Evolutionary genetics: Ambiguous role of CCR5 in Y. pestis infection

Mecsas and colleagues suggest that a deficiency in the chemokine receptor CCR5 in humans is unlikely to confer protection against plague, based on their study of Yersinia pestis infection in Ccr5-deficient mice. They were testing the hypothesis that a mutation in the CCR5 gene, frequently found in Caucasians, may have been selected for in the past because it provided protection against (bubonic) plague; the mutation, called CCR5Delta32, is characterized by a 32-base-pair deletion. We have also tested this hypothesis by using Y. pestis infection in mice and, in addition, we have done phagocytosis experiments with macrophages from wild-type and Ccr5-deficient mice. Although, like Mecsas et al., we did not see any difference in the survival of the two groups of mice, we did find that there was a significantly reduced uptake of Y. pestis by Ccr5-deficient macrophages in vitro. Our results indicate that the role of Ccr5 in Y. pestis infection may therefore be more complex than previously thought.     

DNA details

Handy helpers in this week's issue include a dual-purpose device for vertical electrophoresis and electroblotting, a triple-tray gel box and news of a new patent sequence data bank.     

Peripheral organs control central neurogenesis in the leech

Interactions between developing nerve centres and peripheral targets are known to affect neuronal survival and thus regulate the adult number of neurons in many systems. Here we provide evidence that peripheral tissues can also influence cell numbers by stimulating the production of neurons. In the leech Hirudo medicinalis, there is a population of several hundred neurons that is found only in the two segmental ganglia that innervate the genitalia and which seem to be added gradually during post-embryonic maturation. By monitoring 5-bromo-2'-deoxyuridine incorporation immunohistochemically, we have now determined that these neurons are actually born late in embryogenesis, well after all other central neurons are born and after efferent and afferent projections are established between these ganglia and the periphery. Ablation of the male genitalia early in embryogenesis, or evulsion of the nerves that connect them to the ganglia, prevent the birth of these neurons. However, they fail to appear ectopically when male genitalia are transplanted to other segments, despite innervation by local ganglia. We conclude that the generation of the late-appearing neurons depends on a highly localized signal produced by the male genitalia, to which only the ganglia that normally innervate these organs have the capacity to respond.