Figure 6. Reconstitution of aak-2 in ASI partially rescues dauer exit.

A. daf-2; aak-2 animals exit dauer when kept on plates at the restrictive temperature (25 °C), while daf-2 animals maintain dauer. Reconstitution of aak-2 in only the ASI neurons restores dauer maintenance to ∼60% of daf-2; aak-2 double mutants. Non-transgenic siblings do not show any improved dauer maintenance. Animals exiting dauers grew to adulthood in each case. We did not examine these dauers beyond day 15 only because it became increasingly difficult to maintain these plates contamination free and prevent the dauers from escaping the plates. B-C. RNAi-mediate knockdown of atgl-1 delays dauer exit for daf-2; aak-2 (B) and daf-7; aak-2 (C) animals but does not allow for dauer maintenance beyond the time that a 100% of vector treated animals have exited the stage and resumed growth. While relative to daf-7 mutants, daf-7; mgl-1; mgl-3 triple mutants have low fat levels, they maintain dauer as well as daf-7 mutants (C). Each of the graphed data in A-C reflects the averages of 5 plates of 100 animals per genotype. A representative result is shown. The indicated results were repeated in at least three independent trials.