Keller & Miller (K&M) make a persuasive case for the role of mutation-selection balance in the persistence of such disorders as schizophrenia. However, there is evidence relating illness liability to creativity, which seems to imply balancing selection. I argue for a hybrid position, where schizotypal personality traits can have fitness advantages or disadvantages, with mutational load and neurodevelopmental conditions determining which outcome is observed. (Published Online November 9 2006).

Three reservations about Keller & Miller's (K&M's) argument are explored: Serious validity problems afflict epidemiological criteria discriminating disorders from non-disorders, so high rates may be misleading. Normal variation need not be mild disorder, contrary to a possible interpretation of K&M's article. And, rather than mutation-selection balance, true disorders may result from unselected combinations of normal variants over many loci. (Published Online November 9 2006).

Given that natural selection is so powerful at optimizing complex adaptations, why does it seem unable to eliminate genes (susceptibility alleles) that predispose to common, harmful, heritable mental disorders, such as schizophrenia or bipolar disorder? We assess three leading explanations for this apparent paradox from evolutionary genetic theory: (1) ancestral neutrality (susceptibility alleles were not harmful among ancestors), (2) balancing selection (susceptibility alleles sometimes increased fitness), and (3) polygenic mutation-selection balance (mental disorders reflect the inevitable (...) mutational load on the thousands of genes underlying human behavior). The first two explanations are commonly assumed in psychiatric genetics and Darwinian psychiatry, while mutation-selection has often been discounted. All three models can explain persistent genetic variance in some traits under some conditions, but the first two have serious problems in explaining human mental disorders. Ancestral neutrality fails to explain low mental disorder frequencies and requires implausibly small selection coefficients against mental disorders given the data on the reproductive costs and impairment of mental disorders. Balancing selection (including spatio-temporal variation in selection, heterozygote advantage, antagonistic pleiotropy, and frequency-dependent selection) tends to favor environmentally contingent adaptations (which would show no heritability) or high-frequency alleles (which psychiatric genetics would have already found). Only polygenic mutation-selection balance seems consistent with the data on mental disorder prevalence rates, fitness costs, the likely rarity of susceptibility alleles, and the increased risks of mental disorders with brain trauma, inbreeding, and paternal age. This evolutionary genetic framework for mental disorders has wide-ranging implications for psychology, psychiatry, behavior genetics, molecular genetics, and evolutionary approaches to studying human behavior. (Published Online November 9 2006) Key Words: adaptation; behavior genetics; Darwinian psychiatry; evolution; evolutionary genetics; evolutionary psychology; mental disorders; mutation-selection balance; psychiatric genetics; quantitative trait loci (QTL). (shrink)

This chapter offers a review of standard views about the requirements for natural selection to shape evolution and for the sorts of ‘units’ on which selection might operate. It then summarizes traditional arguments for genic selectionism, i.e., the view that selection operates primarily on genes (e.g., those of G. C. Williams, Richard Dawkins, and David Hull) and traditional counterarguments (e.g., those of William Wimsatt, Richard Lewontin, and Elliott Sober, and a diffuse group based on life history strategies). (...) It then offers a series of responses to the arguments, based on more contemporary considerations from molecular genetics, offered by Carmen Sapienza. A key issue raised by Sapienza concerns the degree to which a small number of genes might be able to control much of the variation relevant to selection operating on such selectively critical organs as hearts. The response to these arguments suggests that selection acts on many levels at once and that sporadic selection, acting with strong effects, can act successively on different key traits (and genes) while maintaining a balance among many potentially conflicting demands faced by organisms within an evolving lineage. (shrink)

The target article skillfully evaluates data on mental disorders in relation to predictions from evolutionary genetic theories of neutral evolution, balancing selection, and polygenic mutation-selection balance, resulting in a negative outlook for the likelihood of success finding genes for mental disorders. Nevertheless, new conceptualizations, methods, and continued interactions across disciplines provide hope.

Keller & Miller's (K&M's) conclusion appears to be correct; namely, that common, harmful, heritable mental disorders are largely maintained at present frequencies by mutation-selection balance at many different loci. However, their “paradox” is questionable. (Published Online November 9 2006).

Genetic variability and diversity are the result of a mutation-selection balance that acts permanently within and between species. The presence of deleterious mutations is a necessary consequence of this process and thus the price paid by a species for its capacity for further evolution (Haldane 1937, Am Nat 71:337–349). Recent estimations of mutation rate in the human lineage has revived the debate as to whether the high number of deleterious mutations poses a severe problem for the (...) future of mankind. Theoretical considerations allow a scenario in which the survival of the human race is maintained by truncation selection of deleterious mutations that removes as many mutations as appear anew in every generation. In this case our genetic burden is carried by those individuals that suffer a genetic death resulting from random distribution of deleterious alleles. Nevertheless, one has to ask whether the mutation rate may set absolute limits on the complexity of a species. (shrink)

