Abstract
Neuronal DEG/ENaC (degenerin and epithelial Na
+
channel) Na
+
channels have been implicated in touch sensation. For example, MEC-4 is expressed in touch neurons in
Caenorhabditis elegans
and mediates gentle-touch response. Similarly, homologous mammalian ASIC2 and ASIC3 are expressed in sensory neurons and produce touch phenotypes when knocked out in mice. Here, we show that novel DEG/ENaC subunits DELM-1 and DELM-2 (degenerin-like channel mechanosensory linked-1 and degenerin-like channel mechanosensory linked-2) are expressed in glia associated with touch neurons in
C. elegans
and that their knock-out causes defects in mechanosensory behaviors related to nose touch and foraging, which are mediated by OLQ and IL1 sensory neurons. Cell-specific rescue supports that DELM-1 and DELM-2 are required cell-autonomously in glia to orchestrate mechanosensory behaviors. Electron microscopy reveals that in
delm-1
knock-outs, OLQ and IL1 sensory neurons and associated glia are structurally normal. Furthermore, we show that knock-out of DELM-1 and DELM-2 does not disrupt the expression or cellular localization of TRPA-1, a TRP channel needed in OLQ and IL1 neurons for touch behaviors. Rather, rescue of the
delm-1
nose-touch-insensitive phenotype by expression of a K
+
channel in socket glia and of a cationic channel in OLQ neurons suggests that DELM channels set basal neuronal excitability. Together, our data show that DELM-1 and DELM-2 are expressed in glia associated with touch neurons where they are not needed for neuronal structural integrity or cellular distribution of neuronal sensory channels, but rather for their function.
