These neurons are implicated in the regulation of aging, the Vorinostat response to stress conditions and the control of a state of developmental arrest called the dauer larva. Previously, we and others have shown that trx-1 deletion shortens lifespan and increases sensitivity to oxidative stress, though it itself does not affect dauer formation. These findings implicate TRX-1 in processes that regulate aging and stress resistance, which raises the question whether it is involved in mechanisms implicated in the regulation of dauer formation. The C. elegans dauer larva has evolved as a tightly-regulated, long-lived and stress-resistant developmental stage only triggered when the animals encounter harsh environmental conditions. We have identified the C. elegans thioredoxin TRX-1 as a novel modulator of the insulin-like neuropeptide DAF-28 during dauer formation. We found that trx-1 suppresses the Daf-c phenotype of all daf-28 insulin-like mutant alleles tested and that this suppression requires a functional DAF-2 insulin-like receptor. Genetic rescue experiments demonstrated that redox-independent functions of transgenic TRX-1 provided specifically in ASJ neurons can restore the suppression exerted by trx-1 deletion on the Daf-c phenotype of daf-28 mutants. The suppression observed at the genetic level is also manifest at the cellular level specifically during dauer formation: GFP reporters of trx-1 and daf-28 display opposing expression patterns in dauers, which is in contrast to what is observed in growing L2/L3 larvae. Moreover, functional TRX-1 is required for the down-regulation of a GFP reporter of daf-28 during dauer formation, a mechanism that is likely mediated by DAF-28-dependent feedback regulation. Our data suggest that TRX-1 contributes to the regulation of insulin-like neuropeptide expression, in particular DAF-28, during dauer formation in response to a changing environment. Previously, mammalian Trx1 has been proposed to participate in the redox regulation that mediates insulin secretion via NADPH as a signaling molecule. However, we have shown in this report that TRX-1 function in dauer formation does not require its redox activity, suggesting that TRX-1 contributes to the down-regulation of daf-28 expression during dauer formation via mechanisms other than redox regulation of neuropeptide production and/or release. It has recently been found in mammals that key neuronal lipid metabolites act as hypothalamic signaling mediators that monitor energy status and contribute to maintaining organism metabolic homeostasis. Cancer etiology is clearly PLX-4720 connected to a cell��s ability to remove or tolerate lesions in DNA by repair and translesion DNA synthesis.