Martijn Dekkers et al. (2006) European Worm Meeting "Dissecting Gustatory Plasticity in C. elegans Using Mammalian Receptors"

Martijn Dekkers, Gert Jansen, John McCafferty, Michelle Teng

[European Worm Meeting, 2006]

Martijn Dekkers1, Michelle Teng2, John McCafferty, Gert Jansen1. We use C. elegans to study the molecular and cellular mechanisms of salt perception, using behavioural assays and calcium imaging. We discriminate three distinct responses to NaCl: First, attraction to NaCl concentrations ranging from 0.1 to 200 mM. Second, avoidance of higher concentrations. Third, avoidance of an otherwise attractive NaCl concentration after prolonged exposure. We call this latter behaviour gustatory plasticity. Previous studies have shown that chemo attraction to NaCl is mediated primarily by ASE, and to a lesser extent by ASI, ADF and ASG, and avoidance of high concentrations of NaCl is mediated by ASH (Bargmann & Horvitz, 1991). In our lab we have identified 85 proteins and five pairs of gustatory neurons that mediate gustatory plasticity. Based on our results we propose a model in which prolonged exposure to 100 mM of NaCl, elicits a signal from the ASE neurons, leading to sensitisation of the avoidance signalling ASI, ADF, ADL and ASH neurons. This results in avoidance of low concentrations of NaCl.. In an effort to identify the roles of the individual cells in gustatory plasticity we expressed either a TRP channel or a G-Protein Coupled Receptor (GPCR) in the neurons that have been implicated in gustatory plasticity. This allows us to specifically activate those cells. The TRP channel that we use is the mammalian capsaicin receptor VR-1. Normally C. elegans does not respond to capsaicin. Previously it has been shown that expression of VR-1 in the ASH neurons results in avoidance of capsaicin (Tobin et al 2002). We have generated animals that express the VR-1 receptor in the ASE, ASI, ADL and ADF neurons. We are currently testing their responses to capsaicin and the effects of preexposure to NaCl on this response, using behavioural assays.. The GPCRs that we have chosen are the mouse SSTR-2 somatostatin receptor and the human CCR-5 chemokine receptor. We have expressed these receptors in the ASH cells, and tested the responses in a novel avoidance assay. We found that the transgenic animals display specific avoidance behaviour to the ligands of the receptors, indicating that these GPCRs are integrated into the endogenous C. elegans signalling machinery, which is remarkable, given the evolutionary distance between the species. We are now making constructs to express these GPCRs in the other cells to assess their role in gustatory plasticity.

MT1685

Caenorhabditis elegans

MT2609

Caenorhabditis elegans

MT2633

Caenorhabditis elegans

MT1684

Caenorhabditis elegans

MT1098

Caenorhabditis elegans

MT2509

Caenorhabditis elegans

JU1960

Caenorhabditis elegans

Plenefisch JD et al. (1994) Worm Breeder's Gazette "Cloning mua-3: Some Observations on the New Molecular Era"

Plenefisch JD, Hedgecock EM

[Worm Breeder's Gazette, 1994]

Cloning mua-3: some observations on the new Molecular Era John Plenefisch and Edward Hedgecock, Dept. of Biology, Johns Hopkins University, Baltimore MD 21218

Parham C et al. (1994) Worm Breeder's Gazette "Tc4 and Tc5: What Makes Them Move and Why It Matters"

Beinhorn J, Collins JJ, Butze K, Parham C

[Worm Breeder's Gazette, 1994]

Tc4 and Tc5: what makes them move and why it matters Christi Parham, Kristie Butze, Joanna Beinhorn and John Collins. Dept. of Biochemistry and Molecular Biology, University of New Hampshire. Durham, NH 03824