The role of fixed charges present at the surface of biological membranes is usually described by the Gouy-Chapman-Grahame theory of the electric double-layer where the Grahame equation is applied independently on each side of the membrane and where the capacitive charges are disregarded. In this article, we generalize the Gouy-Chapman-Grahame theory by taking into account both intrinsic charges and capacitive charges, in the density value of the membrane surface charges. In the first part, we show that capacitive charges couple electrostatic (...) potentials present on both sides of the membrane. The intensity of this coupling depends both on the value of the membrane specific capacitance and the transmembrane electric potential difference. In the second part, we suggest some physiological implications of membrane electric double-layers. (shrink)

The chapter explains why evolutionary genetics – a mathematical body of theory developed since the 1910s – eventually got to deal with culture: the frequency dynamics of genes like “the lactase gene” in populations cannot be correctly modeled without including social transmission. While the body of theory requires specific justifications, for example meticulous legitimations of describing culture in terms of traits, the body of theory is an immensely valuable scientific instrument, not only for its modeling power but also (...) for the amount of work that has been necessary to build, maintain, and expand it. A brief history of evolutionary genetics is told to demonstrate such patrimony, and to emphasize the importance and accumulation of statistical knowledge therein. The probabilistic nature of genotypes, phenogenotypes and population phenomena is also touched upon. Although evolutionary genetics is actually composed by distinct and partially independent traditions, the most important mathematical object of evolutionary genetics is the Mendelian space, and evolutionary genetics is mostly the daring study of trajectories of alleles in a population that explores that space. The ‘body’ is scientific wealth that can be invested in studying every situation that happens to turn out suitable to be modeled as a Mendelian population, or as a modified Mendelian population, or as a population of continuously varying individuals with an underlying Mendelian basis. Mathematical tinkering and justification are two halves of the mutual adjustment between the body of theory and the new domain of culture. Some works in current literature overstate justification, misrepresenting the relationship between body of theory and domain, and hindering interdisciplinary dialogue. (shrink)

The causal nature of evolution is one of the central topics in the philosophy of biology. The issue concerns whether equations used in evolutionary genetics point to some causal processes or purely phenomenological patterns. To address this question the present article builds well-defined causal models that underlie standard equations in evolutionary genetics. These models are based on minimal and biologically plausible hypotheses about selection and reproduction, and generate statistics to predict evolutionary changes. The causal reconstruction (...) of the evolutionary principles shows adaptive evolution as a genuine causal process, where fitness and selection are both causes of evolution. 1 Introduction2 The Philosophical Puzzle3 Causal Models4 Causal Foundations of Evolutionary Genetics4.1 Univariate quantitative genetics model4.1.1 The causal graph4.1.2 Structural equations4.1.3 Deriving evolutionary transition functions4.2 One-locus population genetics model5 Evolution as a Causal Process5.1 Selection as a causal process5.2 Causes of evolutionary change6 Conclusion. (shrink)

The causal nature of evolution is one of the central topics in the philosophy of biology. The issue concerns whether equations used in evolutionary genetics point to some causal processes or purely phenomenological patterns. To address this question the present article builds well-defined causal models that underlie standard equations in evolutionary genetics. These models are based on minimal and biologically plausible hypotheses about selection and reproduction, and generate statistics to predict evolutionary changes. The causal reconstruction (...) of the evolutionary principles shows adaptive evolution as a genuine causal process, where fitness and selection are both causes of evolution. 1 Introduction2 The Philosophical Puzzle3 Causal Models4 Causal Foundations of Evolutionary Genetics4.1 Univariate quantitative genetics model4.1.1 The causal graph4.1.2 Structural equations4.1.3 Deriving evolutionary transition functions4.2 One-locus population genetics model5 Evolution as a Causal Process5.1 Selection as a causal process5.2 Causes of evolutionary change6 Conclusion. (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).

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)

In 1873, within two years of the publication of The Descent of Man, Friedrich Max Mueller wrote: There is one difficulty which Mr Darwin has not sufficiently appreciated … There is between the whole animal kingdom on the one side, and man, even in his lowest state, on the other, a barrier which no animal has ever crossed, and that barrier is – Language … If anything has a right to the name of specific difference, it is language, as we (...) find it in man, and in man only … If we removed the name of specific difference from our philosophic dictionaries, I should still hold that nothing deserves the name of man except what is able to speak … a speaking elephant or an elephantine speaker could never be called an elephant.' and ‘If a pig were ever to say to me, “I am a pig” it would ipso facto cease to be a pig’. (shrink)

At the interface of developmental biology and evolutionary biology, the very criteria of scientific knowledge are up for grabs. A central issue is the status of evolutionary genetics models, which some argue cannot coherently be used with complex gene regulatory network (GRN) models to explain the same evolutionary phenomena. Despite those claims, many researchers use evolutionary genetics models jointly with GRN models to study evolutionary phenomena. This dissertation compares two recent research projects in (...) which researchers jointly use the two kinds of models. I use methods from the empirical social sciences, such as digital corpus analysis, content analysis, and structured case analysis. I infer three primary conclusions about projects of the kind studied. First, they employ an implicit concept of gene that enables the joint use of both kinds of models. Second, they pursue more epistemic aims besides mechanistic explanation of phenomena. Third, they don’t work to create and export broad synthesized theories. Rather, they focus on phenomena too complex to be understood by a common general theory, they distinguish parts of the phenomena, and they apply models from different theories to the different parts. For such projects, seemingly incompatible models are synthesized largely through mediated representations of complex phenomena. (shrink)

