The overarching aim of this thesis was to investigate how proton-sensitive members of the C. elegans DEG/ENaC family regulate cellular processes and drive behaviour. In the initial screen, I identified five C. elegans DEG/ENaCs subunits that can form proton-sensitive homomeric channels when expressed in vitro in Xenopus oocytes. These could be further clustered into two groups based on their response to neutral and low pH in vitro: One group that is inhibited by increasing concentrations of protons (ACD-5 and DEL-4, as well as the previously identified ACD-1 (Wang et al., 2008)) and the other one that can be activated by increasing concentrations of protons (ASIC-1, ACD-2 and DEL-9). Exploration of cellular expression pattern and amino acid sequence similarity revealed that C. elegans DEG/ENaCs can form clusters that reflect expression in neuronal or non-neuronal tissue but these clusters do not correspond to the electrophysiological properties presented here. Further electrophysiological characterisation of candidate subunits showed that increasing concentrations of protons inhibit or activate the homomeric channels in a dose-dependent manner. The ACD-5 and DEL-4, which are inhibited by low pH, show specific pH ranges in which the channel is open or closed, which might reflect their physiological environment in vivo. A similar observation has been made for the human ENaC currents, they are regulated by a pH range that is comparable to the one in epithelia where ENaCs are expressed (Collier and Snyder, 2009). The electrophysiological characterisation confirmed previous results that the C. elegans DEG/ENaCs are highly diverse in their ion selectivity (Fechner et al., 2020). This again, is likely to reflect their diverse physiological function in vivo. Based on expression pattern and in vitro electrophysiological evidence, I further characterised one candidates of each group in more detail, DEL-9 which belongs to the group that is activated by low pH and ACD-5 which is inhibited by low pH. Interestingly, both can be expressed in neuronal and non-neuronal tissue, suggesting that their proton-sensing properties are important for various physiological processes and are not restricted to neuronal functioning, and mutants of either gene show defects in rhythmic behaviours. This fits well with evidence across species that DEG/ENaCs and ASICs are involved in regulating cellular excitability and communication to modulate behaviour (Du et al., 2014, Wemmie et al., 2003, Wemmie et al., 2002, Voglis and Tavernarakis, 2008). Finally, in the last chapter, I identified daf-7/TGFβ-like signalling as the regulatory genetic pathway for neuronal and global upregulation of ACD-5 in dauers and post-dauers. I have further explored the genetic relationship between daf-7/TGFβ and acd-5 and explored potential behaviours relating to expression in ASK sensory neurons. Taking together the evidence presented suggests that at some level ACD-5 regulation depends on food and that ACD-5 is implicated in food-sensing: It is expressed in the chemosensory ASK neuron and in the intestine, it is implicated in food-sensing behaviours, and it is regulated by TGFβ-like signalling which again is a developmental pathway linked to food abundance.