When eukaryotic cells are subjected to stress, they respond by downregulating growth-associated genes and upregulating genes that promote survival. In trypanosomes, gene regulation relies almost entirely on post-transcriptional mechanisms because mRNA is synthesised in multigenic arrays – but how might this affect the stress response? On page 3002, Mark Carrington and colleagues address this question by analysing mRNA dynamics in Trypanosoma brucei (which causes African sleeping sickness) after heat shock. The authors show that several aspects of the T. brucei heat-shock response are similar to that of mammalian cells; for instance, the number of polysomes per cell decreases rapidly after heat shock, as do the levels of many mRNA species (although some become more prevalent). In addition, processing bodies (P-bodies) increase in number, and cytoplasmic stress-granule-like structures accumulate at the cell periphery. Notably, however, stress granules can form without the site-specific phosphorylation of eIF2α, which is usually a requirement for stress-granule formation in mammalian cells. Moreover, the authors show that the 5′-3′ endonuclease XRNA accumulates rapidly at a focus in the cell posterior after heat shock. These results identify key differences between the mammalian and trypanosomal heat-shock responses.