The
daf-35 mutant is developmentally arrested at the L3 stage. The arrested larvae are morphologically similar to dauer larvae and they accumulate fat. The mutant phenotype of
daf-35 is very similar to that of previously described mutant alleles of
let-363 (C.elegans ortholog of TOR kinase) and
daf-15 (ortholog of raptor). We identified F54C8.5, which encodes an ortholog of the Rheb GTPase (another component of the TOR signaling pathway), as the gene defined by the
daf-35 mutation, which is a candidate null allele. Since partial loss of
daf-15 and
let-363 function extends adult life span, we investigated the effects of
daf-35 RNAi treatment. When exposure to RNAi was started with parents of the tested animals we observed delayed or arrested growth. These observations, at least in part, agreed with previously reported F54C8.5 RNAi effects, such as slow growth, abnormal locomotion, sterile progeny, and thin, clear appearance (Simmer at al. 2003, Kamath at al. 2003). RNAi treatment starting at the L4 stage resulted in normal development and increased median lifespan, but not maximum lifespan. Work is in progress to investigate the expression pattern of
daf-35 and to determine the regions of the
daf-35 promoter that are essential for regulation of its expression.