This new study seem to have pretty much proven that
mtDNAis inherited from both parents. I assume that this would lead to most age estimates of ancient human populations that heavily depending on
mtDNA, being discarded. Is this right?
What other things would be affected by this discovery?
Neurons are metabolically active cells with high energy demands at locations distant from the cell body. As a result, these cells are particularly dependent on mitochondrial function, as reflected by the observation that diseases of mitochondrial dysfunction often have a neurodegenerative component. Recent discoveries have highlighted that neurons are reliant particularly on the dynamic properties of mitochondria. Mitochondria are dynamic organelles by several criteria. They engage in repeated cycles of fusion and fission, which serve to intermix the lipids and contents of a population of mitochondria. In addition, mitochondria are actively recruited to subcellular sites, such as the axonal and dendritic processes of neurons. Finally, the quality of a mitochondrial population is maintained through mitophagy, a form of autophagy in which defective mitochondria are selectively degraded. We review the general features of mitochondrial dynamics, incorporating recent findings on mitochondrial fusion, fission, transport and mitophagy. Defects in these key features are associated with neurodegenerative disease. Charcot-Marie-Tooth type 2A, a peripheral neuropathy, and dominant optic atrophy, an inherited optic neuropathy, result from a primary deficiency of mitochondrial fusion. Moreover, several major neurodegenerative diseases—including Parkinson's, Alzheimer's and Huntington's disease—involve disruption of mitochondrial dynamics. Remarkably, in several disease models, the manipulation of mitochondrial fusion or fission can partially rescue disease phenotypes. We review how mitochondrial dynamics is altered in these neurodegenerative diseases and discuss the reciprocal interactions between mitochondrial fusion, fission, transport and mitophagy.
In the past decade, our view of mitochondrial dynamics has expanded from a curious phenomenon into an integral cell biological process influencing many cellular functions and ultimately survival ( 1, 2). Once thought to be solitary and rigidly structured, mitochondria are now appreciated to constitute a population of organelles that migrate throughout the cell, fuse and divide, and undergo regulated turnover. These dynamic processes regulate mitochondrial function by enabling mitochondrial recruitment to critical subcellular compartments, content exchange between mitochondria, mitochondrial shape control, mitochondrial communication with the cytosol and mitochondrial quality control. As a result, mitochondria can readily adapt to changes in cellular requirements, whether due to physiological or environmental imperatives. When mitochondrial dynamics is disrupted, cellular dysfunction ensues. Here we discuss the human diseases associated with abnormalities in mitochondrial dynamics.