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Department of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205

Correspondence to Craig Montell: cmontell{at}jhmi.edu

Drosophila transient receptor potential (TRP) serves dual roles as a cation channel and as a molecular anchor for the PDZ protein, INAD (inactivation no afterpotential D). Null mutations in trp cause impairment of visual transduction, mislocalization of INAD, and retinal degeneration. However, the impact of specifically altering TRP channel function is not known because existing loss-of-function alleles greatly reduce protein expression. In the current study we describe the isolation of a set of new trp alleles, including trp¹⁴ with an amino acid substitution juxtaposed to the TRP domain. The trp¹⁴ flies stably express TRP and display normal molecular anchoring, but defective channel function. Elimination of the anchoring function alone in trp¹²⁷², had minor effects on retinal morphology whereas disruption of channel function caused profound light-induced cell death. This retinal degeneration was greatly suppressed by elimination of the Na⁺/Ca²⁺ exchanger, CalX, indicating that the cell death was due primarily to deficient Ca²⁺ entry rather than disruption of the TRP-anchoring function.

Abbreviations used in this paper: Arr2, arrestin2; CalX, Na⁺/Ca²⁺ exchanger; ERG, electroretinogram; hsp70, heat shock protein 70; INAC, inactivation no afterpotential C, encodes PKC; INAD, inactivation no afterpotential D; ninaE, neither inactivation nor afterpotential E (encodes Rh1); norpA, no receptor potential A, encodes PLC; RDGC, retinal degeneration C; Rh1, rhodopsin 1; TRP, transient receptor potential; TRP, transient receptor potential ; TRPL, transient receptor potential-like.

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