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First published online March 23, 2005

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TRP the light fantastic

TRP ion channels are key components of several sensory signalling cascades, including those responsible for light transduction. G-protein-coupled receptors initiate these cascades but it is unclear how the TRP channels are subsequently activated. Raghu Padinjat and co-workers have used a forward-genetic screen to investigate TRP-channel activation in vivo, using Drosophila phototransduction as a model system (see p. 1373). In the Drosophila mutant rdgA, lack of diacylglycerol kinase activity leads to constitutive TRP-channel activity and retinal degeneration. In a genetic screen for suppression of the rdgA retinal degeneration phenotype, the authors identify su(1) and Su(100) as new alleles of InaD, a gene encoding a PDZ-domain protein that clusters components of the light transduction pathway, including TRP, into a macromolecular signalling complex. Additional experiments indicate that rescue of the rdgA phenotype correlates with reduced levels of phospholipase Cß (PLCß), and that light, Gq (the G protein needed for activation of PLCß by rhodopsin), and PLCß all modulate retinal degeneration in rdgA flies. The authors therefore conclude that lipid products of phosphoinositide hydrolysis play key roles in TRP-channel activation in vivo.

Related articles in JCS:

Functional INAD complexes are required to mediate degeneration in photoreceptors of the Drosophila rdgA mutant

Plamen Georgiev, Isaac Garcia-Murillas, Danny Ulahannan, Roger C. Hardie, and Padinjat Raghu
JCS 2005 118: 1373-1384. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content