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Gene expression in Drosophila Poly mutant and wild-type

ABSTRACT: The Poly mutant was identified as a previously uncharacterised, but essential gene in Drosphila. Loss of Poly reults in lethality at the third larval instar stage, but only after a stage of extreme larval longevity. We aimed to assess the consequences of loss of the Poly gene on glocal gene expression by microarray analysis. Metabolism is altered in Poly mutants and here we find altered gene expression in insulin signaling pathways. Four biological replicates each of Poly mutant and wild-type larvae were used to assess gene expression on FL002 microarrays (GPL5135) . These data reveal that Poly is a mediatior of insulin receptor/TOR signaling.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE32637 | GEO | 2012/01/17

SECONDARY ACCESSION(S): PRJNA146967

REPOSITORIES: GEO

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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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Gene expression in Drosophila Poly mutant and wild-type

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