Inositol 1,4,5- trisphosphate receptor function in Drosophila insulin producing cells

Neha Agrawal, Nisha Padmanabhan, Gaiti Hasan

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)e6652
JournalPLoS ONE
Issue number8
Publication statusPublished - 14 Aug 2009


  • Animals
  • Base Sequence
  • Blotting, Western
  • DNA Primers
  • Drosophila/growth & development
  • Energy Metabolism
  • Feeding Behavior
  • Immunohistochemistry
  • Inositol 1,4,5-Trisphosphate Receptors/genetics
  • Insulin/biosynthesis
  • Mutation
  • RNA Interference
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction


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