Traditionally, models of pleiotropy have predicted that evolutionary rate of genes is related negatively with pleiotropy as the number of traits of an organism increases, the evolutionary rates of genes in the organisms population decrease. So natural selection will frequently maximize vigor in youth at the expense of vigor later on and thereby produce a declining vigor senescence during adult life. Antagonistic pleiotropy and mutation accumulation contribute. Pleiotropy can have an effect on the evolutionary rate of genes and allele frequencies. Williams biologist 1,458 words exact match in snippet view article the genecentered view of evolution in the 1960s. Mutation accumulation ma and antagonistic pleiotropy ap have each been hypothesized to explain the evolution of senescence or deteriorating fitness in old age. Williams 1957 paper pleiotropy, natural selection, and the evolution of senescence is one of the most influential in 20th century evolutionary biology, and contains at least 3 foundational ideas. Protein networks, pleiotropy and the evolution of senescence daniel e. Natural selection can support lethal and harmful alleles, if their effects are felt after reproduction.
August weismann 1891 was the first person to put forward an evolutionary theory of aging which included senescence through mecha. Theory that aging is due to genes that are beneficial in early life, and deleterious late in life. This evolutionary theory, suggested by peter medawar9,10, considers aging as a byproduct of natural selection. Demographers and public health specialists have been surprised by the rapid increases in life expectancy, espe. These findings integrate molecular and evolutionary models of senescence, and should aid in. Contribution number 92 from the department of natural science, michigan state university. I explain these results with a simple mathematical model combining assumptions of the antagonistic pleiotropy theory for the evolution of senescence with data on network topology. Source of information on the evolution of agingsenescence. Pleiotropy is defined as a situation in which a single gene controls more than one trait. As selection pressure declines gradually, it would be more natural to expect senescence to be a similar gradual process, happening at all ages with deterioration approximately inverse to selection pressure, i. An example of negatively pleiotropic gene action of the. By standard population genetic reasoning, selection for pleiotropy should be too weak to matter.
Introduction since the 1940s, evolutionary biologists have argued that the agerelated decrease in the force of natural selection leads inexorably to the evolution of ageing medawar, 1946. Read antagonistic pleiotropy, mortality source interactions, and the evolutionary theory of senescence, evolution on deepdyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips. Senescence, the endogenous deterioration of health at later ages, can be explained in terms of evolution. The widespread occurrence of senescence is explained by observing that i the force of natural selection is generally weaker at late ages than at early ages, and ii the acquisition of greater longevity usually involves some. Mutation with positive effect on fitness when young can increase even if it has negative effects late in life.
According to the mutation accumulation theory of senescence, loci affecting a given fitnessrelated trait are subject to mutation to deleterious alleles with effects that are. Antagonistic pleiotropy and mutation accumulation influence. Testing evolutionary models of senescence in a natural. As organisms age, the effectiveness of natural selection weakens, leading to age. The possibility that genes might increase fitness at one age and also decrease it at another was mentioned by early theorists, but the first strong advocate of this mechanism of the evolution of senescence was williams 1957, who noted that natural selection will tend to maximize vigor in the young at the expense of vigor later in life. As discussed below, antagonistic pleiotropy is key to understanding many aspects of aging, especially the relationship between aging and cancer. Pleiotropy has significance for the theory of evolution. The population genetic basis for the decline with age in sensitivity of fitness to changes in survival and fecundity is discussed. Evolutionary mechanisms of senescence springerlink. He began his hypothesis with the idea that ageing can cause earlier senescence due to the competitive nature of life. Jul 01, 2003 in this paper we have developed a model of physiological senescence evolution, via the antagonistic pleiotropy mechanism, focusing our analyses on the two fitness measures, r and r, since one of the two often provides the appropriate index of evolutionary success under various forms of population regulation mylius and diekmann 1995. As a result, lateacting deleterious alleles will be under weaker purifying selection and will tend to reach higher frequencies, compared with earlyacting one. Haldane wondered why the dominant mutation that causes huntingtons disease remained in the population, and why natural selection had not eliminated it. The deleterious alleles that currently cause degeneration and disease during our long years of postreproductive life were infrequently expressed in our evolutionary and historical past.
This neglect may be attributed to a number of causes. Antagonistic pleiotropy, evolution, extrinsic hazard, interactions, senescence. Williams pleiotropy, natural selection, and the evolution of senescence. Pdf senescence has long been a public health challenge as well as a. Senescence is not due to group selection but to the decline with age in the force of. Oct 11, 2018 antagonistic pleiotropy, as it applies to aging, hypothesizes that animals possess genes that enhance fitness early in life but diminish it in later life and that such genes can be favored by natural selection because selection is stronger early in life even as they cause the aging phenotype to emerge. This theory proposes that ageing is due to the build up of telomereinduced senescent cells within the body. Antagonistic pleiotropy ap is today the bestaccepted theory for the evolutionary origin of aging. While very few studies have investigated selection on life span and senescence in natural insect populations, comparisons of laboratory. Williams 1957 paper pleiotropy, natural selection, and the evolution of senescence is one of the most.
