Primary cilia are microtubule-based organelles that function as sensory antennae for extracellular stimuli. They are involved in the function of several intercellular signalling pathways, including ligand-dependent sonic hedgehog (Shh) signalling, but little is known about how these organelles respond to extracellular stress. Now, Paul Chapple and co-workers (p. 4297) investigate the response of primary cilia to heat shock. Exposure of mammalian cells to high temperatures in vitro results in the shortening and loss of primary cilia by resorption and reduces Shh signalling. Similarly, exposure of zebrafish embryos to high temperatures reduces the number and length of primary cilia in the tail. In mammalian cells, inhibition of histone deacetylases (HDACs) decreases the heat-shock-dependent loss of cilia, which suggests that the axoneme-localized tubulin deacetylase HDAC6 mediates cilia resorption. The activity of the cytosolic chaperone heat shock protein 90 (Hsp90) is also required for maintenance of primary cilia, and HDAC6 and Hsp90 partially colocalise within ciliary axonemes. These results suggest that ciliary resorption attenuates cilia-mediated signalling pathways in response to extracellular stress and that resorption is regulated, in part, by HDAC6 and Hsp90.