Receptor oligomerization plays a key role in maintaining genome stability and restricting protein mutagenesis. When properly folded, protein monomers assemble as oligomeric receptors and interact with environmental ligands. In a gene-centered view, the ligand specificity expressed by these receptors is assumed to be causally predetermined by the cell genome. However, this mechanism does not fully explain how differentiated cells have come to express specific receptor repertoires and which combinatorial codes have been explored to activate their associated signaling pathways. It is (...) our contention that the plasma membrane acts as the locus where several contextual cues may be integrated. As such it allows the semiotic selection of those receptor configurations that provide cells with the minimum essential requirements for agency. The occurrence of protein misfolding makes it impossible for receptor monomers to assemble along the membrane and to sustain meaningful relationships with environmental ligands. How could a cell lineage deal with these loss-of-function mutations during evolution and restrain gene redundancy accordingly? In this paper, we will be arguing that the easiest way for bacteria clones to accomplish this goal is by getting rid of cells expressing mutated receptor proteins. The mechanism sustaining this cell selection is also occurring in many somatic tissues and its function is currently believed to counteract in vivo protein mutagenesis. Our discussion will be mainly focused on the significance and semiotic nature of the interplay between membrane receptors and the epigenetic control of gene expression, as mediated by the control of mismatched repairing and protein folding mechanisms. (shrink)

In a recent comment on the HFEA’s public consultation on sex selection, Soren Holm claimed that proponents of family balancing are committed to embrace a laissez faire approach. Given that arguments in support of sex selection for family balancing also support sex selection for other social reasons, advocates of family balancing, he asserts, are simply inconsistent when calling for a limit on access to sex selection. In this paper, I argue that proponents of family balancing are (...) in no way inconsistent. Provided their advocacy of family balancing is aimed at preventing a severe distortion of the natural sex ratio, they are entirely justified in insisting on restrictions to sex selection. The real question is whether a concern for the sex ratio does indeed call for a limit on sex selection. Based on a recent survey on gender preferences and data from several Gender Clinics, I argue that a restriction on sex selection to family balancing is unwarranted. In the absence of any evidence for a pending sex ratio distortion, we are actually required to adopt a laissez faire approach to sex selection. (shrink)

Evolutionary gradualism, the randomness of mutations, and the hypothesis that natural selection exerts a pervasive and substantial influence on evolutionary outcomes are pair-wise logically independent. Can the claims about selection and mutation be used to formulate an argument for gradualism? In his Genetical Theory of Natural Selection, R.A. Fisher made an important start at this project in his famous “geometric argument” by showing that a random mutation that has a smaller effect on two or more (...) phenotypes will have a higher average fitness than a random mutation that has a larger phenotypic effect. Motoo Kimura’s demonstration that a gene’s probability of fixation depends on both the selection coefficient and the effective population size shows that Fisher’s argument for gradualism was mistaken. Here we analyze Fisher’s argument and explain how Kimura’s theory leads to a conclusion that Fisher did not anticipate. We identify a fallacy that reasoning about fitness differences and their evolutionary consequences should avoid. We then distinguish forward-directed from backward-directed versions of gradualism. The backward-directed thesis about a single mutation may be correct, but the forward-directed thesis is not. After that we consider a sequence of random mutations that all affect the same cluster of phenotypes and Allen Orr’s idea that there is an optimal sequence of mutation sizes, moving from larger to smaller as the population approaches a fixed optimum. This provides a likelihood justification for a forward-directed version of gradualism when there is a fixed optimum, but it also provides an argument against forward-directed gradualism if the optimum shifts substantially as the population evolves. Finally, we consider whether genome-wide association studies (GWASs) can furnish empirical evidence that bears on the truth of gradualism. The version of gradualism that GWASs directly bear on concerns the phenotypic effect size of a gene after it arises by mutation and has reached an appreciable frequency, not the phenotypic size of the mutation event itself. (shrink)

A growing number of researchers suggest that female homosexuality is at least in part influenced by genetic factors. Unlike for male homosexuality, few familial studies have attempted to explore maintenance of this apparently fitness-detrimental trait in the population. Using multiple recruitment methods, we explored fecundity and sexual orientation within the pedigrees of 1,458 adult female respondents. We compared 487 homosexual and 163 bisexual with 808 heterosexual females and 30,203 of their relatives. Our data suggest that the direct fitness of homosexual (...) females is four times lower than the direct fitness of heterosexual females of corresponding ages. The prevalence of nonheterosexuality within the homosexual female respondents’ families appear to be more than four times higher than the basal prevalence in the Italian population. Pedigree size and relative fecundity in both the paternal and maternal sides of the homosexual women’s families were significantly higher than in the heterosexuals’ families. If confirmed, the relative average fecundity increase within the family seems to offset the loss in fitness due to the low direct fitness of homosexual females. Therefore, the balanced fecundity in the homosexual females’ families may allow the trait to be maintained at a low-frequency equilibrium in the population. (shrink)

This article proposes an Analytic Hierarchy Process Dempster-Shafer and similarity-based network selection algorithm for the scenario of dynamic changes in user requirements and network environment; combines machine learning with network selection and proposes a decision tree-based network selection algorithm; combines multiattribute decision-making and genetic algorithm to propose a weighted Gray Relation Analysis and genetic algorithm-based network access decision algorithm. Firstly, the training data is obtained from the collaborative algorithm, and it is used as the training set, and (...) the network attributes are used as the attribute set, and the continuous attributes are discretized by dichotomization, and the attribute that can make the greatest information gain is selected as the division feature, and a decision tree with strong generalization ability is finally obtained, which is used as the decision basis for network access selection. The simulation results show that the algorithm proposed in this thesis can effectively improve user service quality under three services, and the algorithm is simple and effective with low complexity. It first uses AHP-DS hierarchical analysis to establish a recursive hierarchy for the network selection problem and obtains the subjective weights of network attributes through the judgment matrix. Then, it uses a genetic algorithm to adjust the subjective weight, defines the fitness function in the genetic algorithm-based on gray correlation analysis, adjusts the weights of the selection operator, crossover operator, and variation operator in the genetic algorithm, and gets the network with the largest fitness as the target network, which can effectively improve the user service quality. (shrink)

Quartz & Sejnowski find flaws in standard theories of neural selection, which they propose to repair by introducing Lamarckian mechanisms for anatomical refinement that are analogous to directed mutation in evolution. The reversal of cause and effect that these mechanisms require is no more plausible in an explanation of cognition than it is in an explanation of evolution.

