Mitochondrial DNA Damage and Longevity in Rockfish

Rougheye rockfish are one of the few species to show negligible senescence, a comparative lack of the usual evident consequences of aging. Other examples include lobsters, naked mole-rats, some tortoise species, and some clam species such as the ocean quahog. Individuals still die after a comparatively long life, and so there are evidently still processes of degeneration gnawing away, but for many of these species it is hard to measure age via the normal metrics of vigor, growth, reproduction, and changes in various aspects of biochemistry. There is little to no meaningful change and decline until close to the end.

Mitochondria are the power plants of the cell, responsible for generating chemical energy stores to power cellular processes. They are descended from symbiotic bacteria and contain a remnant of that bacterial DNA. Damage to this mitochondrial DNA is considered to contribute to aging via a complex chain of conseqeunces that leads to a growing number of malfunctioning cells overtaken by dysfunctional mitochondria. This study of mitochondrial damage and longevity is interesting for having been carried out in a negligibly senescent species:

The mitochondrial theory of ageing proposes that the cumulative effect of biochemical damage in mitochondria causes mitochondrial mutations and plays a key role in ageing. Numerous studies have applied comparative approaches to test one of the predictions of the theory: that the rate of mitochondrial mutations is negatively correlated with longevity. Comparative studies face three challenges in detecting correlates of mutation rate: covariation of mutation rates between species due to ancestry, covariation between life history traits, and difficulty obtaining accurate estimates of mutation rate.

We address these challenges using a novel Poisson regression method to examine the link between mutation rate and lifespan in rockfish (Sebastes). This method has better performance than traditional sister-species comparisons when sister species are too recently diverged to give reliable estimates of mutation rate. Rockfish are an ideal model system: they have long life spans with indeterminate growth and little evidence of senescence, which minimizes the confounding tradeoffs between lifespan and fecundity.

We show that lifespan in rockfish is negatively correlated to rate of mitochondrial mutation, but not the rate of nuclear mutation. The life history of rockfish allows us to conclude that this relationship is unlikely to be driven by the tradeoffs between longevity and fecundity, or by the frequency of DNA replications in the germline. Instead the relationship is compatible with the hypothesis that mutation rates are reduced by selection in long-lived taxa to reduce the chance of mitochondrial damage over its lifespan, consistent with the mitochondrial theory of ageing.



When citing the exotic (rarely seen) species such as turtles, rockfish and then lobster and NM rat please note that Nick Lane in his excellent book "Power, Sex, Suicide: Mitochondria and the Meaning of Life" also mentions a far more common species, bird. You can barely discern an old bird from a young one.

Bird, comparable in size to a rat, lives six times as long. You can bet that his point is about the mitochondria and ROS management.

Posted by: JohnN at June 8th, 2015 2:14 PM
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