The relation of recombination to mutational advance.
TL;DR: It is shown that this calculation does not apply for mutant genes that act advantageously only when in some special combinations with one or more other mutant genes, and that as far as these cases of special synergism are concerned recombining lines have no evolutionary advantage over non-recombining ones.
Abstract: The method of calculation is shown wherebt a formula has been derived that approximately the ratio of the rate of accumulation of advantageous mutant genes in a population that undergoes recombination to the rate in an otherwise non-recombining one. A table is given showing the ratios thus found for different frequencies of advantageous mutations and different degrees of their advantage. It is shown that this calculation does not apply for mutant genes that act advantageously only when in some special combinations with one or more other mutant genes, and that as far as these cases of special synergism are concerned recombining lines have no evolutionary advantage over non-recombining ones. Other limitations of the formula are pointed out and assessed. It is explained that most factors that retard the rate of recombination—for expample, linkage, rarity of outbreeding, intercalation of sexual reproduction between more frequent cycles of sexual propagation, and partial isolation between subpopulations—must usually cause little long-term retardation of the speed of advance that is fostered by recombination. Moreover, even where long-term evolutions has virtually ceased, recombination of mutant genes still confers upon a population the means of adopting short-term genetic “dodges”, that adjust it to ecological and “physical” changes in its circumstances, much more rapidly than would be possible for a comparable asexual population. Under conditions where only stability of type is needed, a non-recombining does not actually degenerate as a result of an excess of mutation over selection, after the usual equilibrium between these pressures is reached. However, a irreversible ratchet mechanism exists in the non-recombining species (unlike the recombining ones) that prevents selection, even if intensified, from reducing the mutational loads below the lightest that were in existence when the intensified selection started, whereas, contrariwise, “drift”, and what might be called “selective noise” must allow occasional slips of the lightest loads in the direction of increased weight.
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TL;DR: E Epidemiological as well as functional and structural studies suggest that RNA viruses can tolerate restricted types and numbers of mutations during any specific time point during their evolution, which may open new avenues for combating viral infections.
Abstract: RNA viruses exploit all known mechanisms of genetic variation to ensure their survival. Distinctive features of RNA virus replication include high mutation rates, high yields, and short replication times. As a consequence, RNA viruses replicate as complex and dynamic mutant swarms, called viral quasispecies. Mutation rates at defined genomic sites are affected by the nucleotide sequence context on the template molecule as well as by environmental factors. In vitro hypermutation reactions offer a means to explore the functional sequence space of nucleic acids and proteins. The evolution of a viral quasispecies is extremely dependent on the population size of the virus that is involved in the infections. Repeated bottleneck events lead to average fitness losses, with viruses that harbor unusual, deleterious mutations. In contrast, large population passages result in rapid fitness gains, much larger than those so far scored for cellular organisms. Fitness gains in one environment often lead to fitness losses in an alternative environment. An important challenge in RNA virus evolution research is the assignment of phenotypic traits to specific mutations. Different constellations of mutations may be associated with a similar biological behavior. In addition, recent evidence suggests the existence of critical thresholds for the expression of phenotypic traits. Epidemiological as well as functional and structural studies suggest that RNA viruses can tolerate restricted types and numbers of mutations during any specific time point during their evolution. Viruses occupy only a tiny portion of their potential sequence space. Such limited tolerance to mutations may open new avenues for combating viral infections.
1,468 citations
TL;DR: In this article, the authors examined the dynamics of evolutionary adaptation, the genetic bases of adaptation, tradeoffs and the environmental specificity of adaptation and the origin and evolutionary consequences of mutators.
Abstract: Microorganisms have been mutating and evolving on Earth for billions of years. Now, a field of research has developed around the idea of using microorganisms to study evolution in action. Controlled and replicated experiments are using viruses, bacteria and yeast to investigate how their genomes and phenotypic properties evolve over hundreds and even thousands of generations. Here, we examine the dynamics of evolutionary adaptation, the genetic bases of adaptation, tradeoffs and the environmental specificity of adaptation, the origin and evolutionary consequences of mutators, and the process of drift decay in very small populations.
1,359 citations
Book•
01 Dec 1998
TL;DR: Geary presents a theoretical bridge linking parenting, mate choices, and competition, with children's development and sex differences in brain and cognition, in a lively and nuanced application of Darwin's insight to help explain the authors' heritage and their place in the natural world.
Abstract: Why do girls tend to earn better grades in school than boys? Why are men still far more likely than women to earn degrees in the fields of science, technology, engineering, and mathematics? And why are men on average more likely to be injured in accidents and fights than women? These and many other questions are the subject of both informal investigation in the media and formal investigation in academic and scientific circles. In his landmark book "Male, Female: The Evolution of Human Sex Differences", author David Geary provided the first comprehensive evolutionary model to explain human sex differences. Using the principles of sexual selection such as female choice and male-male competition, the author systematically reviewed and discussed the evolution of sex differences and their expression throughout the animal kingdom, as a means of not just describing but explaining the same process in Homo sapiens. Now, over ten years since the first edition, Geary has completed a massive update, expansion and theoretical revision of his classic text. New findings in brain and genetic research inform a wealth of new material, including a new chapter on sex differences in patterns of life history development; expanded coverage of genetic research (e.g. DNA finger printing to determine paternity as related to male-male competition in primates); fatherhood in humans; cross-cultural patterns of sex differences in choosing and competing for mates; and, genetic, hormonal, and socio-cultural influences on the expression of sex differences. Finally, through his motivation to control framework (introduction in the first edition and expanded in "The Origin of Mind", 2005), Geary presents a theoretical bridge linking parenting, mate choices, and competition, with children's development and sex differences in brain and cognition. The result is an even better book than the original - a lively and nuanced application of Darwin's insight to help explain our heritage and our place in the natural world.
