doi:10.1038/nindia.2009.154 Published online 16 June 2009
When levels of a recently identified gene 'Orai' are reduced in the Drosophila nerve cells, the entry of calcium ions into its cells is nullified, according to a new research1. This impairs flight in adult Drosophila. The research suggests that drugs that can raise the calcium ion entry into neurons could be of therapeutic value. The finding holds promise for neurodegenerative conditions and metabolic diseases characterised by similar dysregulated intracellular calcium ion homeostasis.
Life evolved in sea water that contained a number of ions including calcium (Ca2+). At some stage of cellular evolution, Ca2+ began to be used as a regulatory molecule. When eukaryotic cells evolved with cellular compartments and endo-membranes, Ca2+ containing intracellular compartments were formed.
As organisms became more complex, these compartments acquired new roles in cell communication. In cells of the nervous system a well-defined source of signaling Ca2+ is the extracellular medium. However, Ca2+ is also stored inside neurons but the relevance of these stores in neuronal function is poorly understood. The recently identified Orai gene encodes a channel that helps to refill these stores inside the cells from extracellular medium.
"Significantly, raising the level of Orai and consequently store-operated calcium entry (SOCE) in neurons, can restore flight to varying extents to Drosophila mutants for an intracellular Ca2+-release channel — the inositol 1,4,5-trisphosphate receptor," says Gaiti Hasan, one of the co-authors of the study.