It is widely assumed that the strongest case for permitting non‐medical sex selection is where parents aim at family balance. This piece criticizes one representative attempt to justify sex selection for family balance. Kluge (2007) assumes that some couples may seek sex selection because they hold discriminatory values, but this need not impugn those who merely have preferences, without evaluative commitments, for a particular sex. This is disputed by those who see any sex selection (...) as inherently sexist because it upholds stereotypes about the sexes. This article takes an alternative approach. I argue that, even if we accept that preference‐based selection is unobjectionable, a policy permitting selection for family balancing does a poor job of distinguishing between value‐based and preference‐based selection. If we wish to permit only preference‐based sex selection we should seek to identify parents’ motives. If we wish to justify a family balancing policy, other arguments are needed. (shrink)

The existing numerous adaptive variants of differential evolution have been improved the search ability of classic DE to certain extent. Nevertheless, those variants of DE do not obtain the promising performance in solving black box problems with unknown features, which is mainly because the adaptive rules of those variants are designed according to their designers’ cognition on the problem features. To enhance the optimization ability of DE in optimizing black box problems with unknown features, a differential evolution with autonomous (...) class='Hi'>selection of mutation strategies and control parameters is proposed in this paper, inspired by autonomous decision-making mechanism of reinforcement learning. In ASDE, a historical experience archive with population features is utilized to preserve accumulated historical experience of the combination of mutation strategies and control parameters. Furthermore, the accumulated historical experience can be autonomously mapped into rules repository, and the individuals can choose the combination of mutation strategies and control parameters according to those rules. Additionally, an updating and utilization mechanism of the historical experience is designed to assure that the historical experience can be effectively accumulated and utilized efficiently. Compared with some state-of-the-art intelligence algorithms on 15 functions of CEC2015, 28 functions of CEC2017, and parameter extraction problems of the photovoltaic model, ASDE has the advantages of solution accuracy, convergence speed, and robustness in solving black box problems with unknown features. (shrink)

Schizophrenia has attracted more than its fair share of evolutionary-based theories. The theories involving balancing selection are based on the assumption that the incidence of schizophrenia is invariant across time and place. Modern epidemiology allows us to reject this dogmatic belief. Once variations in the genetic and epidemiological landscape of schizophrenia are acknowledged, more productive research models can be generated. (Published Online November 9 2006).

The selfish goal metaphor is interesting and intriguing. It accounts for the idiosyncrasies and inconsistencies in peoples' goal pursuits without invoking free will, self-regulatory, or self-control failures. However, people pursue multiple goals, sometimes simultaneously. We argue that the model proposed in the target article may gain significant theoretical and practical value if the principles underlying goal selection and/or balancing on a moment-to-moment basis are clearly specified and integrated with the notion of the selfish goal.

This paper aims to propose an improved learning algorithm for feature selection, termed as binary superior tracking artificial bee colony with dynamic Cauchy mutation. To enhance exploitation capacity, a binary learning strategy is proposed to enable each bee to learn from the superior individuals in each dimension. A dynamic Cauchy mutation is introduced to diversify the population distribution. Ten datasets from UCI repository are adopted as test problems, and the average results of cross-validation of BSTABC-DCM are compared (...) with other seven popular swarm intelligence metaheuristics. Experimental results demonstrate that BSTABC-DCM could obtain the optimal classification accuracy and select the best representative features for the UCI problems. (shrink)

Adaptive mutation is defined as a process that, during nonlethal selections, produces mutations that relieve the selective pressure whether or not other, nonselected mutations are also produced. Examples of adaptive mutation or related phenomena have been reported in bacteria and yeast but not yet outside of microorganisms. A decade of research on adaptive mutation has revealed mechanisms that may increase mutation rates under adverse conditions. This article focuses on mechanisms that produce adaptive mutations in one strain (...) of Escherichia coli, FC40. These mechanisms include recombination-induced DNA replication, the placement of genes on a conjugal plasmid, and a transient mutator state. The implications of these various phenomena for adaptive evolution in microorganisms are discussed. BioEssays 22:1067–1074, 2000. © 2000 John Wiley & Sons, Inc. (shrink)

The most benign rationale for sex selection is deemed to be “family balancing.” On this view, provided the sex distribution of an existing offspring group is “unbalanced,” one may legitimately use reproductive technologies to select the sex of the next child. I present four novel concerns with granting “family balancing” as a justification for sex selection: families or family subsets should not be subject to medicalization; sex selection for “family balancing” entrenches heteronormativity, inflicting harm in at least (...) three specific ways; the logic of affirmative action is appropriated; the moral mandate of reproductive autonomy is misused. I conclude that the harms caused by family balancing are sufficiently substantive to override any claim arising from a supposed right to sex selection as an instantiation of procreative autonomy. (shrink)

Adaptive mutation is defined as a process that, during nonlethal selections, produces mutations that relieve the selective pressure whether or not other, nonselected mutations are also produced. Examples of adaptive mutation or related phenomena have been reported in bacteria and yeast but not yet outside of microorganisms. A decade of research on adaptive mutation has revealed mechanisms that may increase mutation rates under adverse conditions. This article focuses on mechanisms that produce adaptive mutations in one strain (...) of Escherichia coli, FC40. These mechanisms include recombination-induced DNA replication, the placement of genes on a conjugal plasmid, and a transient mutator state. The implications of these various phenomena for adaptive evolution in microorganisms are discussed. BioEssays 22:1067–1074, 2000. © 2000 John Wiley & Sons, Inc. (shrink)

