NG Paper on Mitochondrial DNA and Aging

One of the rapidly growing areas of interest in aging research is the role played by mitochondria DNA. What are mitochondria? This site explains:

Mitochondria are structures within cells that convert the energy from food into a form that cells can use. Although most DNA is packaged in chromosomes within the nucleus, mitochondria also have a small amount of their own DNA. This genetic material is known as mitochondrial DNA or mtDNA. In humans, mitochondrial DNA spans about 16,500 DNA building blocks (base pairs), representing a fraction of the total DNA in cells.

Mitochondrial DNA contains 37 genes, all of which are essential for normal mitochondrial function. Thirteen of these genes provide instructions for making enzymes involved in oxidative phosphorylation. Oxidative phosphorylation is a process that uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source. The remaining genes provide instructions for making molecules called transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), which are chemical cousins of DNA. These types of RNA help assemble protein building blocks (amino acids) into functioning proteins.

Mitochondrial genes are among the estimated 20,000 to 25,000 total genes in the human genome.

The latest issue of Nature Genetics has this Brief Communication piece which further illustrates the impressive and exciting advances that are being made in aging research. Here is the abstract:

"DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice" by Marc Vermulst et. al.

Mitochondrial DNA (mtDNA) mutations are thought to have a causal role in many age-related pathologies. Here we identify mtDNA deletions as a driving force behind the premature aging phenotype of mitochondrial mutator mice, and provide evidence for a homology-directed DNA repair mechanism in mitochondria that is directly linked to the formation of mtDNA deletions. In addition, our results demonstrate that the rate at which mtDNA mutations reach phenotypic expression differs markedly among tissues, which may be an important factor in determining the tolerance of a tissue to random mitochondrial mutagenesis.

Cheers,
Colin

P.S. the image of the "anatomy of the cell" is provided via the Lucile Packard Children’s Hospital website at Stanford.