Abstract
BK(Ca) channels, originally discovered in Drosophila melanogaster as slowpoke (slo), are recognized for their roles in cellular and organ physiology. Pharmacological approaches implicated BK(Ca) channels in cellular and organ protection possibly for their ability to modulate mitochondrial function. However, the direct role of BK(Ca) channels in regulating mitochondrial structure and function is not deciphered. Here, we demonstrate that BK(Ca) channels are present in fly mitochondria, and slo mutants show structural and functional defects in mitochondria. slo mutants display an increase in reactive oxygen species and the modulation of ROS affected their survival. We also found that the absence of BK(Ca) channels reduced the lifespan of Drosophila, and overexpression of human BK(Ca) channels in flies extends life span in males. Our study establishes the presence of BK(Ca) channels in mitochondria of Drosophila and ascertains its novel physiological role in regulating mitochondrial structural and functional integrity, and lifespan.