TGFb -like and insulinlike pathways regulate dauer entry and recovery. Since the Daf-c (dauer formation constitutive) phenotype associated with
daf-2(lf) (insulin receptor-like) can be fully suppressed by
daf-16(lf) (fork-head-like transcription factor),
daf-16 was considered to be the terminal dauer-promoting gene of the insulin-like pathway and the sole output of the
daf-2/IR signal. Likewise,
daf-3 (smad transcription factor) is considered to be the terminal dauer-promoting gene of the
daf-7/TGFb -like pathway. These two signaling pathways may converge by regulating the
daf-12 (nuclear hormone receptor) activity. A third signaling pathway for dauer arrest is suggested by the finding that
daf-16(0);
daf-3(0) animals can still form partial dauers in response to pheromone. In order to identify the components in the putative third signaling pathway, we screened for Daf-c mutations in a
daf-16(0);
daf-3(0) background. No Daf-c mutations in either the TGFb or insulin-like pathways were expected to be isolated from this screen. Surprisingly,
mg293, one of the two alleles isolated from this screen, is likely to be an allele of
daf-2 based on its map position and a complementation test. The Daf-c phenotype caused by
daf-2(lf) was expected to be suppressed by
daf-16(0). But the result suggested that a
daf-3(0) mutation can relieve this suppression. To directly test this possibility, we constructed a
daf-16(0);
daf-2(0);
daf-3(0) strain ,using a known
daf-2(0) allele. At all temperatures tested, this triple mutant gives rise to transient partial dauers. This result indicates a
daf-16-independent
daf-2 output that is normally masked by the
daf-3(+) function. This
daf-2 output affects dauer entry but not recovery and it may well be the third signaling pathway. Since
daf-12 is the most downstream dauer-promoting gene and can mutate to Daf-c (likely gf) alleles, which also give rise to transient partial dauers, we hypothesize that
daf-12 and its co-factors may be the targets of the
daf-16-independent
daf-2 signal. We performed a suppressor screen on the Daf-c
daf-12(
rh273) strain and have obtained 12 suppressors. We are currently analyzing these suppressors and testing whether they (and
daf-12 itself) are the targets for the
daf-16-independent
daf-2 signal.