This commentary on research results from last year is a good introduction to the topic of protein translation errors and their relationship with species longevity. Translation is one of the steps in the complex process of gene expression, in which genes are used as a blueprint to assemble proteins. Nothing is perfect and errors take place in translation, as everywhere else. Such errors are in effect a form of damage, causing issues for the cell until the broken protein is removed.
It is fairly well established that greater levels of the cellular maintenance processes of autophagy, responsible for removing damaged proteins, metabolic waste, and failing cellular structures, can result in slowed aging in a range of species. It sounds plausible that reducing the rate at which malformed proteins are produced would be beneficial for similar reasons, but this is harder to prove one way or another. The present laboratory is made up of the biochemistry of similar species with different life spans, translation machinery, and error rates. Unfortunately there are also many other differences: the study of aging is made very challenging by the inability to completely isolate mechanisms of interest, and dial