Publication Date



Open access

Embargo Period


Degree Type


Degree Name

Doctor of Philosophy (PHD)


Physiology and Biophysics (Medicine)

Date of Defense


First Committee Member

Laura Bianchi

Second Committee Member

H. Peter Larsson

Third Committee Member

Gerhard Dahl

Fourth Committee Member

Michael Kim

Fifth Committee Member

David M. Miller III


Neuronal DEG/ENaC Na+ channels have been implicated in touch sensation. For example, MEC-4 is expressed in touch neurons in C. 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 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 the idea that DELM-1 and DELM-2 are required cell-autonomously in glia to orchestrate mechanosensory behaviors. Electron microscopy reveals that OLQ and IL1 sensory neurons and associated glia are structurally normal in delm-1 knockouts. Furthermore, we show that knockout 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. Taken 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 touch neuron function.


DEG/ENaC; glia; touch