The strategy that the protozoan parasite Trypanosoma brucei — which causes fatal disease in humans and cattle — uses to evade its host's immune defences is the subject of a News & Views article on page 172. Elsewhere in this issue, Dean et al. provide further molecular insights into the workings of this pathogen (pictured, with red blood cell). They focus on the cell-differentiation events associated with its transmission between host and vector (S.Dean et al. Nature 459, 213–217; 2009).


In response to the metabolites citrate or cis-aconitate, trypanosomes differentiate from a non-dividing, stumpy form — the form thought to be taken up by the parasite's tsetse fly vector from the mammalian host's bloodstream — to a dividing form found in the fly's midgut.

The parasite becomes sensitive to the metabolite signals through exposure to low temperatures, which the fly often experiences while feeding at dusk or dawn. But the surface molecules responsible for transmitting the signals to the microbe have remained elusive.

Dean and colleagues find that trypanosomes sense citrate through the PAD family of cell-surface transporter proteins. Only the stumpy form seems to express these proteins, establishing it as the competent stage in the parasite's life cycle for transmission from its mammalian host to the fly.

The authors also find that reducing PAD expression decreases citrate-induced trypanosome differentiation. PAD proteins could therefore potentially be used as molecular markers when screening for compounds that promote transition to the non-dividing, and so less-virulent, stumpy form.