evolutionary biology of longevity
Introduction
Life is inherently hazardous. Preservation of life has included evolution of mechanisms that regulate longevity & reproduction along with evolution of species. For example, size confers a survival advantage & larger organisms tend to live longer & reproduce at a slower rate than smaller organisms. The development of the central nervous system also confers a survival advantage. Compare, for example, maximum life span of chimpanzees (50 years) vs humans (113 years).
Comparative analysis of genomic sequences across species suggests that relatively few genes may account for the evolution of longevity & of human intelligence.[1]
Evidence in support of this notion may be found in genes showing lineage-specific variationin copy number when the human genome is compared with the genomes of the great apes[2].
Mechanisms for evolution of species include:
- alternative splicing
- gene duplication[3]
- evolution of conserved non-coding sequences involved in gene regulation
- regions near genes involved in neuronal adhesion (primates)[5]
- cis-regulatory regions near genes expressed in the fetal brain[6]
- often near genes associated with transcription & DNA binding & near telomeres[7]
- Sirt1 appears to confer longevity benefit of calorie restriction through actions in the hypothalamus
- microsatellite instability[4]
- mutation
The relative contributions of various mechanism for evolution of species not well understood.
More general terms
Additional terms
- biology of aging
- evolutionary divergent human protein
- genes showing lineage-specific variation in copy number
- human longevity protein
References
- ↑ 1.0 1.1 Cutler RG, the Evolutionary Biology of Senescence, In: Biology of Aging
- ↑ 2.0 2.1 Fortna A, Kim Y, MacLaren E, Marshall K, Hahn G, Meltesen L, Brenton M, Hink R, Burgers S, Hernandez-Boussard T, Karimpour- Fard A, Glueck D, McGavran L, Berry R, Pollack J, Sikela JM. Lineage-specific gene duplication and loss in human and great ape evolution. PLoS Biol. 2004 Jul;2(7):E207. Epub 2004 Jul 13. PMID: https://www.ncbi.nlm.nih.gov/pubmed/15252450
- ↑ 3.0 3.1 Kopelman NM, Lancet D, Yanai I. Alternative splicing and gene duplication are inversely correlated evolutionary mechanisms. Nat Genet. 2005 Jun;37(6):588-9. Epub 2005 May 15. PMID: https://www.ncbi.nlm.nih.gov/pubmed/15895079
- ↑ 4.0 4.1 Journal Watch 25(16):130, 2005 Hammock EA, Young LJ. Microsatellite instability generates diversity in brain and sociobehavioral traits. Science. 2005 Jun 10;308(5728):1630-4. PMID: https://www.ncbi.nlm.nih.gov/pubmed/15947188
- ↑ 5.0 5.1 Prabhakar S et al Accelerated evolution of conserved noncoding sequences in humans. Science. 2006 Nov 3;314(5800):786. PMID: https://www.ncbi.nlm.nih.gov/pubmed/17082449
- ↑ 6.0 6.1 Torgerson DG et al Evolutionary processes acting on candidate cis-regulatory regions in humans inferred from patterns of polymorphism and divergence. PLoS Genet. 2009 Aug;5(8):e1000592. Epub 2009 Aug 7. PMID: https://www.ncbi.nlm.nih.gov/pubmed/19662163
- ↑ 7.0 7.1 Pollard KS et al Forces shaping the fastest evolving regions in the human genome. PLoS Genet. 2006;2(10):e168 PMID: https://www.ncbi.nlm.nih.gov/pubmed/17040131