From The Origin of Species to the origin of bacterial flagella

There is little hope for a vaccine for African sleeping sickness, and most of the drugs currently used to treat it are old, not particularly effective and difficult to use in the conditions that prevail in sub-Saharan Africa, where the disease is endemic. So the discovery of a new class of molecule that might be targeted by drug intervention could be an important boost to the field. The sleeping sickness parasite Trypanosoma brucei is a protozoon equipped with a whip-like flagellum. RNA interference (RNAi) knock-down experiments show that a functioning flagellum is essential for Trypanosoma's survival in the bloodstream. That makes the flagellum a possible point of therapeutic attack, and proteomic analysis points to a number of trypanosome-specific flagellar proteins that could be targeted. On the cover, monstrous cells of bloodstream-form trypanosomes formed by a failure of cell division in cells with defective flagella.

Many prokaryotic protein complexes underlie polar asymmetry. In Caulobacter crescentus, a flagellum is built exclusively at the pole that arose from the previous cell division. The basis for this pole specificity is unclear but could involve a cytokinetic birth scar that marks the newborn pole as the flagellum assembly site. We identified two developmental proteins, TipN and TipF, which localize to the division septum and the newborn pole after division. We show that septal localization of TipN/F depends on cytokinesis. Moreover, TipF, a c-di-GMP phosphodiesterase homolog, is a flagellum assembly factor that relies on TipN for proper positioning. In the absence of TipN, flagella are assembled at ectopic locations, and TipF is mislocalized to such sites. Thus TipN and TipF establish a link between bacterial cytokinesis and polar asymmetry, demonstrating that division does indeed leave a positional mark in its wake to direct the biogenesis of a polar organelle.