Background: The Inositol 1,4,5-trisphosphate receptor (InsP(3)R) is an InsP(3) gated intracellular Ca(2+)-release channel. Characterization of Drosophila mutants for the InsP(3)R has demonstrated that InsP(3)-mediated Ca(2+) release is required in Drosophila larvae for growth and viability.
Methodology/principal findings: To understand the molecular basis of these growth defects a genome wide microarray analysis has been carried out with larval RNA obtained from a strong InsP(3)R mutant combination in which 1504 independent genes were differentially regulated with a log(2) of fold change of 1 or more and P<0.05. This was followed by similar transcript analyses from InsP(3)R mutants where growth defects were either suppressed by introduction of a dominant suppressor or rescued by ectopic expression of an InsP(3)R transgene in the Drosophila insulin like peptide-2 (Dilp2) producing cells.
Conclusions/significance: These studies show that expression of transcripts related to carbohydrate and amine metabolism is altered in InsP(3) receptor mutant larvae. Moreover, from a comparative analysis of genes that are regulated in the suppressed and rescued conditions with the mutant condition, it appears that the organism could use different combinations of pathways to restore a 'normal' growth state.