Infection with the wMel and wMelPop strains of Wolbachia leads to higher levels of melanization in the hemolymph of Drosophila melanogaster, Drosophila simulans and Aedes aegypti.

Introduction of the life-shortening strain of Wolbachia pipientis, wMelPop, into the key dengue vector, Aedes aegypti, and the anti-pathogen effects in Wolbachia-infected hosts highlights the need for more research into its interactions with its original host, Drosophila melanogaster, and the novel mosquito host. The visual difference in darkness between the eggs of wMelPop Wolbachia-infected and uninfected mosquito hosts after egg deposition led to further investigation into melanization levels of the insects. Both D. melanogaster and A. aegypti infected with wMelPop showed increased levels of melanization, especially in females. This result was also seen in D. melanogaster and Drosophila simulans infected with the closely related wMel strain. D. simulans infected with other strains of Wolbachia did not display this difference. HPLC analysis of hemolymph from mosquitoes showed that this difference was not due to dopamine levels in the host as they were no different in wMelPop-infected and control mosquitoes before or after blood feeding.

Inhibition of Melanization by a Parasitoid Serine Protease Homolog Venom Protein Requires Both the Clip and the Non-Catalytic Protease-Like Domains.

Endoparasitoid wasps inject a variety of components into their host hemocoel at oviposition to facilitate successful development of their progeny. Among these are venom proteins which have been shown to play crucial roles in host regulation. A serine protease homolog (SPH)-like venom protein from Cotesia rubecula was previously shown to inhibit melanization in the host hemolymph by blocking activation of prophenoloxidase to phenoloxidase, a key enzyme in melanin formation. Similar to other SPHs, Vn50 consists of a clip and a protease-like (SPL) domain. Protein modeling demonstrated that Vn50 has a very similar structure to known SPHs and functional analysis of Vn50 domains expressed in insect cells indicated that neither of the domains on its own has an inhibitory effect on melanization.