By Michael R. Rose, Caleb E. Finch
Aging is a kind of topics that many biologists believe is essentially unknown. hence, they typically think cozy supplying super facile generalizations which are both unsupported or at once refuted within the experimental literature. regardless of this unlucky precedent, getting older is a truly vast phenomenon that calls out for integration past the mere accumulating jointly of effects from disparate laboratory organisms. With this in brain, half One deals numerous varied artificial views. The editors, Rose and Finch, supply a verbal synthesis of the sphere that intentionally makes an attempt to examine getting older from each side, the evolutionary and the molecular. The articles by way of Charlesworth and Clark either supply inhabitants genetic views on getting older, the previous extra mathematical, the latter extra experimental. Bell takes a very assorted method, arguing that getting older is probably not the results of evolutionary forces. Bell's version in its place proposes that getting older might come up from the revolutionary deterioration of power host pathogen interactions. this can be the 1st specific e-book of this version. It marks whatever of a go back to the kind of getting older theories that predominated within the 1950's and 1960's, theories just like the somatic mutation and mistake disaster theories. we are hoping that the reader could be interested in the distinction in perspectives among the articles in keeping with evolutionary idea and that of Bell. MR. Rose and C. E. Finch (eds. ), Genetics and Evolution of getting older, 5-12, 1994. © 1994 Kluwer educational Publishers. The J aniform genetics of getting older 2 Michael R. Rosel & Caleb E.
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Additional resources for Genetics and Evolution of Aging
Selection occurs in HIV populations during serial passage in cell culture. , 1991). , 1992). , 1991), and may occur even in highly conserved regions of the viral genome. Hoxie et al. (1991) found that the passage of attenuated HIV-l with low binding affinity for CDA cells eventually resulted in the appearance of cytopathic variants whose binding affinities were comparable with those of normal cytopathic HIV-2 isolates. , 1991). L'Age-Stehr et al. (1990) observed the evolution of a shorter latent period and increased virulence towards T-cells when HIV was maintained in cell culture.
1991). , 1990). Within-host selection in relation to other theories The material that I have reviewed above shows that all the preconditions required by the hypothesis of within-host selection are met, at least in some instances. Whether or not they are generally true must await the accumulation of evidence. However, the availability of methods for amplifying viral genomes present at very low abundance in host tissues will make it possible to decide very soon whether the single most important and most surprising observation which the theory requires, the universality of persistent viral infection, is really the case.
Partridge, L. H. Barton, 1993. Optimality, mutation, and the evolution of ageing. Nature 362: 305-311. , P. Pignatelli & L. Partridge, 1993. Evolutionary effects of selection on age at reproduction in larval and adult Drosophila melanogaster. Evolution 47: 445-455. , 1984. Laboratory evolution of postponed senescence in Drosophila melanogaster. Evolution 38: 1004--1010. R. & B. Charlesworth, 1981. Genetics of life history of Drosophila melanogaster. II. Exploratory selection experiments. Genetics 97: 187-196.