Dataset Information

E-MEXP-1513

ABSTRACT: Transcription profiling by array of Drosophila melanogaster wild type, Nurf301 mutant and hop[Tum-1] mutant third instar larvae

PROVIDER: E-MEXP-1513 | ExpressionAtlas | 2014-10-10

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MEXP-1513-analysis-methods.tsv	Tabular
	E-MEXP-1513-atlasExperimentSummary.Rdata	Rdata
	E-MEXP-1513-configuration.xml	Xml
	E-MEXP-1513-percentile-ranks.tsv	Tabular
	E-MEXP-1513.condensed-sdrf.tsv	Tabular

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Project description:Intracellular Ca2+ release through the Inositol 1,4,5-Triphosphate Receptor (InsP3R) is a feature of all multicellular organisms in which it shapes the temporal and spatial aspects of calcium signaling in cells, affecting several developmental and physiological processes. Mutants in the InsP3R gene of Drosophila (itpr) exhibit a range of defects which include growth defects and larval lethality.The Drosophila Insulin-like peptides (ILPs) are encoded by multigene families that are expressed in the brain and other tissues. Upon secretion, these peptides likely serve as hormones, neurotransmitters, and growth factors. In Drosophila melanogaster, molecular genetic studies have revealed Drosophila ILPs as elements of a conserved insulin signaling pathway, and as in other animal models, it appears to play a key role in metabolism, growth, reproduction, and aging. Previous work from our group has shown that InsP3R function can be rescued by ectopically expressing InsP3R in dilp cells or can be compensated by altering the activity of Sarco-Endoplasmic Reticulum Calcium-ATPase (SERCA). To understand the molecular basis of larval lethality and growth defect in Drosophila InsP3R mutants and to decipher possible cross talk of itpr gene with other signaling pathways we have carried out genome wide microarray experiments. We have compared the transcript profiles of i) itpr mutant larvae and wild type larvae, ii) dilp rescue larvae with itpr mutant larvae iii) itpr and SERCA double mutant larvae with itpr mutant larvae. By this we have identified genes whose levels are altered in itpr mutants and are restored towards wild type in dilp rescue larvae with itpr mutant larvae and itpr and SERCA double mutants. Our experiments help in identify genes that are regulated by changes in intracellular Ca2+ in the context of larval viability may contribute to the better understanding of the major human pathologies caused by calcium misbalance or by dysregulation of the insulin/IGF pathway.

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E-MEXP-1513

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