A substantial portion of the human genome has been found to consist of simple sequence repeats, including microsatellites and minisatellites. Microsatellites, tandem repeats of 1–6 nucleotides, form the template for dynamic mutations, which involve heritable changes in the lengths of repeat sequences. In recent years, a large number of human disorders have been found to be caused by dynamic mutations, the most common of which are trinucleotide repeat expansion diseases. Dynamic mutations are common to numerous nervous system disorders, including Huntington's (...) disease, various spinocerebellar ataxias, fragile X syndrome, fragile X tremor/ataxia syndrome, Friedreich ataxia and other neurodegenerative disorders. The involvement of dynamic mutations in brain disorders will be reviewed, with a focus on the large group caused by CAG/glutamine repeat expansions. We will also outline a proposed role of tandem repeat polymorphisms (TRPs), with unique ‘digital’ genetic distributions, in modulating brain development and normal function, so as to generate additional mutational diversity upon which natural selection may act. BioEssays 29:525–535, 2007. © 2007 Wiley Periodicals, Inc. (shrink)

The human Y chromosome contains very low levels of nucleotide variation. It has been variously hypothesized that this invariance reflects historic reductions in the human male population, a very recent common ancestry, a slow rate of molecular evolution, an inability to evolve adaptively, or frequent selective sweeps acting on genes borne on the Y chromosome. We propose an alternative theory in which human Y chromosome evolution is driven by mutations in the maternally inherited mitochondrial genome, which impair male fertility and (...) ultimately lead to a reduction in the effective population size (Ne) and consequently the variability of the Y chromosome. BioEssays 24:275–279, 2002. © 2002 Wiley Periodicals, Inc.; DOI 10.1002/bies.10062. (shrink)

Somatic mutations arising in human skin cancers are heterogeneously distributed across the genome, meaning that certain genomic regions (e.g., heterochromatin or transcription factor binding sites) have much higher mutation densities than others. Regional variations in mutation rates are typically not a consequence of selection, as the vast majority of somatic mutations in skin cancers are passenger mutations that do not promote cell growth or transformation. Instead, variations in DNA repair activity, due to chromatin organization and transcription factor (...) binding, have been proposed to be a primary driver of mutational heterogeneity in melanoma. However, as discussed in this review here, recent studies indicate that chromatin organization and transcription factor binding also significantly modulate the rate at which UV lesions form in DNA. The authors propose that local variations in lesion susceptibility may be an important driver of mutational hotspots in melanoma and other skin cancers, particularly at binding sites for ETS transcription factors. (shrink)

A widely accepted tenet of evolutionary biology is that spontaneous mutations occur randomly with regard to their fitness effect. However, since the mutation rate varies along a genome and this variation can be subject to selection, organisms might evolve lower mutation rates at loci where mutations are most deleterious or increased rates where mutations are most needed. In fact, mechanisms of targeted hypermutation are known in organisms ranging from bacteria to humans. Here we review the main forces (...) driving the evolution of local mutation rates and identify the main limiting factors. Both targeted hyper‐ and hypomutation can evolve, although the former is restricted to loci under very frequent positive selection and the latter is severely limited by genetic drift. Nevertheless, we show how an association of repair with transcription or chromatin‐associated proteins could overcome the drift limit and lead to non‐random hypomutation along the genome in most organisms.Editor's suggested further reading in BioEssays Stress‐induced mutation via DNA breaks in Escherichia coli: A molecular mechanism with implications for evolution and medicine Abstract. (shrink)

A major barrier to recombination between bacterial species lies in the mismatch repair system, a complex of proteins that has evolved to proof‐read freshly replicated DNA. It now appears that a second system, involving an inducible DNA recombination, repair and mutagenesis pathway, also regulates interspecies recombination, but in a positive way, being required for recombination between Escherichia coli and Salmonella typhimurium(1). Thus the rate at which newly emerging species of bacteria diverge can be seen as a balance between a (...) permissive state associated with inducible repair and recombination, and the proof‐reading of intermediates in the recombination pathway by the mismatch correction system. (shrink)

If natural selection chose where new mutations occur it might well favour placing them near existing polymorphisms, thereby avoiding disruption of areas that work while adding novelty to regions where variation is tolerated or even beneficial. Such a system could operate if heterozygous sites are recognised and ‘repaired’ during the initial stages of crossing over. Such repairs involve an extra round of DNA replication, providing an opportunity for further mutations, thereby raising the local mutation rate. If so, the (...) changes in heterozygosity that occur when populations grow or shrink could feed back to modulate both the rate and the distribution of mutations. Here, I review evidence from isozymes, microsatellites and single nucleotide polymorphisms that this potential is realised in real populations. I then consider the likely implications, focusing particularly on how these processes might affect microsatellites, concluding that heterozygosity does impact on the rate and distribution of mutations. (shrink)

The mutation-selection hypothesis may extend to understanding normal personality variation. Traits such as emotional stability, agreeableness, and conscientiousness figure strongly in mate selection and show evidence of non-additive genetic variance. They are linked with reproductively relevant outcomes, including longevity, resource acquisition, and mating success. Evolved difference-detection adaptations may function to spurn individuals whose high mutation load signals a burdensome relationship load. (Published Online November 9 2006).

