[
Parasitol Today,
1992]
Like particle physics, biology is now a big expensive business, and like CERN, the genome projects alternately provoke admiration and detraction. Some feel that it would be more valuable to go for specific genes of interest rather than fill databases with sequences of junk DNA. The detractors would also say that the costs entailed, the limited intellectual and practical payback, and the ethical worries are too big to justify. But like the mythological juggernaut, once started it won't stop and it is indisputable that exciting information will come out of these efforts. Like some of the best discoveries many will be unexpected and have repercussions of immense value. This is indisputable on statistical grounds alone; the Caenorhabditis elegans genome is estimated to contain tens of thousands of genes. However, genome projects cannot be justified by serendipity and they do have obvious immediate value for tracing the genes involved in cancer and other inheritable disorders, and indeed for the multiple technological spin-offs. The C. elegans genome project is already bearing luscious fruit, of the 34 genes reported so far some of which have sequence similarity with genes such as glutathione reductase, an immunogenic protein from Trichostrongylus colubriformis, acetyl-CoA acetyltransferase and various other enzymes, growth factors and signal transducing components. Up-to-date cDNA data will be published by John Sulston and his colleagues in the early issues of Nature Genetics, due out this month.
[
Journal of Physiology,
2005]
The TRPV4 ion channel, previously named vanilloid receptor-related osmotically activated channel (VR-OAC), functions in vivo in the transduction of osmotic and mechanical stimuli. In trpv4 null mice, TRPV4 was found to be necessary for the maintenance of systemic osmotic equilibrium, and for normal thresholds in response to noxious mechanical stimuli. In a Caenorhabditis elegans TRPV mutant transgenic for mammalian TRPV4, the mammalian transgene was directing the osmotic and mechanical avoidance response in the context of the ASH ''''nociceptive'''' neurone. Molecular mechanisms of gating of TRPV4 in vivo are not known at this point and have to be determined.
[
Pflugers Arch - European Journal of Physiology,
2005]
The transient receptor potential vanilloid 4 (TRPV4) ion channel was named initially vanilloid-receptor-related osmotically activated channel (VR-OAC). Preliminary answers to the question, "What is the function of the trpv4 gene in live animals ?" are highlighted briefly in this review. In trpv4 null mice, TRPV4 is necessary for the maintenance of osmotic equilibrium, and in Caenorhabditis elegans transgenic for mammalian TRPV4, TRPV4 directs the osmotic avoidance response in the context of the ASH "nociceptive" neuron. The molecular mechanisms of gating of TRPV4 in vivo need to be determined; in particular, whether TRPV4 in live animals is gated via phosphorylation of defined amino-acid residues or more directly through the osmotic stimulus itself.
[
Peptides,
2015]
Forward or reverse movement in Caenorhabditis elegans is the result of sequential contraction of muscle cells arranged along the body. In larvae, muscle cells are innervated by distinct classes of motorneurons. B motorneurons regulate forward movement and A motorneurons regulate backward movement. Ablation of the D motor neurons results in animals that are uncoordinated in either direction, which suggests that D motorneurons regulate the interaction between the two circuits. C. elegans locomotion is dictated by inputs from interneurons that regulate the activity of motorneurons which coordinate muscle contraction to facilitate forward or backwards movement. As C. elegans moves through the environment, sensory neurons interpret chemical and mechanical information which is relayed to the motor neurons that control locomotory direction. A mechanosensory input known as light nose touch can be simulated in the laboratory by touching the nose of the animal with a human eyebrow hair. The recoil reaction that follows from light nose touch appears to be primarily mediated by glutamate release from the polymodal sensory neuron ASH. Numerous glutamate receptor types are found in different neurons and interneurons which suggest that several pathways may regulate the aversive response. Based on the phenotypes of mutants in which neuropeptide processing is abolished, neuropeptides play a role in circuit regulation. The light touch response is also regulated by transient receptor channel proteins and degenerin/epithelial sodium channels which modulate the activity of sensory neurons involved in the nose touch response.