The pore canal protein snsl is required for cuticular lipids transport and cuticle barrier function in the migratory locust, Locusta migratoria.

Lipids are important components of the insect cuticle protecting against desiccation and xenobiotic penetration. Delivery of lipids to the cuticular surface occurs through pore canals, which are a nano-canal system formed by the epidermis, running through the procuticle and terminating at the epicuticle, where they ramify as wax-canals. The molecular mechanisms of cuticular lipids deposition in insects are poorly understood. Here, we identified the pore canal protein Snsl (Snustorr snarlik) in the migratory locust Locusta migratoria (LmSnsl) and investigated its function in cuticular lipid transport and cuticle barrier construction. We found that LmSnsl was specifically expressed in the integument and had a high expression level before ecdysis when a new cuticle is formed. Silencing of LmSnsl by RNA interference (RNAi) caused a lethal phenotype during or shortly after molting. In addition, RNAi against LmSnsl resulted in a decrease in cuticular lipids and in the accumulation of internal lipids. The pore canals of dsLmSnsl animals are deformed and contain less luminal material. Furthermore, we found that cuticle permeability to xenobiotics was enhanced in dsLmSnsl-treated nymphs that were, consistently, more susceptible to insecticides. These animals were also prone to pathogen invasion suggesting that cuticle lipids act in pathogen defense. Taken together, our results indicate that the locust Snsl protein is needed for pore canal integrity required for the transport of lipids from the epidermis to the cuticle to constitute a barrier against xenobiotics and pathogens.