This article deals with the relations in the triangle state–society–business in modern Russia. It is shown against Russian historical background, that the absolutist state in this country could never be identified with the society and these relations were shaped under its strong domination. The ethics of rule-following characteristic for market economy in general did not develop in Russia. The breakdown of communist Russia and market reforms proceeding since 1992 did not change this situation significantly. The period of political alliance between (...) big business and government was followed by restoration of state dominance in somewhat modified forms. Both periods were characterized by corruption, which contrary to Putin’s slogans, increases in Russia. In the article I show the evolution of Putin administration’s policy which changed from emphasizing and improving legal institutions to selective use of legal norms depending on personal loyalty. Main forms of state exploitation of Russian business are described. The conclusion is that Russian experience of balancing state and market should be called negative. (shrink)

Using data obtained during a retrospective interview study of 30 women who had undergone genetic testing—BRCA1/2 mutation searching—this paper describes how women, previously diagnosed with breast/ovarian cancer, perceive their role in generating genetic information about themselves and their families. It observes that when describing their motivations for undergoing DNA testing and their experiences of disclosing genetic information within the family these women provide care based ethical justifications for their actions. Finally, it argues that generating genetic information and disclosing this (...) information to kin raise different types of ethical issues. The implications of these findings for ethical debates about informed choice in the context of genetic testing are discussed. (shrink)

Using data obtained during a retrospective interview study of 30 women who had undergone genetic testing—BRCA1/2 mutation searching—this paper describes how women, previously diagnosed with breast/ovarian cancer, perceive their role in generating genetic information about themselves and their families. It observes that when describing their motivations for undergoing DNA testing and their experiences of disclosing genetic information within the family these women provide care based ethical justifications for their actions. Finally, it argues that generating genetic information and disclosing this (...) information to kin raise different types of ethical issues. The implications of these findings for ethical debates about informed choice in the context of genetic testing are discussed. (shrink)

Natural selection is the populational process whereby, for instance, the relative number of a variant better suited to a given environment’s attributes increases over generations. In other words, a population’s makeup is altered, over generations, to suit the requirements of a particular environment. Niche construction is the process whereby an environment’s attributes can be stably modified by organisms, over generations, to suit requirements of those organisms. Should the latter process, when it occurs, be considered as significant for the complementary (...) fit between organism and environment as the former? According to mainstream evolutionary theory, random genetic mutation is the only source of novel, unlearned, trans-generationally persistent behavior. A growing number of biologists and philosophers of science, however, maintain that organisms are capable of generating such behavior, in response to, for instance, trans-generationally persistent environmental change, by way of phenotype-mediated, developmentally plastic mechanisms that do not require mutation. Should mechanisms of this sort be more generally recognized as the source of the selectable variation that selection operates on? Niche construction theory answers “yes” to both these questions, and the result is a debate over the comprehensiveness of mainstream evolutionary theory. (shrink)

In “Spandrels,” Gould and Lewontin criticized what they took to be an all-too-common conviction, namely, that adaptation to current environments determines organic form. They stressed instead the importance of history. In this paper, we elaborate upon their concerns by appealing to other writings in which those issues are treated in greater detail. Gould and Lewontin’s combined emphasis on history was three-fold. First, evolution by natural selection does not start from scratch, but always refashions preexisting forms. Second, preexisting forms are (...) refashioned by the selection of whatever mutational variations happen to arise: the historical order of mutations needs to be taken into account. Third, the order of environments and selection pressures also needs to be taken into account. (shrink)

The 1940s and 1950s were marked by intense debates over the origin of drug resistance in microbes. Bacteriologists had traditionally invoked the notions of ‘training’ and ‘adaptation’ to account for the ability of microbes to acquire new traits. As the field of bacterial genetics emerged, however, its participants rejected ‘Lamarckian’ views of microbial heredity, and offered statistical evidence that drug resistance resulted from the selection of random resistant mutants. Antibiotic resistance became a key issue among those disputing physiological vs. (...) genetic explanations of variation in bacteria. Postwar developments connected with the Lysenko affair gave this debate a new political valence.Proponents of the neo-Darwinian synthesis weighed in with support for the genetic theory. However, certain features of drug resistance seemed inexplicable by mutation and selection, particularly the phenomenon of ‘multiple resistance’—the emergence of resistance in a single strain against several unrelated antibiotics. In the late 1950s, Tsutomu Watanabe and his collaborators solved this puzzle by determining that resistance could be conferred by cytoplasmic resistance factors rather than chromosomal mutation. These R factors could carry resistance to many antibiotics and seemed able to promote their own dissemination in bacterial populations. In the end, the vindication of the genetic view of drug resistance was accompanied by a recasting of the ‘gene’ to include extrachromosomal hereditary units carried on viruses and plasmids. (shrink)

We study the effects of environmental catastrophes on the evolution of a population of sensory-motor agents with individually evolving mutation rates, and compare these effects in a variety of control systems. A catastrophe makes the balance shift toward the need for evolutionary novelty, and we observe the mutation rate evolve upwards. As the population adapts the sensory-motor strategies to the new environment and the balance shifts toward a need for evolutionary memory, the mutation rate falls. (...) These observations support the hypothesis that second-order evolution of the mutation flexibly balances the need for evolutionary “novelty” and “memory,” both of which are controlled by the mutation rate. (shrink)

