The genetics of calcium signaling in Drosophila melanogaster.

Biochim Biophys Acta

National Center for Biological Sciences, Tata Institute of Fundamental Research, Bangalore, India.

Published: August 2012

Background: Genetic screens for behavioral and physiological defects in Drosophila melanogaster, helped identify several components of calcium signaling of which some, like the Trps, were novel. For genes initially identified in vertebrates, reverse genetic methods have allowed functional studies at the cellular and systemic levels.

Scope Of Review: The aim of this review is to explain how various genetic methods available in Drosophila have been used to place different arms of Ca2+ signaling in the context of organismal development, physiology and behavior.

Major Conclusion: Mutants generated in genes encoding a range of Ca2+ transport systems, binding proteins and enzymes affect multiple aspects of neuronal and muscle physiology. Some also affect the maintenance of ionic balance and excretion from malpighian tubules and innate immune responses in macrophages. Aspects of neuronal physiology affected include synaptic growth and plasticity, sensory transduction, flight circuit development and function. Genetic interaction screens have shown that mechanisms of maintaining Ca2+ homeostasis in Drosophila are cell specific and require a synergistic interplay between different intracellular and plasma membrane Ca2+ signaling molecules.

General Significance: Insights gained through genetic studies of conserved Ca2+ signaling pathways have helped understand multiple aspects of fly physiology. The similarities between mutant phenotypes of Ca2+ signaling genes in Drosophila with certain human disease conditions, especially where homologous genes are causative factors, are likely to aid in the discovery of underlying disease mechanisms and help develop novel therapeutic strategies. This article is part of a Special Issue entitled Biochemical, biophysical and genetic approaches to intracellular calcium signalling.

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Source
http://dx.doi.org/10.1016/j.bbagen.2011.11.002DOI Listing

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