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https://doi.org/10.1371/journal.pone.0006652
Title: | Inositol 1,4,5- trisphosphate receptor function in Drosophila insulin producing cells | Authors: | Agrawal N. Padmanabhan N. Hasan G. |
Keywords: | double stranded RNA inositol 1,4,5 trisphosphate inositol 1,4,5 trisphosphate receptor insulin like peptide 2 peptide hormone peptides and proteins protein Ddc transcription factor GAL4 unclassified drug inositol 1,4,5 trisphosphate receptor insulin primer DNA animal cell animal tissue article body size controlled study Drosophila feeding disorder genetic strain growth disorder growth regulation insulin producing cell larval development lethality microbial viability nerve cell nonhuman phenotype point mutation protein depletion protein domain protein expression protein function pupation regulatory mechanism RNA interference signal transduction survival tissue specificity animal biosynthesis energy metabolism feeding behavior genetics growth, development and aging immunohistochemistry metabolism mutation nucleotide sequence physiology reverse transcription polymerase chain reaction Western blotting Animals Base Sequence Blotting, Western DNA Primers Drosophila Energy Metabolism Feeding Behavior Immunohistochemistry Inositol 1,4,5-Trisphosphate Receptors Insulin Mutation Reverse Transcriptase Polymerase Chain Reaction RNA Interference Signal Transduction |
Issue Date: | 2009 | 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. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0006652 | Rights: | Attribution 4.0 International | Abstract: | The Inositol 1,4,5- trisphosphate receptor (InsP3R) 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 InsP3 signaling pathway at a systemic level, we are studying Drosophila mutants for the InsP3R (itpr) gene. Here, we show that growth defects precede larval lethality and both are a consequence of the inability to feed normally. Moreover, restoring InsP3R 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 InsP3R 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 InsP3R activity in non-overlapping neuronal domains independently rescues larval itpr phenotypes by non-cell autonomous mechanisms. � 2009 Agrawal et al. | Source Title: | PLoS ONE | URI: | https://scholarbank.nus.edu.sg/handle/10635/161833 | ISSN: | 19326203 | DOI: | 10.1371/journal.pone.0006652 | Rights: | Attribution 4.0 International |
Appears in Collections: | Staff Publications Elements |
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