Kemppainen KK, Kemppainen E, Jacobs HT. The alternative oxidase AOX does not rescue the phenotype of tko25t mutant flies. G3 (Bethesda). 2014 Aug 21;4(10):2013-21. PMID: 25147191; PMCID: PMC4199707.
From the abstract: "A point mutation [technical knockout(25t) (tko(25t))] in the Drosophila
gene coding for mitoribosomal protein S12 generates a phenotype of
developmental delay and bang sensitivity. tko(25t) has been intensively
studied as an animal model for human mitochondrial diseases ... Transgenic expression in Drosophila
of the alternative oxidase (AOX) derived from Ciona intestinalis has
previously been shown to mitigate the toxicity of respiratory chain
inhibitors and to rescue mutant and knockdown phenotypes ... We therefore tested whether AOX
expression could compensate the mutant phenotype of tko(25t) ... We conclude that AOX
does not rescue tko(25t) and that the mutant phenotype is not solely due
to limitations on electron flow in the respiratory chain, but rather to
a more complex metabolic defect. The future therapeutic use of AOX in
disorders of mitochondrial translation may thus be of limited value."