Thermal adaptation and clinal mitochondrial DNA variation of European anchovy

http://rspb.royalsocietypublishing.org/content/281/1792/20141093.short

It seems that anchovies broadly possess one of two mtDNA types, and which type a fish possesses is related to the latitudes at which it lives. This paper shows that ocean temperature is the strongest of the investigated possible determinants of anchovy mtDNA haplotype. The authors discuss the specific molecular effects of the differences between haplotypes, including some residue changes in Complex III. They speculate on the OXPHOS implications of these changes, but don't consider proton leak, which I think may be affected by the residue changes (they're on the side of the complex, though I can't see immediately if these sites are where the complex contacts the membrane). Generally -- a fun example of possible environment adaptation in mtDNA haplotypes.

Global Genetic Determinants of Mitochondrial DNA Copy Number

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0105242

These guys screen yeast for nuclear genes whose deletions lead to a disappearance of mtDNA. Lots of the hits are mitochondrial proteins (54.9%), including a really big set involved in the mitochondrial ribosome. Other hits include a dozen genes involved in nucleic acid metabolism, ATP(4, 5, 14) and GRX (involved in Fe-S cluster formation) and a couple of dozen of miscellaneous functionality. Interesting to speculate on the mechanisms leading to mtDNA loss -- autophagy due to mitochondrial dysfunction, or some more direct mechanism? If the autophagy link is the case, and mitochondrial dysfunction is recognised through membrane potential, then the ATP genes are interesting, as the mitochondrion can presumably (?) maintain its membrane potential without Complex V. Perhaps there's a role for ROS signalling marking a dysfunctional mitochondrion here? If the absence of Complex V means the other complexes end up pumping protons against a higher and higher gradient, churning out more ROS as they do so?

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Progressive increase in mtDNA 3243A>G heteroplasmy causes abrupt transcriptional reprogramming

Progressive increase in mtDNA 3243A>G heteroplasmy causes abrupt transcriptional reprogramming

Mitochondria contain their own genetic material: mtDNA. Each mitochondrion may contain several copies of their mtDNA, and the cell will generally contain many mitochondria. A mutation in an mtDNA can sometimes proliferate, resulting in an inhomogeneous population of wild-type and mutant mtDNA molecules. This is called heteroplasmy. The authors find that, for a particular mutation considered, changing the balance of wild-type to mutant mtDNAs, abrupt changes in the expression profile of the nuclear genome occurs, drawing an analogy with phase transitions. 

Tumour-derived PTH-related protein triggers adipose tissue browning and cancer cachexia

Tumour-derived PTH-related protein triggers adipose tissue browning and cancer cachexia

Cachexia is a condition often observed in cancer patients, associated with muscle wasting, frailty and weight loss. Although cachetic patients often ingest less food, they are also in a state of negative energy balance which cannot be corrected with nutritional supplementation. This has been linked to greater thermogenesis in brown fat tissue. The authors use a Lewis lung carcinoma murine model to identify a key secreted factor PTHrP which mediates muscle wasting in fat tissue.

High frequency of homoplasmic mitochondrial DNA mutations in human tumors can be explained without selection

High frequency of homoplasmic mitochondrial DNA mutations in human tumors can be explained without selection

The authors generated a model to track mitochondrial heteroplasmy in cells. They simulated mtDNA, which randomly accumulated mutations at each generation, according to a Poisson process. At cell division, each mtDNA molecule was randomly chosen and replicated, so that the total copy number of mtDNAs doubled from 5 to 10. The mtDNA molecules were then randomly, but equally, split between the two daughter cells. Following successive generations of this process, the authors found consistently that a macroscopic fraction of cells in the model would contain a homoplasmic mutation. This model argues against the idea that selection is required for homoplasmy to occur, which is sometimes thought to be the case in particular forms of cancer.

Tumorigenicity of hypoxic respiring cancer cells revealed by a hypoxia–cell cycle dual reporter

Tumorigenicity of hypoxic respiring cancer cells revealed by a hypoxia–cell cycle dual reporter

The Warburg effect is the observation that, during tumorigenesis, there exists a metabolic shift from oxidative phosphorylation to glycolysis. In this report, the authors highlight the metabolic heterogeneity of cancer, by developing a dual reporter of HIF (hypoxia-inducible factor) and cell division. They find, in HEK 293T cells, that there exists a sub-population of non-HIF and non-cycling cells. These cells overexpressed certain mitochondrial genes and had an increased oxygen consumption, suggesting they respire aerobically. Despite this, they were found to be unexpectedly tumorigenic, relative to their glycolytic counterparts.