By Jan Vijg
Getting older has lengthy considering been ascribed to the sluggish accumulation of DNA mutations within the genome of somatic cells. although, it's only lately that the mandatory subtle know-how has been built to start trying out this conception and its effects. Vijg severely experiences the concept that of genomic instability as a potential common reason for getting older within the context of a brand new, holistic knowing of genome functioning in advanced organisms due to contemporary advances in sensible genomics and structures biology. It presents an up to date synthesis of present examine, in addition to a glance forward to the layout of ideas to retard or opposite the deleterious results of getting older. this is often rather very important in a time once we are urgently attempting to get to the bottom of the genetic component to aging-related ailments. in addition, there's a starting to be public reputation of the critical of knowing extra concerning the underlying biology of getting older, pushed through carrying on with demographic switch.
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Extra info for Aging of the Genome: The Dual Role of DNA in Life and Death
Medawar proposed that aging was the necessary result of constitutional mutations, accumulated in the germ line over evolutionary time, that reduce ﬁtness late in life. As mentioned above, in the wild only a small fraction of a birth cohort will reach advanced age while continuing to reproduce. Therefore, the later the adverse effects of such mutations manifest after the period of ﬁrst reproduction, the less likely that they will be weeded out by natural selection. The frequencies of such alleles, especially in small populations, will then drift randomly from generation to generation.
Cancer is one of them. Tumor-suppressor genes are obviously advantageous for young organisms and mutations inactivating such genes would not be passed on to many offspring. Apoptosis, or programmed cell death, and cellular senescence, irreversible mitotic arrest, are both critical processes for suppressing tumorigenesis in mammals78. Both responses are highly conserved in eukaryotic organisms also for reasons other than suppressing cancer. Apoptosis, for example, plays an essential role in embryonic development and also later in maintaining normal tissue homeostasis.
Melanogaster, the fruit ﬂy. Clare and Luckinbill61 restricted reproduction of this organism to late age, thereby increasing the intensity of selection during the later portion of the lifespan. They did this for 21–29 generations, at two different THE LOGIC OF AGING 33 larval densities. Populations with high and uncontrolled numbers of competing larvae responded strongly to selection for late-life reproduction, with the length of adult life increasing by as much as 50%. Under such conditions selection produced true-breeding long-lived lines.
Aging of the Genome: The Dual Role of DNA in Life and Death by Jan Vijg