Abstract
In Caenorhabditis elegans, gentle touch is sensed by the anterior (ALM and AVM) and posterior (PLM) touch receptor neurons. Anterior, but not posterior, touch is affected by several stress conditions via the action of AKT kinases and the DAF-16/FOXO transcription factor. Here we show that a ubiquitination-dependent mechanism mediates such effects. AKT-1/AKT kinase and DAF-16 alter the transcription of mfb-1, which encodes an E3 ubiquitin ligase needed for the ubiquitination of the mechanosensory channel subunit MEC-4. Ubiquitination of MEC-4 reduces the amount of MEC-4 protein in the processes of ALM neurons and, consequently, the mechanoreceptor current. Even under nonstress conditions, differences in the amount of MFB-1 appear to cause the PLM neurons to be less sensitive to touch than the ALM neurons. These studies demonstrate that modulation of surface mechanoreceptors can regulate the sensitivity to mechanical signals.