The critical role of Arabidopsis electron-transfer flavoprotein ubiquinone oxidereductase during dark induced starvation

Abstract

In mammals, electron-transfer flavoprotein:ubiquinone oxidoreductase (ETFQO) accepts electrons from the electron-transfer flavoprotein (ETF) and reduces ubiquinone. ETF is the physiological electron acceptor for at least nine mitochondrial matrix flavoprotein dehydrogenases involved in straight-chain fatty acid β-oxidation, catabolisms of several amino acids, and choline metabolism. Thus mammalian mitochondrial proteins, ETF and ETFQO, plays a key role in multiple metabolic pathways, and are important in supplying mitochondria with respiratory substrates auxiliary to those derived from sucrose. In humans, mutations in either ETF or ETF-QO results in the fatal genetic disease, type II Glutaric acidemia. In contrast to the situation in mammals, nothing is yet known about the function of ETF and ETF-QO in plants so far. Here we will describe a genetic, molecular, and biochemical analysis of an unique Arabidopsis homologue of ETFQO.