Wolbachia pipientis is known to infect only arthropods and nematodes (mainly filarial worms). A unique feature shared by the two Phyla is the ability to replace the exoskeleton, a process known as ecdysis. This shared characteristic is thought to reflect a common ancestry. Arthropod moulting is induced by the steroid hormone 20-hydroxyecdysone (20E) and a role for ecdysteroids in nematode ecdysis has also been suggested. Removing Wolbachia from filarial worms impairs the host’s development. From analyses of the genome of Wolbachia harboured by the filarial nematode Brugia malayi and that of its host, the bacterium may provide a source of heme, an essential component of cytochrome P450’s that are necessary for steroid hormone biosynthetic pathways. In arthropods, Wolbachia is a reproductive manipulator, inducing various phenotypic effects that may be due to differences in host physiology, in particular, endocrine-related processes governing development and reproduction. Insect steroids have well-defined roles in the coordination of multiple developmental processes, and in adults they control important aspects of reproduction, including ovarian development, oogenesis, sexual behaviour, and in some taxa vitellogenin biosynthesis. According to some authors ecdysteroids may also act as sex hormones. In insects sex differentiation is generally thought to be a strictly genetic process, in which each cell decides its own sexual fate based on its sex chromosome constitution, but, surprisingly, recent data demonstrate that in Drosophila sex determination is not cell-autonomous, as it happens in mammals. Thus the presence of signals coordinating the development of a gender-specific phenotype cannot be excluded. This could explain why Wolbachia interferes with insect reproduction; and also could explain why Wolbachia interferes with insect development. Thus, is “sex (=reproduction) and stripping (=ecdysis)” the key to the intimate relationship between Wolbachia and its host?
- wolbachia, arthropods, nematodes, ecdysis, ecdysteroids, insulin, hormonal pathways