Makhnyeva 2015 Abstract MiPschool Greenville 2015

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Effect of cGMP-dependent protein kinase (PKG) signaling on mitochondrial content in Drosophila melanogaster subjected to anoxia and reoxygenation.


Makhnyeva O, Dawson-Scully K, Milton SL (2015)

Event: MiPschool Greenville 2015

Ischemic stroke is one of the leading causes of human death worldwide. It occurs due to the high susceptibility of neurons to anoxia and reoxygenation. Unlike mammals, the fruit fly Drosophila melanogaster withstands low oxygen levels without pathology [1]. It was previously shown that the fruit flies carrying the Rover allele of the foraging gene (forR), express a cGMP-dependent protein kinase (PKG) with high enzymatic activity, whereas fruit flies with the Sitter allele of for (fors) express a low-enzymatic activity PKG; it was also demonstrated that upon return to normal oxygen levels after anoxia, the forR flies survive better than fors flies [2]. From mammalian research, it is also known that the activated NO/PKG signaling cascade induces mitochondrial biogenesis but the exact mechanism is not known [3].

The present study attempts to elucidate whether different levels of enzymatic activity of PKG have an effect on mitochondrial content in Drosophila brains and whole bodies before and after exposure to anoxic stress. Here, the mitochondrial content was assessed by measuring citrate synthase enzymatic activity and by determining protein expression levels of cytochrome c oxidase subunit IV (COX IV) and cytochrome c (Cyt c) by Western blotting. From preliminary results, forR fruit flies had higher citrate synthase enzymatic activity rates in brains when subjected to normal oxygen levels; in addition, these fruit flies showed higher basal levels of COX IV and cytochrome c in whole body homogenates compared to the fors flies. Interestingly, mitochondrial protein levels increased upon reoxygenation in both types of Drosophila.

Results of this study may lead to a better understanding of fruit fly’s innate anoxia-tolerance strategies and the protective role of increased PKG signaling. Subsequently, this knowledge may be used to identify potential therapeutic targets to prevent detrimental neurological effects of an ischemic stroke in humans.

Labels: MiParea: mt-Biogenesis;mt-density, nDNA;cell genetics 

Stress:Ischemia-reperfusion, Oxidative stress;RONS  Organism: Drosophila 

Enzyme: Complex IV;cytochrome c oxidase 

Event: Poster 


Dept Biol Sc, Florida Atlantic Univ, FL, USA. -

References and acknowledgements

  1. Krishnan SN, Sun Y-A, Mohsenin A, Wyman RJ, Haddad GG (1997) Behavioral and electrophysiologic responses of Drosophila melanogaster to prolonged periods of anoxia. J Insect Physiol 43:203-10.
  2. Dawson-Scully K, Bukvic D, Chakaborty-Chatterjee M, Ferreira R, Milton S, Sokolowski M (2010) Controlling anoxic tolerance in adult Drosophila via the cGMP-PKG pathway. J Experim Biol 213:2410-16.
  3. Nisoli E, Clementi E, Paolucci C, Cozzi V, Tonello C, Sciorati C, Bracale R, Valerio A, Francolini M, Moncada S, Carruba MO (2003) Mitochondrial biogenesis in mammals: the role of endogenous nitric oxide. Sc 299:896–9.