Description
Inhibition of insulin/IGF-1 signaling (IIS) represents a promising avenue for the treatment of mitochondrial diseases, although many of the molecular mechanisms underlying this beneficial effect remain elusive. Here, we analyze the transcriptome of a well established model for mitochondrial deficiency, gas-1(fc21) mutant nematodes, which when placed in a genetic context of IIS inhibition, undergo metabolic rewiring leading to a massive lifespan extension Overall design: 5 biological replicates each of wild-type, gas-1(fc21) and age-1(hx546);gas-1(fc21) mutant nematodes (L4 stage) were analyzed by RNA Next Generation Sequencing