Dissecting Independent Channel and Scaffolding Roles of the Drosophila Transient Receptor Potential Channel

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 <tex-math>$trp^{14}$</tex-math> with an amino acid substitution juxtaposed to the TRP domain. The <tex-math>$trp^{14}$</tex-math> flies stably express TRP and display normal molecular anchoring, but defective channel function. Elimination of the anchoring function alone in <tex-math>$trp^{\Delta 1272}$</tex-math>, 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 <tex-math>$Na^{+}/Ca^{2+}$</tex-math> exchanger, CalX, indicating that the cell death was due primarily to deficient Ca<sup>2+</sup> entry rather than disruption of the TRP-anchoring function..

Medienart:

E-Artikel

Erscheinungsjahr:

2005

Erschienen:

2005

Enthalten in:

Zur Gesamtaufnahme - volume:171

Sprache:

Englisch

Beteiligte Personen:

Wang, Tao [VerfasserIn]
Jiao, Yuchen [VerfasserIn]
Montell, Craig [VerfasserIn]

Links:

Volltext

Themen:

Biological sciences
Health sciences
Physical sciences
Research-article

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

JST045651256