This response (a) integrates non-equilibrium evolutionary genetic models, such as coevolutionary arms-races and recent selective sweeps, into a framework for understanding common, harmful, heritable mental disorders; (b) discusses the forms of ancestral neutrality or balancing selection that may explain some portion of mental disorder risk; and (c) emphasizes that normally functioning psychological adaptations work against a backdrop of mutational and environmental noise. (Published Online November 9 2006).

According to evolutionary, genetic, and endocrinal perspectives, gender differences are modulated by the interaction between intra-uterine stress, genetic equipments, and the availability of the facilitating environment during the newborn period. The social message of fitness over obstacles during socialization and the discussion of secure/non-secure attachment styles should take into consideration the brain functions, which are altered differently in response to intra- and extra-uterine stress in each gender.

I investigate how theoretical assumptions, pertinent to different perspectives and operative during the modeling process, are central in determining how nature is actually taken to be. I explore two different models by Michael Turelli and Steve Frank of the evolution of parasite-mediated cytoplasmic incompatility, guided, respectively, by Fisherian and Wrightian perspectives. Since the two models can be shown to be commensurable both with respect to mathematics and data, I argue that the differences between them in the (1) mathematical presentation of (...) the models, (2) explanations, and (3) objectified ontologies stem neither from differences in mathematical method nor the employed data, but from differences in the theoretical assumptions, especially regarding ontology, already present in the respective perspectives. I use my "set up, mathematically manipulate, explain, and objectify" (SMEO) account of the modeling process to track the model-mediated imposition of theoretical assumptions. I conclude with a discussion of the general implications of my analysis of these models for the controversy between Fisherian and Wrightian perspectives. (shrink)

The analysis of genetic and epigenetic mechanisms of the genotype–phenotypic connection has, so far, only been possible in a handful of genetic model systems. Recent technological advances, including next‐generation sequencing methods such as RNA‐seq, ChIP‐seq and RAD‐seq, and genome‐editing approaches including CRISPR‐Cas, now permit to address these fundamental questions of biology also in organisms that have been studied in their natural habitats. We provide an overview of the benefits and drawbacks of these novel techniques and experimental approaches that can now (...) be applied to ecological and evolutionary vertebrate models such as sticklebacks and cichlid fish. We can anticipate that these new methods will increase the understanding of the genetic and epigenetic factors influencing adaptations and phenotypic variation in ecological settings. These new arrows in the methodological quiver of ecologist will drastically increase the understanding of the genetic basis of adaptive traits – leading to a further closing of the genotype–phenotype gap. -/- . (shrink)

This paper outlines a critique of the use of the genetic variance–covariance matrix (G), one of the central concepts in the modern study of natural selection and evolution. Specifically, I argue that for both conceptual and empirical reasons, studies of G cannot be used to elucidate so-called constraints on natural selection, nor can they be employed to detect or to measure past selection in natural populations – contrary to what assumed by most practicing biologists. I suggest that the search for (...) a general solution to the difficult problem of identifying causal structures given observed correlation’s has led evolutionary quantitative geneticists to substitute statistical modeling for the more difficult, but much more valuable, job of teasing apart the many possible causes underlying the action of natural selection. Hence, the entire evolutionary quantitative genetics research program may be in need of a fundamental reconsideration of its goals and how they correspond to the array of mathematical and experimental techniques normally employed by its practitioners. (shrink)

A common worry about the genetic engineering of human beings is that it will reduce human genetic diversity, creating a biological monoculture that could not only increase our susceptibility to disease but also hasten the extinction of our species. Thus far, however, the evolutionary implications of human genetic modification remain largely unexplored. In this paper, I consider whether the widespread use of genetic engineering technology is likely to narrow the present range of genetic variation, and if so, whether this (...) would in fact lead to the evolutionary harms that some authors envision. By examining the nature of biological variation and its relation to population immunity and evolvability, I show that not only will genetic engineering have a negligible impact on human genetic diversity, but also that it will be more likely to ensure rather than undermine the health and longevity of the human species. (shrink)

The idea of genetic assimilation, that environmentally induced phenotypes may become genetically fixed and no longer require the original environmental stimulus, has had varied success through time in evolutionary biology research. Proposed by Waddington in the 1940s, it became an area of active empirical research mostly thanks to the efforts of its inventor and his collaborators. It was then attacked as of minor importance during the ‘‘hardening’’ of the neo-Darwinian synthesis and was relegated to a secondary role for decades. (...) Recently, several papers have appeared, mostly independently of each other, to explore the likelihood of genetic assimilation as a biological phenomenon and its potential importance to our understanding of evolution. In this article we briefly trace the history of the concept and then discuss theoretical models that have newly employed genetic assimilation in a variety of contexts. We propose a typical scenario of evolution of genetic assimilation via an intermediate stage of phenotypic plasticity and present potential examples of the same. We also discuss a conceptual map of current and future lines of research aimed at exploring the actual relevance of genetic assimilation for evolutionary biology. (shrink)

Uchiyama et al. propose a unified model linking cultural evolutionary theory to behavior genetics (BG) to enhance generalizability, enrich explanation, and predict how social factors shape heritability estimates. A consideration of culture evolution is beneficial but insufficient for purpose. I submit that their proposed model is underdeveloped and their emphasis on heritability estimates misguided. I discuss their ambiguous conception of culture, neglect of social structure, and the lack of a general theory in BG.

