1 ptp-3/mIn1 mIs14. Strains were raised at 25°C and the embryonic lethality of non-GFP-expressing animals quantitated.