Objective: Stand-to-sit task is an important daily function, but there is a lack of research evidence on whether knee osteoarthritis affects the postural balance during the task. This study aimed to compare individuals with knee OA and asymptomatic controls in postural balance and identify kinematic and lower extremity muscle activity characteristics in individuals with knee OA during the stand-to-sit task.Methods: In total, 30 individuals with knee OA and 30 age-matched asymptomatic controls performed the 30-s Chair Stand Test at (...) self-selected speeds. Motion analysis data and surface electromyography were collected while participants performed the 30sCST. To quantify postural balance, the displacement of the center of mass and the peak instantaneous velocity of the CoM were calculated. The kinematic data included forward lean angles of the trunk and pelvic, range of motion of the hip, knee, and ankle joints in the sagittal plane. The averaged activation levels of gluteus maximus, vastus lateralis, vastus medialis, rectus femoris, biceps femoris, tibialis anterior, and medial head of gastrocnemius muscles were indicated by the normalized root mean square amplitudes.Results: Compared with the asymptomatic control group, the knee OA group prolonged the duration of the stand-to-sit task, demonstrated significantly larger CoM displacement and peak instantaneous CoM velocity in the anterior-posterior direction, reduced ankle dorsiflexion RoM, greater anterior pelvic tilt RoM, and lower quadriceps femoris and muscles activation level coupled with higher BF muscle activation level during the stand-to-sit task.Conclusion: This study indicates that individuals with knee OA adopt greater pelvic forward lean RoM and higher BF muscle activation level during the stand-to-sit task. However, these individuals exist greater CoM excursion in the anterior-posterior direction and take more time to complete the task. This daily functional activity should be added to the rehabilitation goals for individuals with knee OA. The knee OA group performs reduced ankle dorsiflexion RoM, quadriceps femoris, and TA activation deficit. In the future, the rehabilitation programs targeting these impairments could be beneficial for restoring the functional transfer in individuals with knee OA. (shrink)

There is growing evidence that mutations can arise in non‐dividing cells (both bacterial and mammalian) in the absence of chromosomal replication. The processes that are involved are still largely unknown but may include two separate mechanisms. In the first, DNA lesions resulting from the action of endogenous mutagens may give rise to RNA transcripts with miscoded bases. If these confer the ability to initiate DNA replication, the DNA lesions may have an opportunity to miscode during replication and thus could give (...) rise to apparently ‘adaptive’ mutations. A second mechanism is suggested by recent work in starved bacteria, showing that there is much more turnover of chromosomal DNA than has been previously thought. This could permit polymerase errors to lead to mutations in non‐dividing cells. Such cryptic DNA synthesis, which may essentially replace existing DNA rather than duplicating it, could, in principle, act as an additional source of variability on which selection may act, initially in the absence of cell division. In mammals such processes would undoubtedly have implications for germ cell mutagenesis and carcinogenesis. (shrink)

We hypothesize that heritable epigenetic changes can affect rates of fitness increase as well as patterns of genotypic and phenotypic change during adaptation. In particular, we suggest that when natural selection acts on pure epigenetic variation in addition to genetic variation, populations adapt faster, and adaptive phenotypes can arise before any genetic changes. This may make it difficult to reconcile the timing of adaptive events detected using conventional population genetics tools based on DNA sequence data with environmental drivers of (...) adaptation, such as changes in climate. Epigenetic modifications are frequently associated with somatic cell differentiation, but recently epigenetic changes have been found that can be transmitted over many generations. Here, we show how the interplay of these heritable epigenetic changes with genetic changes can affect adaptive evolution, and how epigenetic changes affect the signature of selection in the genetic record. (shrink)

De Vries' mutation theory has not stood the test of time. The supposed mutations of Oenothera were in reality complex recombination phenomena, ultimately explicable in Mendelian terms, while instances of large-scale mutations were found wanting in other species. By 1915 the mutation theory had begun to lose its grip on the biological community; by de Vries' death in 1935 it was almost completely abandoned. Yet, as we have seen, during the first decade of the present century it achieved (...) an enormous popularity. As this paper has tried to suggest, one of the principal reasons for this was that de Vries' theory served as a banner around which a whole crowd of disaffected Darwinians or anti-Darwinians could rally. However, not all of those who favored de Vries did so for quite the same reasons. Underlying the multitude of views ran several common threads: a dissatisfaction with current Darwinian theory born out of misunderstanding natural selection, a general misunderstanding of the nature of species, and a prejudice against speculative, nontestable theories in biology.Supporters of de Vries were not the only opponents of Darwinism, nor was the mutation theory the only alternative to natural selection. In the early twentieth century a number of theories had been proposed to explain away the problems which Darwin had left unsolved. There was the idea of orthogenesis, championed by the American paleontologists Cope, Osborn and others; organic selection (or orthoplasy) was championed by M. M. Baldwin and C. Lloyd Morgan; there were the concepts of convergent evolution proposed by Hermann Friedmann, the theory of physiological selection by John George Romanes, and the concepts of reproductive divergence by H. M. Vernon. Virtually none of these men either accepted or were strong supporters of the de Vriesian theory, for each had his own particular ‘ism” to advocate as the major factor in evolution. The existence of a large number of such theories, each purporting to be the explanation, was characteristic of evolutionary theory at the turn of the century. It is to a large extent the emphasis on such fragmentary concepts that retarded development of the comprehensive theory of evolution which emerged in the 1920's and 1930's. For the historian, however, a study of these alternative theories is instructive in trying to understand the inherent difficulties which Dawwinian theory posed to biologists at the time. De Vries' mutation theory serves historically as a mirror to reflect the critical mood of a generation hostile to the theory of natural selection.It has often been claimed that it was impossible to understand the mechanism of natural selection until it could be placed in genetic and mathematical terms. It is certainly true that great strides have been made in population genetics and the treatment of evolutionary concepts with mathematical tools in the last forty years. But the very people who developed the genetical and mathematical approach to evolution were already convinced of the essential correctness of Darwinian theory before they started. Advances in an understanding of Mendelian heredity aided greatly in solving one important issue for evolutionists: the origin of variations. And the rigor with which selection acted could best be studied by observing changes in gene frequencies (calculated mathematically) over a number of generations. But as this paper has shown, two of the basic problems which biologists faced in evaluating Darwinian theory at the turn of the century-the nature of species, and the criteria of what constituted an acceptable explanation in biological science-could not be answered directly by mathematics. What mathematical and genetical theory did do was to help convince the skeptics of the validity of the Darwinian proposition.The change in explanatory criteria which many hailed as de Vries' most important contribution to evolutionary theory seems to have been part of a general emergence of twentieth-century biology from the domination of theorizers in the nineteenth. It also marked the emergence of America from the domination of biological, and particularly evolutionary, influence of Europeans. The change occurred in three areas: in the kinds of questions asked: testable versus non-testable; in the kind of data sought: quantitative versus qualitative; and in the kinds of theories proposed: analytical and reductive—the attempt to see complex processes in terms of simpler components-as opposed to synthetic and speculative. Although ultimately wrong in his idea, de Vries and his theories rode high on the wave of “experimentalism” which was the harbinger of a new era in evolutionary theory. (shrink)