What role does non-genetic inheritance play in evolution? In recent work we have independently and collectively argued that the existence and scope of non-genetic inheritance systems, including epigenetic inheritance, niche construction/ecological inheritance, and cultural inheritance—alongside certain other theory revisions—necessitates an extension to the neo-Darwinian Modern Synthesis (MS) in the form of an Extended Evolutionary Synthesis (EES). However, this argument has been challenged on the grounds that non-genetic inheritance systems are exclusively proximate mechanisms that serve the ultimate function of calibrating (...) organisms to stochastic environments. In this paper we defend our claims, pointing out that critics of the EES (1) conflate non-genetic inheritance with early 20th-century notions of soft inheritance; (2) misunderstand the nature of the EES in relation to the MS; (3) confuse individual phenotypic plasticity with trans-generational non-genetic inheritance; (4) fail to address the extensive theoretical and empirical literature which shows that non-genetic inheritance can generate novel targets for selection, create new genetic equilibria that would not exist in the absence of non-genetic inheritance, and generate phenotypic variation that is independent of genetic variation; (5) artificially limit ultimate explanations for traits to gene-based selection, which is unsatisfactory for phenotypic traits that originate and spread via non-genetic inheritance systems; and (6) fail to provide an explanation for biological organization. We conclude by noting ways in which we feel that an overly gene-centric theory of evolution is hindering progress in biology and other sciences. (shrink)

In his book The Biotech Century Jeremy Rifkin makes arguments about the dangers of market-driven genetic biotechnology in medical and agricultural contexts. Believing that Darwinism is too compromised by a competitive ethic to resist capitalist depredations of the genetic commons, and perhaps hoping to pick up anti-Darwinian allies, he turns for support to unorthodox non-Darwinian views of evolution. The Darwinian tradition, more closely examined, contains resources that might better serve his argument. The robust tradition associated with Theodosius Dobzhansky, Ernst Mayr, (...) and others provides an alternative, scientifically sound basis for challenging the rhetoric of genetic reductionism. (shrink)

On the one hand, much has been written on Theodosius Dobzhansky’s central role in the development of the field of population genetics and modern evolutionary theory, as well as on his sociopolitical worldview in the middle of the Twentieth Century. On the other hand, much has also been written on Dobzhansky’s role in the institutionalization of genetics in Brazil, where he spent a considerable amount of time. Unfortunately, these literatures developed without any points of intersection or cross-reference. (...) This article places Dobzhansky’s work in Brazil in the broader contexts of the science and politics of its historical period. (shrink)

While prior models of the evolution of altruism have assumed that organisms reproduce asexually, this paper presents a model of the evolution of altruism for sexually reproducing organisms using Hardy–Weinberg dynamics. In this model, the presence of reciprocal altruists allows the population to evolve to a stable polymorphic population where the majority of organisms are altruistic. Further, adding stochasticity leads to even larger numbers of altruists, while adding stochasticity to an analogous asexual model leads to more selfish organisms. The contrast (...) between these outcomes demonstrates why it may be important to pay attention to the underlying genetics of a population. (shrink)

We formulate the following hypothesis: Life's origin may have occurred during the lower Archaean at a time when the environmental temperature was higher than it is at present. Preliminary consequences of this hypothesis are studied from the point of view of molecular evolution. We restrict our attention to implications regarding the genetic code. We conclude that alternative assignment of termination codons may be understood in terms of: (a) the elevated temperatures to which the progenote may initially have been exposed; and (...) (b) the subsequent response of its genome to the opportunity provided by the eventual loss of hyperthermal genetic expression during a thermal transition (TT) period, which was triggered off by the evolution of the dynamic Earth. (shrink)

In this paper, I propose a populational schema of modeling that consists of: a linear AFSV schema, and a higher-level schema employing the genetic algorithm. The basic ideas of the proposed solution are as follows: whole populations of models are considered at subsequent stages of the modeling process, successive populations are subjected to the activity of genetic operators and undergo selection procedures, the basis for selection is the evaluation function of the genetic algorithm. The schema can be applied to automate (...) the modeling of the mind/brain by means of artificial neural networks: the structure of each network is modified by genetic operators, modified networks undergo a learning cycle, and successive populations of networks are verified during the selection procedure. The whole process can be automated only partially, because it is the researcher who defines the evaluation function of the genetic algorithm. (shrink)