1,156 citations
TL;DR: If the deleterious mutation rate per genome per generation is greater than 1, then the greater efficiency of selection against these mutations in sexual populations may be responsible for the evolution of sex and related phenomena.
Abstract: The origin and maintenance of sexual reproduction continues to be an important problem in evolutionary biology. If the deleterious mutation rate per genome per generation is greater than 1, then the greater efficiency of selection against these mutations in sexual populations may be responsible for the evolution of sex and related phenomena. In modern human populations detrimental mutations with small individual effects are probably accumulating faster than they are being eliminated by selection.
1,079 citations
TL;DR: Longitudinal studies suggest that the prevalence of seed‐transmitted endophytes can increase rapidly over time, and estimates of infection frequency have revealed variable levels of infection with especially high prevalence in the subfamily Pooideae.
Abstract: Over the past 20 yr much has been learned about a unique symbiotic interaction between fungal endophytes and grasses. The fungi (Clavicipitaceae, Ascomycota) grow intercellularly and systemically in aboveground plant parts. Vertically transmitted asexual endophytes forming asymptomatic infections of cool‐season grasses have been repeatedly derived from sexual species that abort host inflorescences. The phylogenetic distribution of seed‐transmitted endophytes is strongly suggestive of cocladogenesis with their hosts. Molecular evidence indicates that many seed‐transmitted endophytes are interspecific hybrids. Superinfection may result in hyphal fusion and parasexual recombination. Most endophytes produce one or more alkaloid classes that likely play some role in defending the host plant against pests. Hybridization may have led to the proliferation of alkaloid‐production genes among asexual endophytes, favoring hybrids. The ergot alkaloid ergovaline, lolitrems, and lolines are produced by only a ...
981 citations
Cites background from "The relation of recombination to mu..."
...Another potential factor selecting for interspecific hybrids, not mutually exclusive with the first, is Muller’s ratchet, the accumulation of marginally deleterious mutations in clonal lineages (Muller 1964; Lynch et al. 1993; Moran 1996; Bidochka 2001)....
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TL;DR: There is no basic biological reason why reproduction, variation and evolution can not go indefinitely without sexuality or sex; therefore, sex is not, in an absolute sense, a necessity, it is a "luxury."
Abstract: FPROM the genetic point of view it is advantageous to begin by considering sex in the broader sense of sexuality. It is not generally realized that genetics has finally solved the age-old problem of the reason for the existence (i.e., the function) of sexuality and sex, and that only geneticists can properly answer the question, \"Is sex necessary ?\" There is no basic biological reason why reproduction, variation and evolution can not go o01 indefinitely without sexuality or sex; therefore, sex is not, in an absolute sense, a necessity, it is a \"luxury.\" It is, however, highly desirable and useful, and so it becomes necessary in a relativistic sense, when our competitorspecies also are endowed with sex, for sexless beings, although often at a temporary advantage, can not keep up the pace set by sexual beings in the evolutionary race and, wheii readjustments are called for, they must eventually lose out. Thus sexual beings form most of the central and the continuing portions of the evolutionary tree from which ever and again new sexless end-twigs sprout off. Whatever the secondary needs of present-day somatoplasm may be, there is no fundamental protoplasmic need for rejuvenation of the germ plasm through sexual union, no reason to believe that \"protoplasmic stimulation\" is per se produced by mingling of unlike germ plasms, nor any evidence that variation of the hereditary particles is induced by \"panmixia.\" A more reasonable claim might be made out for the new genetic concept of \"heterosis\" as furnishing the function of sexuality and
1,173 citations
Journal Article•
702 citations
TL;DR: In this paper, the authors present a mathematical treatment of biological evolution and its mechanism, which is not possible for me to represent the high tradition of Josiah Willard Gibbs by offering you a Mathematical Treatment.
Abstract: I t is not possible for me to represent the high tradition of Josiah Willard Gibbs by offering you a mathematical treatment. Nevertheless, the subject of biological evolution and its mechanism must be of great interest to yourselves, as the most exemplary products of its operation. Perhaps, then, our reconnaissance flight over these biological jungles, and our attempts to measure certain aspects of them, may serve to entice some of you or, through you, some of those with whom your influence counts, into bringing your higher powered mental tools to bear in the more effective and more elegant mapping and analysis of this territory. If so, my intention to inveigle you into it will have been successfully accomplished. To those philosophers who declare \"I think, therefore I am,\" their own existence seems the one complete certainty. To others, it does not seem so certain that they do think, nor even that they produce a significant imprint on reality in general. I t is, however, evident that they, along with all things living, if they do exist, are utter improbabilities, far less plausible than any other phenomena that have been encountered. Herein we shall at tempt to assess how fantastically unlikely we and our fellow creatures are, and by what means such preposterous anomalies could have come about. The old-time philosopher still insists that such extravagances of organization could have arisen only by design, inasmuch as accident cannot be expected to convert itself into order. However, a dispassionate examination of the rules of this game of life should throw some light on the question of how such a massive compounding of improbabilities may have taken place.
69 citations