In both biology and the human sciences, social groups are sometimes treated as adaptive units whose organization cannot be reduced to individual interactions. This group-level view is opposed by a more individualistic one that treats social organization as a byproduct of self-interest. According to biologists, group-level adaptations can evolve only by a process of natural selection at the group level. Most biologists rejected group selection as an important evolutionary force during the 1960s and 1970s but a positive literature (...) began to grow during the 1970s and is rapidly expanding today. We review this recent literature and its implications for human evolutionary biology. We show that the rejection of group selection was based on a misplaced emphasis on genes as “replicators” which is in fact irrelevant to the question of whether groups can be like individuals in their functional organization. The fundamental question is whether social groups and other higher-level entities can be “vehicles” of selection. When this elementary fact is recognized, group selection emerges as an important force in nature and what seem to be competing theories, such as kin selection and reciprocity, reappear as special cases of group selection. The result is a unified theory of natural selection that operates on a nested hierarchy of units.The vehicle-based theory makes it clear that group selection is an important force to consider in human evolution. Humans can facultatively span the full range from self-interested individuals to “organs” of group-level “organisms.” Human behavior not only reflects the balance between levels of selection but it can also alter the balance through the construction of social structures that have the effect of reducing fitness differences within groups, concentrating natural selection (and functional organization) at the group level. These social structures and the cognitive abilities that produce them allow group selection to be important even among large groups of unrelated individuals. (shrink)

Despite its widespread existence, the adaptive role of aneuploidy (the abnormal state of having an unequal number of different chromosomes) has been a subject of debate. Cellular aneuploidy has been associated with enhanced resistance to stress, whereas on the organismal level it is detrimental to multicellular species. Certain aneuploid karyotypes are deleterious for specific environments, but karyotype diversity in a population potentiates adaptive evolution. To reconcile these paradoxical observations, this review distinguishes the role of aneuploidy in cellular versus organismal evolution. (...) Further, it proposes a population genetics perspective to examine the behavior of aneuploidy on a populational versus individual level. By altering the copy number of a significant portion of the genome, aneuploidy introduces large phenotypic leaps that enable small cell populations to explore a wide phenotypic landscape, from which adaptive traits can be selected. The production of chromosome number variation can be further increased by stress‐ or mutation‐induced chromosomal instability, fueling rapid cellular adaptation. (shrink)

