Normal Phototransduction in Drosophila Photoreceptors Lacking an InsP3 Receptor Gene

Raghu, Padinjat; Colley, Nansi Jo; Webel, Rebecca; James, T Njuguna; Hasan, Gaiti; Danin, Michal; Selinger, Zvi; Hardie, Roger C.

doi:10.1006/mcne.2000.0846

Cited by 123 publications

(106 citation statements)

References 62 publications

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“…A variety of studies indicate that IP 3 is not the critical second messenger. Release of caged IP 3 does not mimic the light response [144], and mutation of the only IP 3 -receptor encoded in the Drosophila genome has no impact on phototransduction [145,146]. Furthermore, IP 3 does not activate TRPL in an in vitro expression system [147].…”

Section: The Trpc Cation Channelsmentioning

confidence: 99%

Phototransduction and retinal degeneration in Drosophila

Wang

Montell

2007

Pflugers Arch - Eur J Physiol

257

303

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Drosophila visual transduction is the fastest known G-protein-coupled signaling cascade and has therefore served as a genetically tractable animal model for characterizing rapid responses to sensory stimulation. Mutations in over 30 genes have been identified, which affect activation, adaptation, or termination of the photoresponse. Based on analyses of these genes, a model for phototransduction has emerged, which involves phosphoinoside signaling and culminates with opening of the TRP and TRPL cation channels. Many of the proteins that function in phototransduction are coupled to the PDZ containing scaffold protein INAD and form a supramolecular signaling complex, the signalplex. Arrestin, TRPL, and Gα q undergo dynamic light-dependent trafficking, and these movements function in long-term adaptation. Other proteins play important roles either in the formation or maturation of rhodopsin, or in regeneration of phosphatidylinositol 4,5-bisphosphate (PIP 2 ), which is required for the photoresponse. Mutation of nearly any gene that functions in the photoresponse results in retinal degeneration. The underlying bases of photoreceptor cell death are diverse and involve mechanisms such as excessive endocytosis of rhodopsin due to stable rhodopsin/arrestin complexes and abnormally low or high levels of Ca 2+ . Drosophila visual transduction appears to have particular relevance to the cascade in the intrinsically photosensitive retinal ganglion cells in mammals, as the photoresponse in these latter cells appears to operate through a remarkably similar mechanism.

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Section: The Trpc Cation Channelsmentioning

confidence: 99%

Phototransduction and retinal degeneration in Drosophila

Wang

Montell

2007

Pflugers Arch - Eur J Physiol

257

303

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“…Indeed, visual transduction in Drosophila photoreceptors lacking the itpr gene is also normal (Raghu et al, 2000). To identify neural processes sensitive to InsP 3 R activity, motor functions like the jump response, climbing speed, and cleaning reflex were tested in adult viable itpr mutants and found to be unimpaired.…”

Section: Introductionmentioning

confidence: 99%

Loss of Flight and Associated Neuronal Rhythmicity in Inositol 1,4,5-Trisphosphate Receptor Mutants ofDrosophila

Banerjee¹,

Lee²,

Venkatesh³

et al. 2004

J. Neurosci.

119

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“…The central role played by IP 3 Rs in a wide range of cellular responses is reflected by the high level of lethality resulting from gene knockout observed in both Drosophila (Acharya et al, 1997;Venkatesh and Hasan, 1997) and mice (Matsumoto et al, 1996). Nevertheless, careful analysis has enabled, for example, the functions of IP 3 Rs in cerebellum in mice (Inoue et al, 1998) and phototransduction in Drosophila to be studied (Acharya et al, 1997;Raghu et al, 2000). Caenorhabditis elegans is also proving to be a powerful system for understanding IP 3 signaling function.…”

Section: Introductionmentioning

confidence: 99%

Regulated Disruption of Inositol 1,4,5-Trisphosphate Signaling inCaenorhabditis elegansReveals New Functions in Feeding and Embryogenesis

Walker

Gower

et al. 2002

MBoC

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Inositol 1,4,5-trisphosphate (IP 3 ) is an important second messenger in animal cells and is central to a wide range of cellular responses. The major intracellular activity of IP 3 is to regulate release of Ca 2ϩ from intracellular stores through IP 3 receptors (IP 3 Rs). We describe a system for the transient disruption of IP 3 signaling in the model organism Caenorhabditis elegans. The IP 3 binding domain of the C. elegans IP 3 R, ITR-1, was expressed from heat shock-induced promoters in live animals. This results in a dominant-negative effect caused by the overexpressed IP 3 binding domain acting as an IP 3 "sponge." Disruption of IP 3 signaling resulted in disrupted defecation, a phenotype predicted by previous genetic studies. This approach also identified two new IP 3 -mediated processes. First, the up-regulation of pharyngeal pumping in response to food is dependent on IP 3 signaling. RNA-mediated interference studies and analysis of itr-1 mutants show that this process is also IP 3 R dependent. Second, the tissue-specific expression of the dominant-negative construct enabled us to circumvent the sterility associated with loss of IP 3 signaling through the IP 3 R and thus determine that IP 3 -mediated signaling is required for multiple steps in embryogenesis, including cytokinesis and gastrulation. Inositol 1,4, ) is an important and widely used second messenger in animal cells. IP 3 is produced by the hydrolysis of phosphatidylinositol 4,5-bisphosphate after the activation of phospholipase C (PLC). The best understood routes of PLC activation are through the stimulation of G protein-coupled receptors or tyrosine kinase-linked receptors at the cell surface, although the presence of additional isoforms of PLC suggests other possible routes (Rhee and Bae, 1997;Katan, 1998). The only known action of IP 3 is to induce Ca 2ϩ release from intracellular stores through activation of IP 3 receptors (IP 3 Rs) (Berridge, 1993). This pathway and the Ca 2ϩ signals derived from it are central to a wide range of cellular responses (Berridge, 1993(Berridge, , 1997Clapham 1995). INTRODUCTIONTwo challenges in the study of this signaling network are to unravel the different functions played by IP 3 signaling in animals and to develop methods for manipulating these processes and thus advance our understanding of how the specificity of IP 3 signaling is achieved. Recent genetic approaches have provided new insights into IP 3 function in animals. The central role played by IP 3 Rs in a wide range of cellular responses is reflected by the high level of lethality resulting from gene knockout observed in both Drosophila (Acharya et al., 1997;Venkatesh and Hasan, 1997) and mice (Matsumoto et al., 1996). Nevertheless, careful analysis has enabled, for example, the functions of IP 3 Rs in cerebellum in mice (Inoue et al., 1998) and phototransduction in Drosophila to be studied (Acharya et al., 1997;Raghu et al., 2000). Caenorhabditis elegans is also proving to be a powerful system for understanding IP 3 signaling function. IP 3 Rs i...

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Normal Phototransduction in Drosophila Photoreceptors Lacking an InsP3 Receptor Gene

Cited by 123 publications

References 62 publications

Phototransduction and retinal degeneration in Drosophila

Phototransduction and retinal degeneration in Drosophila

Loss of Flight and Associated Neuronal Rhythmicity in Inositol 1,4,5-Trisphosphate Receptor Mutants ofDrosophila

Regulated Disruption of Inositol 1,4,5-Trisphosphate Signaling inCaenorhabditis elegansReveals New Functions in Feeding and Embryogenesis

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