Dr Matthew McKenzie

Following the completion of his PhD in 2002, Dr Matthew McKenzie undertook his postdoctoral research in the laboratory of Professor Michael Duchen, University College London. There he investigated how mitochondrial membrane potential, calcium handling and ATP generation are disrupted in mitochondrial disorders using state-of-the-art confocal imaging techniques.

In 2004, Dr McKenzie returned to Australia to work in Professor Michael Ryan’s laboratory at Melbourne’s La Trobe University. During this time, he received an NHMRC Peter Doherty Fellowship, and subsequently an NHMRC Career Development Fellowship, to study the biogenesis of mitochondrial complex I and how inherited defects can disrupt this process.

In April 2011, Dr McKenzie was recruited by Hudson Institute of Medical Research as a Research Group Leader in the Centre for Genetic Diseases. His current research focuses on interactions between protein complexes involved in mitochondrial fatty acid beta-oxidation (FAO) and oxidative phosphorylation (OXPHOS), and their importance in human disease pathology. The Australian Research Council recently recognised Dr McKenzie’s research excellence with a prestigious Future Fellowship. Additionally, he also receives support from the Australian Mitochondrial Disease Foundation, the William Buckland Foundation, Marshall Edwards Inc., USA, and Monash University.

Selected publications

  • Lim SC, Hroudová J, Van Bergen NJ, Lopez Sanchez MI, Trounce IA, McKenzie M (2016) Loss of the Mitochondrial DNA-encoded protein ND1 results in the disruption of Complex I biogenesis during the early stages of its assembly.  FASEB J, 30:2236-48.

  • Kang Y, Baker MJ, Liem M, Louber J, McKenzie M, Atukorala I, Ang CS, Keerthikumar S, Mathivanan S, Stojanovski D (2016) Tim29 is a novel subunit of the human TIM22 translocase and is involved in complex assembly and stability. Elife, 24;5 pii: e17463.

  • Cagnone GL, Tsai TS, Makanji Y, Matthews P, Gould J, Bonkowski MS, Elgass KD, Wong AS, Wu LE, McKenzie M, Sinclair DA, St. John JC (2016) Restoration of normal embryogenesis by mitochondrial supplementation in pig oocytes exhibiting mitochondrial DNA deficiency. Sci Rep, 6:23229.

  • Lim SC, Carey KT, McKenzie M (2015) Anti-cancer analogues ME-143 and ME-344 exert toxicity by directly inhibiting mitochondrial NADH: ubiquinone oxidoreductase (Complex I). Am J Cancer Res. 5(2):689-701.

  • McKenzie M, Chiotis M, Hroudová J, Lopez Sanchez MI, Lim SC, Cook MJ, McKelvie P, Cotton RG, Murphy M, St John JC, Trounce IA (2014) Capture of somatic mtDNA point mutations with severe effects on oxidative phosphorylation in synaptosome cybrid clones from human brain. Hum Mutat, 35:1476-84.

  • Trounce IA, Crouch PJ, Carey KT, McKenzie M (2013) Modulation of ceramide-induced cell death and superoxide production by mitochondrial DNA-encoded respiratory chain defects in Rattus xenocybrid mouse cells. Biochim Biophys Acta 1827:817-825.

  • Tucker EJ, Hershman SG, Kohrer C, Belcher-Timme CA, Patel J, Goldberger OA, Christodoulou J, Silberstein JM, McKenzie M, Ryan MT, Compton AG, Jaffe JD, Carr SA, Calvo SE, RajBhandary UL, Thorburn DR, Mootha VK (2011) Mutations in MTFMT underlie a human disorder of formylation causing impaired mitochondrial translation. Cell Metab, 14:428-434.

  • McKenzie M, Tucker EJ, Compton AG, Lazarou M, George C, Thorburn DR, Ryan MT (2011) Mutations in the gene encoding C8orf38 block complex I assembly by inhibiting production of the mitochondria-encoded subunit ND1. J Mol Biol, 414:413-426.

  • Dunning CJ*, McKenzie M*, Sugiana C, Lazarou M, Silke J, Connelly A, Fletcher JM, Kirby DM, Thorburn DR, Ryan MT (2007) Human CIA30 is involved in the early assembly of mitochondrial complex I and mutations in its gene cause disease. EMBO J 26:3227-3237. (*joint first authors)

  • McKenzie M, Liolitsa D, Akinshina N, Campanella M, Sisodiya S, Hargreaves I, Nirmalananthan N, Sweeney MG, Abou-Sleiman PM, Wood NW, Hanna MG, Duchen MR (2007) Mitochondrial ND5 gene variation associated with encephalomyopathy and mitochondrial ATP consumption. J Biol Chem, 282:36845-36852.