The evolution of animal senescence canadian journal of. The notion that hamiltons forces of natural selection plateau thus has major implications for our understanding of the aging process and, in particular, of late life. Senescence is not due to group selection but to the decline with age in the force of natural selection acting on individuals. Pleiotropy, natural selection, and the evolution of senescence. Antagonistic pleiotropy, as it applies to aging, hypothesizes that animals possess genes that enhance fitness early in life but diminish it in later life and that such genes can be favored by natural selection because selection is stronger early in life even as they cause the aging phenotype to emerge. Reverse selection for earlylife fitness was applied to laboratory populations of. Only after the evolution of senescence could such an age be approximated. Such mutation accumulation will lead to senescence, as further formalized by haldane haldane, 1942 and medawar medawar, 1952. George williams, then a professor at michigan state university, published a paper in 1957 titled pleiotropy, natural selection, and the evolution of senescence evolution 11 398411. The central hypothesis of antagonistic pleiotropy remains the prevailing evolutionary explanation of senescence. What we can conclude from these mutation accumulation studies is that mutations tend to have an extremely wide window of negative effects, leading to positive pleiotropy across. Early reproduction is favoured by natural selection. There are two ways in which this decline with age in the power of selection can lead to the evolution of senescence.
Williams, for their help in the preparation of this paper. It is shown that this creates a presure of selection that disproportionately favors performance early in life. Selection, of course, will act to minimize the rate of this decline whenever possible. The evolution of human senescence can be explained by reference to the brief life expectancy of our ancestors. In human genetic diseases, a defect in a single gene often can affect a. According to these theories, aging is a byproduct of natural selection. There is a cumulative probability of death with or without senescence. Strong selection for one or two aspects of gene function will automatically bring along some other pleiotropic traits. According to ap theory, aging is a side effect of genes that are selected for their contribution to fertility and other essential components of individual fitness. The word senescence can refer either to cellular senescence or to senescence of the whole organism.
Pleiotropism simple english wikipedia, the free encyclopedia. That is, natural selection cannot eliminate genes that promote earlylife survival but incongruously also promote latelife debility, a concept termed antagonistic pleiotropy. If you need to print pages from this book, we recommend downloading it as a pdf. The evolution of senescence may be explained by two different, but not mutually exclusive, genetic mechanisms. Jun 22, 2004 i explain these results with a simple mathematical model combining assumptions of the antagonistic pleiotropy theory for the evolution of senescence with data on network topology. In this standard view, aging exists because the benefits of enhanced fertility early in life are linked logically or physically to. Contribution number 92 from the department of natural science, michigan. The onset of this neurological disease is on average at age 45. Protein networks, pleiotropy and the evolution of senescence. The rate of senescence shown by any species will reflect the balance between this direct. By 1957, williams introduced the concept of antagonis. Jan 30, 2017 antagonistic pleiotropy and mutation accumulation influence human senescence and disease.
In this paper we have developed a model of physiological senescence evolution, via the antagonistic pleiotropy mechanism, focusing our analyses on the two fitness measures, r and r, since one of the two often provides the appropriate index of evolutionary success under various forms of population regulation mylius and diekmann 1995. In general, the hallmark signature for these evolutionary explanations for senescence is that additive genetic variance i. This decline allows the spread of alleles with deleterious effects on late health. According to this theory, aging is a nonadaptive trait because natural selection is negligent of events that occur in a few longlived animals that provide little additional contribution to offspring numbers. Jul 01, 2003 read antagonistic pleiotropy, mortality source interactions, and the evolutionary theory of senescence, evolution on deepdyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips. One of the most prominent theories on the biochemical causes of ageing is the telomerecell senescence theory. Jan 12, 2016 we show that we should actually expect the rates of agerelated decline in female fertility and offspring performance to diverge under selection.
Williams michigan state university received february 26, 1957 senescence is a widespread phenomenon, but it has been largely neglected by nonmedical biologists. Dec 18, 2019 the mechanism of selection is indirect, the benefit longterm, and it accrues only to the group at the expense of the individual. Organismal senescence involves an increase in death rates andor a decrease in fecundity with increasing age, at least in the latter part of an organisms life cycle. Antagonistic pleiotropy and mutation accumulation influence human senescence and disease. Pdf protein networks, pleiotropy and the evolution of. Natural selection should therefore act in the direction of postponing or eliminating senescence from the life history. In human genetic diseases, a defect in a single gene often can affect a number of traits and have simultaneous diverse. In the ormat proided y the authors and unedited antagonistic. Download pdf aging, cellular senescence, and cancer. It has often been claimed that some heritable features of animals are not the product of adaptation by natural selection. The evolution of senescence under curtailed life span in. Antagonistic pleiotropy and mutation accumulation influence human. From an evolutionary standpoint, this system is thought to have evolved via antagonistic pleiotropy.
Received 28 january 2004 accepted 25 february 2004 published online 5 may 2004 protein networks, pleiotropy and the evolution of senescence daniel e. Williams noted that senescence may be causing many deaths even if animals are not dying of old age. The antagonistic pleiotropy hypothesis predicts that senescence is a consequence of. Jan 24, 2015 aging is very much under selection and it has been proved to be so without any doubt. Pleiotropy, natural selection and the evolution of senescence. A proper hypothesis should be based upon the best information available at the time, and for the case of the evolutionary theory of senescence, hamiltons model of selection is superior. Genomic patterns of pleiotropy and the evolution of complexity. Is antagonistic pleiotropy ubiquitous in aging biology. These findings integrate molecular and evolutionary models of senescence, and should aid in the search for new ageing genes. According to this theory, aging is a nonadaptive trait because natural selection is negligent of events that occur in a few longlived animals that provide. Pdf antagonistic pleiotropy and mutation accumulation influence. According to the mutation accumulation theory of senescence, loci affecting a given fitnessrelated trait are subject to mutation to deleterious alleles with effects that are restricted to certain ages.
1205 1268 876 423 919 868 41 1523 1437 468 1491 521 1532 1220 1397 1022 4 412 878 1053 1522 1522 1298 501 1144 1018 180 428 508 103 1120 1088 911 588 3 862 987 817 111 485 1036 870