A key event in survival

摘要

The parasitic microorganism Trypanosoma bruce/evades recognition by its host's immune system by repeatedly changing its surface coat. The switch in coat follows a risky route, though: DNA break and repair.rnLike many other single-celled pathogens, the protozoan Trypanosoma brucei, which causes African sleeping sickness in humans, undergoes antigenic variation - that is, it periodically switches its variant surface glyco-protein (VSG), the molecule targeted by host antibodies. But how switching is triggered has remained largely elusive. On page 278 of this issue, Boothroyd et al. show that a DNA double-strand break (DSB) upstream of the T. brucei VSG gene is the likely primary event in this process. Their results add to the few, albeit crucial, cases in which DSBs trigger developmental processes: these include mating-type switching in yeast, rearrangements of immune-system genes in humans and meiotic cell division to produce sex germ cells.