Working with scientists from the University of Utah, Cecila Castro, Jules Griffin, Kenneth Murfitt and Eric Miska have published a paper in Nature Neuroscience detailing the role of betaine as a neurotransmitter in the nematode worm (C. elegans). In this study the team examined a receptor called ACR-23, identifying it as a betaine receptor. First, they characterized the betaine transporter SNF-3 and observed that mutations in this transporter led to poor growth in worms which lacked phospholipase C, an important enzyme in cell signalling and also lipid/choline metabolism. Metabolomics was performed in the Department of Biochemistry to characterise these genetically modified worms to understand the underlying mechanisms behind the poor growth. Second, mutations in acr-23 suppressed this, indicating that excess betaine acts via ACR-23.
Interestingly, the publication of WormQTLHD may help link findings in the worm to human disease.