Authors: Roger C Hardie
Publish Date: 2011/02/01
Volume: 461, Issue: 5, Pages: 493-498
Abstract
The history of the discovery of the transient receptor potential TRP cation channel superfamily began in 1969 with Cosens and Mannings isolation of the Drosophila transient receptor potential mutant in which the photoreceptor response decays during continuous illumination Early studies from Minke found that the elementary light response was unaffected in trp mutants and he attributed the defect to an intermediate stage of phototransduction Montell and Rubin cloned the trp gene in 1989 they recognised it as a transmembrane protein but also concluded that it did not encode the lightsensitive channels In 1991 Minke and Selinger proposed that TRP represented a Ca2+ transporter required for refilling intracellular InsP3sensitive Ca2+ stores in turn required for activation of the lightsensitive channels Also in 1991 after developing a photoreceptor patch clamp preparation I showed that the lightsensitive channels themselves were highly permeable to Ca2+ questioning the need for such a dedicated Ca2+ transporter In 1992 in collaboration with Minke I resolved this paradox by showing there were two classes of lightsensitive channels one highly Ca2+ permeable and eliminated in trp mutants This represented the first and compelling evidence that TRP represented a lightsensitive channel and was supported by the cloning of the second lightsensitive channel TRPL by Kellys lab Three years later in 1995 the labs of Montell and Birnbaumer independently cloned TRPC1 the first of 29 vertebrate TRP isoforms distributed amongst seven subfamilies
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