A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Agrawal, N., Padmanabhan, N., Hasan, G. (2009). Inositol 1,4,5- trisphosphate receptor function in Drosophila insulin producing cells.  PLoS ONE 4(8): e6652. (Export to RIS)
FlyBase ID FBrf0208703
Publication Type Research paper
PubMed ID 19680544
PubMed Abstract The Inositol 1,4,5- trisphosphate receptor (InsP(3)R) is an intracellular ligand gated channel that releases calcium from intracellular stores in response to extracellular signals. To identify and understand physiological processes and behavior that depends on the InsP(3) signaling pathway at a systemic level, we are studying Drosophila mutants for the InsP(3)R (itpr) gene. Here, we show that growth defects precede larval lethality and both are a consequence of the inability to feed normally. Moreover, restoring InsP(3)R function in insulin producing cells (IPCs) in the larval brain rescues the feeding deficit, growth and lethality in the itpr mutants to a significant extent. We have previously demonstrated a critical requirement for InsP(3)R activity in neuronal cells, specifically in aminergic interneurons, for larval viability. Processes from the IPCs and aminergic domain are closely apposed in the third instar larval brain with no visible cellular overlap. Ubiquitous depletion of itpr by dsRNA results in feeding deficits leading to larval lethality similar to the itpr mutant phenotype. However, when itpr is depleted specifically in IPCs or aminergic neurons, the larvae are viable. These data support a model where InsP(3)R activity in non-overlapping neuronal domains independently rescues larval itpr phenotypes by non-cell autonomous mechanisms.
DOI 10.1371/journal.pone.0006652
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Language of Publication English
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Publication Type Journal
Abbreviation PLoS ONE
Title PLoS ONE
Publication Year 2006-
ISBN/ISSN 1932-6203
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