Figure 3. Identification of TAX-6 as a target and a positive regulator of DAF-2 signaling. (A to F) TAX-6::GFP was expressed in neurons (open arrows) and in the cytoplasm (solid arrows) and nucleus (arrowheads) of intestinal cells.
tax-6(
p675); Ex[pAK13] animals were imaged at magnifications 100 [(A) to (C)] and 400 [(D) to (F)]. DIC, differential interference contrast. (G) Expression of TAX-6::GFP in the intestine of animals treated with control,
daf-2, or
tax-6 RNAi. The intensity of cytoplasmic and nuclear TAX-6::GFP in the intestine was scored separately. Percentages of worms expressing strong (+++), intermediate (++), weak (+), very weak (+/-), or background (-) TAX-6::GFP in the intestine were averaged from three experiments (n > 39 animals in each experiment). (H) Effects of the
tax-6(
p675) mutation on dauer formation and a synthetic effect with
daf-2 RNAi. WT ('1' and '2'),
daf-16 (
mu86) ('3' and '4'), and
tax-6(
p675) ('5' and '6') animals were treated with
daf-2 ('2,''4,' and '6') or control RNAi ('1,''3,' and '5') at 27C (black, one experiment) or 25C (gray, average of two experiments) (n > 120 animals in each experiment). (I)
daf-16(
mu86) suppressed
tax-6(
p675) dauer formation (average of two experiments, n > 300 animals per experiment). (J)
daf-16(
mu86) suppressed the long life span of
tax-6(
p675) mutant animals (one experiment, n > 80 animals, P < 0.01, log-rank test). (K)
cnb-1 mutants displayed an extended life span (one experiment, n > 80 animals, P < 0.01, log-rank test).