Cuticular sclerotization in insects – A critical review

Sclerotization of cuticle is a vital process for the survival of insects. It is caused by covalent crosslinking of structural proteins and chitin to form hard and often coloured cuticle. During sclerotization, N-acetyldopamine and N-β-alanyldopamine are activated by cuticular enzymes such as phenoloxidase—both laccase and o-diphenoloxidase, peroxidase, quinone isomerase and quinone methide isomerase to reactive intermediates that can form adducts and crosslinks. Four major mechanisms—quinone tanning, quinone methide sclerotization, α,β-sclerotization, and free radical tanning have been identified so far for gluing and bonding the structural proteins with chitin. The biochemistry of the quinone tanning, the first discovered mechanism for hardening is critically evaluated and assessed. The enzymatic and nonenzymatic production of quinone methide, and the critical role of quinone isomerase in quinone methide sclerotization is discussed. The biosynthesis of two sclerotizing precursor associated with α,β-sclerotization is outlined. The critical roles of dehydro N-acetyldopamine and dehydro N-β-alanyldopamine in α,β-sclerotization, and the differential use of N-acetyldopamine and N-β-alanyldopamine in producing coloured versus colourless cuticle is considered. Potential contribution of both peroxidase and laccase for free radical tanning is also briefly examined. The mechanisms of formation of catecholic products in cuticular hydrolysates are investigated. The genes associated with cuticular hardening are briefly described. Sclerotization in other animal systems that use dehydro dopa and its derivatives is also assessed. Melanisation reactions that occur in cuticle and hemolymph and its role in wound healing, defence reactions and cuticular pigmentation is critically evaluated.