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Patterns of gene expression in Drosophila InsP3 receptor mutant larvae reveal a role for InsP3 signaling in carbohydrate and energy metabolism.

ABSTRACT: 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.

SUBMITTER: Kumar S

PROVIDER: S-EPMC3162032 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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Patterns of gene expression in Drosophila InsP3 receptor mutant larvae reveal a role for InsP3 signaling in carbohydrate and energy metabolism.

Kumar Satish S Dey Debleena D Hasan Gaiti G

PloS one 20110825 8

<h4>Background</h4>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.<h4>Methodology/principal findings</h4>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 mu ...[more]

PMID: 21901161

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Project description:B cell lymphoma 2 (Bcl-2) proteins are the central regulators of apoptosis. The two bcl-2 genes in Drosophila modulate the response to stress-induced cell death, but not developmental cell death. Because null mutants are viable, Drosophila provides an optimum model system to investigate alternate functions of Bcl-2 proteins. In this report, we explore the role of one bcl-2 gene in nutrient stress responses.We report that starvation of Drosophila larvae lacking the bcl-2 gene, buffy, decreases survival rate by more than twofold relative to wild-type larvae. The buffy null mutant reacted to starvation with the expected responses such as inhibition of target of rapamycin (Tor) signaling, autophagy initiation and mobilization of stored lipids. However, the autophagic response to starvation initiated faster in larvae lacking buffy and was inhibited by ectopic buffy. We demonstrate that unusually high basal Tor signaling, indicated by more phosphorylated S6K, was detected in the buffy mutant and that removal of a genomic copy of S6K, but not inactivation of Tor by rapamycin, reverted the precocious autophagy phenotype. Instead, Tor inactivation also required loss of a positive nutrient signal to trigger autophagy and loss of both was sufficient to activate autophagy in the buffy mutant even in the presence of enforced phosphoinositide 3-kinase (PI3K) signaling. Prior to starvation, the fed buffy mutant stored less lipid and glycogen, had high lactate levels and maintained a reduced pool of cellular ATP. These observations, together with the inability of buffy mutant larvae to adapt to nutrient restriction, indicate altered energy metabolism in the absence of buffy.All animals in their natural habitats are faced with periods of reduced nutrient availability. This study demonstrates that buffy is required for adaptation to both starvation and nutrient restriction. Thus, Buffy is a Bcl-2 protein that plays an important non-apoptotic role to promote survival of the whole organism in a stressful situation.

Dataset Information

Patterns of gene expression in Drosophila InsP3 receptor mutant larvae reveal a role for InsP3 signaling in carbohydrate and energy metabolism.

Publications

Patterns of gene expression in Drosophila InsP3 receptor mutant larvae reveal a role for InsP3 signaling in carbohydrate and energy metabolism.

Similar Datasets

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