By Jan Vijg
Getting older has lengthy in view that been ascribed to the sluggish accumulation of DNA mutations within the genome of somatic cells. despite the fact that, it's only lately that the required refined expertise has been constructed to start checking out this thought and its effects. Vijg severely studies the idea that of genomic instability as a potential common explanation for getting older within the context of a brand new, holistic figuring out of genome functioning in complicated organisms due to contemporary advances in useful genomics and structures biology. It presents an up to date synthesis of present study, in addition to a glance forward to the layout of innovations to retard or opposite the deleterious results of getting older. this is often really very important in a time once we are urgently attempting to resolve the genetic element of aging-related ailments. in addition, there's a starting to be public attractiveness of the significant of figuring out extra in regards to the underlying biology of getting older, pushed via 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
H. Morgan. First demonstrated in 1998 in Caenorhabditis elegans42, RNAi allows the sequence-speciﬁc silencing of genes using synthetic double-stranded RNAs. Such exogenous RNAs co-opt a ubiquitously expressed, evolutionarily conserved gene-regulatory system consisting of microRNAs (miRNAs; Chapter 3). Endogenous miRNAs are transcribed as single-stranded precursors up to 2000 bp in length and exhibit signiﬁcant secondary structure, resulting in stems and loops. Such primary transcripts are ﬁrst processed in the nucleus and after entering the cytoplasm converted by the RNase III enzyme Dicer into double-stranded 21–23-nucleotide-long mature RNAs.
At this point in time, there are hundreds of mutant genes in a variety of organisms, from yeast and fruit ﬂies to mice, which increase longevity by dampening growth, reproduction, energy metabolism, or nutrient sensing. There are also mutant genes that cause accelerated aging, but these are not always generally accepted due to the difﬁculties in demonstrating that reduced longevity is genuinely due to accelerated aging or merely a result of a disease or developmental defect. This is discussed extensively in Chapter 5.
Nevertheless, the ratchet would operate in all genomes over time and there is no reason to assume that it would not operate in somatic cells of metazoa, especially stem cells which would readily develop into clonal lines creating mosaics for the mutations which have arisen. This situation would be analogous to senescence of a protozoan clone, but signiﬁcantly more complicated in view of the interdependence of different types of somatic cells in metazoan species. In summary, Medawar’s idea of aging as a result of the accumulation in the germ line of mutations creating gene variants with adverse effects on the soma late in life, after the age of ﬁrst reproduction, is a logical explanation for the sheer universality of aging in the animal world.