Molecular Models of Wolbachia-Induced Cytoplasmic Incompatibility Must Account for the Multiplicity of Compatibility Types.

Wolbachia endosymbionts commonly induce cytoplasmic incompatibility, making infected males’ sperm lethal to the embryos unless these are rescued by the same bacterium, inherited from their mother. Causal genes were recently identified but two families of mechanistic models are still opposed. In the toxin-antidote model, interaction between the toxin and the antidote is required for rescuing the embryos. In host modification models, a host factor is misregulated in sperm and rescue occurs through compensation or withdrawal of this modification. While these models have been thoroughly discussed, the multiplicity of compatibility types, i.e., the existence of many mutually incompatible strains, as seen in Culex mosquitoes, has not received sufficient attention. To explain such a fact, host modification models must posit that the same embryonic defects can be induced and rescued through a large variety of host targets. Conversely, the toxin-antidote model simply accommodates this pattern through variations in the toxin-antidote interaction sites.

Advances in Biomaterial’s Modification and Thrombosis Inhibition

With the development of modern medical technology, the clinical range of biomaterial applications have gradually expanded. However, bioactivity on the surface of biomaterials may be reduced and induce thrombus formation that will not only cause serious dysfunction of the biological materials, but can also affect the host. Modification of these biological materials can thus help to retain the biological activity on the surface of the material and inhibit thrombus formation, which underlines the importance of their clinical application. The current review will address the modification of biomaterials and inhibition of thrombosis on the surface of biomaterials.

Intra-specific host sharing in the manipulative parasiteAcanthocephalus dirus: does conflict occur over host modification?

The acanthocephalan parasiteAcanthocephalus dirusinduces a colour change in the intermediate host, the aquatic isopodCaecidotea intermedius, which increases transmission to definitive hosts (creek chub, sunfish). We examined the potential for conflict to occur between infective (cystacanth) and non-infective (acanthor, acanthella) stages ofA. dirusover the level of colour modification that should be induced when these stages share a host. Using a field survey, we showed that host sharing by infective and non-infective stages was relatively common and that infective and non-infective stages differed in their effects on colour modification. Non-infective stages induced a colour change over 40% of the body, whereas infective stages induced a colour change over 80%. Thus, conflict could occur between stages over the level of modification that should be induced. We then showed that mixed-stage infections induced a colour change in the host that was consistent with the level of modification induced by the infective stage. We discuss the potential significance of these results to patterns of host modification and their effects on stage-related survival in nature.