Karl J. Morten

TL;DR: It is shown that the selective removal of mitochondria by autophagy, but not other organelles, during erythropoeisis is essential and that this is a necessary developmental step in erythroid cells.

TL;DR: The metabolic reprogramming of cancer is discussed, possible explanations for the high glucose consumption in cancer cells observed by Warburg, and key experimental practices should be considered when studying the metabolism of cancer.

TL;DR: It is found that mitochondrial SOD2 deficiency exacerbates amyloid burden and significantly reduces metal levels in the brain, while increasing levels of Ser-396 phosphorylated tau.

TL;DR: H-mtTFA levels were investigated in cell lines which were either free of mtDNA or temporarily depleted by treatment with dideoxycytidine, and in tissue from three patients with mtDNA depletion and cytochrome oxidase deficiency, suggesting that either h- mtTFA regulates mtDNA levels, or that h-MTTFA expression may be regulated by a feedback mechanism initiated by MtDNA Depletion.

TL;DR: Evidence is presented for the presence of duplicated mtDNA in 6/11 patients known to have deletions of mitochondrialDNA in muscle, suggesting that this could be a general mechanism for major re-arrangements of mitochondrial DNA.