Evolutionary Conservation Of A Mechanism Of Longevity From Worms To Mammals
Though the study of aging in the nematode model organism C. elegans has provided much insight into this complex process, it is not yet clear whether genes involved in aging in the worm have a similar role in mammals. In a recent study, Dr. Hekimi and colleagues of McGill University (Canada) report that inactivation of the gene mclk1, the murine ortholog of the C. elegans gene clk-1, results in increased cellular fitness and prolonged lifespan in mice.
The gene clk-1 in the worm, as well as mclk1 in mice, encodes an enzyme necessary for the biosynhesis of ubiquinone, an essential cofactor in numerous redox reactions such as mitochondrial respiration. Though lack of the mclk1 gene results in embryonic lethality, the authors were able to study mclk1-/- embryonic stem (ES) cells and show that they are resistant to oxidative stress and exhibit reduced DNA damage when compared to ES cells in which this gene is active. ...
Though the aging process of different organisms will most likely differ due to different physiologies and environments, Dr. Hekimi summarizes the relevance of their findings by concluding that "... the longevity-promoting effect of reducing clk-1/mclk1 activity that was initially observed in C. elegans is conserved in mice, supporting the idea that some molecular mechanisms of aging are shared throughout the animal kingdom."
A number of other genes that affect aging in a wide range of species have also been found in research using the nematode worm C. elegans -- for example:
- daf-2, an insulin-like receptor gene (see Signs Of Aging: Scientists Evaluate Genes Associated With Longevity and Scientists Find What Type Of Genes Affect Longevity)
- the gene for enzyme age-1/PI3 kinase, which plays a role in muscle deterioration (see Researchers Seek Fountain Of Youth Among The Worms)
- DAF-16, also involved in an insulin/glucose pathway (see Researchers Identify Switch That Controls Aging In Worms)
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