Nematodes including free-living C. elegans require sterol for their growth as a nutritional source because C. elegans is unable to biosynthesize sterol de novo. C. elegans shows dauer-like larvae formation upon cholesterol starvation (CS), but the genetic epistasis among abnormal dauer formation (daf) genes during the process remains unclear. To clarify the genetic interactions among
daf-9,
daf-12, and
daf-16 in this process, mRNA levels of these genes upon CS were measured. DAF-9, a cytochrome P450, produces a ligand for DAF-12, a hormone receptor. DAF-16 is a key factor in the
daf-2/insulin-like signaling. We found that CS increased the mRNA levels of
daf-9,
daf-12, and
daf-16. CS also induced DAF-16 nuclear localization, which was positively and negatively regulated by DAF-12 and DAF-9 activities, respectively. We also found that DAF-16, a FOXO transcription factor, enhanced the mRNA levels of
daf-12 but suppressed
daf-9, whereas DAF-9 regulated
daf-12 mRNA level negatively. Concomitantly, CS-induced larval arrest was regulated positively by DAF-12 and DAF-16, but negatively by DAF-9. The effect of
daf-9 mutant on the larval arrest was suppressed by
daf-12 RNAi, placing DAF-12 downstream of DAF-9. These results altogether suggest that circulatory mutual regulation among
daf-9,
daf-12, and
daf-16 at the expression level mediates cholesterol signal to control larval development upon CS. On the other hand, DAF-16 translocation upon CS did not induce
sod-3 expression or extend life span. General sickness or other stresses caused by CS might have hindered the effect of DAF-16 translocation on longevity.