Although the field of bioethics usually emphasizes ethical dilemmas arising from contemporary biomedical research, at another level the foundation of ethical judgments can be explored in the light of evolutionary biology. Two scientific approaches illuminate the relationships between human nature, social environments, and standards of ethical judgment: first, ethology and the observational study of nonhuman primates; second, evolutionary theory and new developments in the understanding of natural selection. Ethology shows that humans, like the species most closely related to us, (...) are naturally both cooperative and competitive. Evolutionary theory can "explain" cooperation at diverse levels of social organization , suggesting which forms of social cooperation are to be expected in specific cases. By focusing on the emotions underlying the sense of justice, moreover, an evolutionary approach can provide a more realistic assessment of the motivations and intentions underlying ethical controversies. Because individuals inevitably have competing claims as well as competing moral obligations, evolutionary bioethics thus teaches the need for balance and judgment. Emotions elicited by the all-too-human tendency to engage in moralistic aggression need to be balanced by reasoned judgment of the consequences of our own actions. The ethicist, no more or less than any other human, needs to be aware of the risks of deceptions and self-deception. Or, to put it more simply, an evolutionary bioethics leads back to the humility of the Socratic injunction: know thyself. Im allgemein üblichen Sinne befaßt sich Bioethik meist mit ethischen Problemstellungen, die durch die Fortschritte der biologischen Forschung hervorgerufen werden. Unter einem anderen Blickwinkel kann sie aber auch die Grundlage ethischer Urteile im Licht der Entwicklungsbiologie untersuchen. Zwei Wissenschaftszweige befassen sich mit dem Verhältnis zwischen der menschlichen Natur, dem sozialen Umfeld und den Standards für ethische Urteile; erstens, die Ethologie und Verhaltensstudien an nichtmenschlichen Primaten; zweitens, die Evolutionstheorie und neue Entwicklungen beim Verständnis der natürlichen Selektion. Die Ethologie zeigt, daß Menschen genauso wie die Tiere, die ihnen am nächsten verwandt sind, von Natur aus sowohl zur Kooperation als auch zur Konkurrenz miteinander neigen. Die Evolutionstheorie kann die verschiedenen Weisen von Kooperation auf den verschiedenen Ebenen sozialer Organisation "erklären" und dabei Hypothesen aufstellen, welche Formen sozialer Zusammenarbeit in spezifischen Fällen erwartet werden können. Soweit sie sich mit den Emotionen befaßt, die dem Sinn für Gerechtigkeit zugrunde liegen, kann die Evolutionstheorie darüber hinaus eine realistischere Einschätzung der Beweggründe und Intentionen vermitteln, die hinter ethischen Kontroversen stehen. Weil Individuen unvermeidlich konkurrierende Ansprüche, aber auch konkurrierende moralische Verpflichtungen haben, zeigt die evolutionäre Bioethik das Bedürfnis nach Ausgleich und Schlichtung. Die Emotionen, die durch die allzu menschliche Neigung zu Aggression im Namen der Moral hervorgerufen werden, rufen nach Ausgleich durch begründete Urteile über die Folgen unserer eigenen Handlungen. Der Ethiker muß sich, nicht mehr und nicht weniger als jeder andere Mensch, des Risikos von Täuschung und Selbsttäuschung bewußt sein. Oder, um es einfacher auszudrücken, evolutionäre Ethik führt zurück zu der Bescheidenheit der Sokratischen Forderung: Erkenne dich selbst. (shrink)

The evolution of sex in eukaryotes represents a paradox, given the “twofold” fitness cost it incurs. We hypothesize that the mutational dynamics of the mitochondrial genome would have favored the evolution of sexual reproduction. Mitochondrial DNA (mtDNA) exhibits a high‐mutation rate across most eukaryote taxa, and several lines of evidence suggest that this high rate is an ancestral character. This seems inexplicable given that mtDNA‐encoded genes underlie the expression of life's most salient functions, including energy conversion. We propose that (...) negative metabolic effects linked to mitochondrial mutation accumulation would have invoked selection for sexual recombination between divergent host nuclear genomes in early eukaryote lineages. This would provide a mechanism by which recombinant host genotypes could be rapidly shuffled and screened for the presence of compensatory modifiers that offset mtDNA‐induced harm. Under this hypothesis, recombination provides the genetic variation necessary for compensatory nuclear coadaptation to keep pace with mitochondrial mutation accumulation. (shrink)

Recent work on the heat-shock protein Hsp90 by Rutherford and Lindquist (1998) has been included among the pieces of evidence taken to show the essential role of developmental processes in evolution; Hsp90 acts as a buffer against phenotypic variation, allowing genotypic variation to build. When the buffering capacity of Hsp90 is altered (e.g., in nature, by mutation or environmental stress), the genetic variation is "revealed," manifesting itself as phenotypic variation. This phenomenon raises questions about the genetic variation before and (...) after what I will call a "revelation event": Is it neutral, nearly neutral, or non-neutral (i.e., strongly deleterious or strongly advantageous)? Moreover, what kinds of evolutionary processes do we take to be at work? Rutherford and Lindquist (1998) focus on the implications of non-neutral variation and selection. Later work by Queitsch, Sangster, and Lindquist (2002) and Sangster, Lindquist, and Queitsch (2004) raises the possibility that Hsp90 buffering may play the role that was played by drift in Sewall Wright's shifting balance model, permitting transition from one adaptive peak to another. However, Ohta (2002) suggests that much of this variation may be nearly neutral, which in turn, would imply a strong role for drift as well as selection. The primary goal of this paper is to illuminate the alternative scenarios and the processes operating in each. At the end, I raise the possibility of a synthesis between evo-devo and nearly neutral evolution. (shrink)

Capturing a scientific change in thinking about personality and individual differences that has been building over the past 15 years, this volume stands at an important moment in the development of psychology as a discipline. Rather than viewing individual differences as merely the raw material upon which selection operates, the contributing authors provide theories and empirical evidence which suggest that personality and individual differences are central to evolved psychological mechanisms and behavioral functioning. The book draws theoretical inspiration from life (...) history theory, evolutionary genetics, molecular genetics, developmental psychology, personality psychology, and evolutionary psychology, while utilizing the theories of the "best and the brightest" international scientists working on this cutting edge paradigm shift. In the first of three sections, the authors analyze personality and the adaptive landscape; here, the authors offer a novel conceptual framework for examining "personality assessment adaptations." Because individuals in a social environment have momentous consequences for creating and solving adaptive problems, humans have evolved "difference-detecting mechanisms" designed to make crucial social decisions such as mate selection, friend selection, kin investment, coalition formation, and hierarchy negotiation. In the second section, the authors examine developmental and life-history theoretical perspectives to explore the origins and development of personality over the lifespan. The third section focuses on the relatively new field of evolutionary genetics and explores which of the major evolutionary forces--such as balancing selection, mutation, co-evolutionary arms races, and drift--are responsible for the origins of personality and individual differences. Existing as a seminal work in the newly emerging evolutionary psychology field, this book is a "must-read" for anyone invested in the development of psychology as a field. (shrink)