Adult nervous system has limited capacity to regenerate after accidental damages. Post injury functional restoration requires proper targeting of the regenerated axon to the postsynaptic partner. In C. elegans both mechanosensory and motor neurons show functional recovery following neuronal injury in early stages of life. Functional restoration declines with age in touch neuron. Identification of pathways that inhibit regrowth is relevant for informing therapeutic strategies for functional recovery. Several mutants are identified that inhibit regeneration of touch neuron in early adult stages. It is not clear among these which are critical for promoting functional regeneration in late adult stages. A comprehensive understanding of how these pathways would be related to the pathways that control organism level aging is also lacking till date. Towards this goal, we axotomized the PLM (Posterior Touch Receptor Neuron) axons in various mutants and compared the functional regeneration at L4 and Day3 stages using the posterior touch response index (PTRI). We found that although some of the mutants known for enhancing axonal regrowth showed improved functional recovery at L4 stage, only few of them showed functional restoration in A3 stage. Other than the previously known
let-7(0), mutants lacking the components of Insulin signaling (IIS) and S6 kinase mutant
rsks-1(0) showed an enhanced recovery at A3 stages. Loss of IGF-1 receptor, DAF-2 or any other downstream kinases like AGE-1, PDK-1, AKT-1/2 in IIS pathway promote functional restoration irrespective of the animal's age. Upon activation, DAF-2 inhibits translocation of the forkhead transcription factor FOXO/ DAF-16 from cytoplasm to nucleus through the downstream kinases. Enhanced recovery in
daf-2(0) is completely dependent on
daf-16. Moreover, we found that in absence of
daf-16, functional recovery is affected in both L4 and A3 stages. This indicated that DAF-16 is important for regeneration. Other than IIS pathway, we found significant recovery in
rsks-1(0). S6 kinase inhibits the downstream kinase AMPK/ AAK-2 and affects DAF-16 activity. We found functional restoration in
rsks-1(0) depends on
aak-2 but is independent of
daf-16. Since both
let-7 miRNA and IIS pathway inhibit axon regeneration, it is important to understand how these two cascades converge and/or diverge. We found that simultaneous loss of
let-7 and
akt-1 increase functional recovery in a synergistic manner. Also, loss of
let-7(0) can completely bypass the requirement of
daf-16 in regeneration. Moreover, functional restoration gets significantly improved in worms lacking both
let-7 and
rsks-1 in comparison to single mutants. Our data reveals that there are independent negative regulators of axon regeneration and their simultaneous removal might be beneficial in overcoming regeneration barrier after neuronal injury.