2,491 research outputs found

    Dennis R. Alexander and Ronald L. Numbers : Biology and Ideology: From Descartes to Dawkins

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    Science has always strived for objectivity, for a ‘‘view from nowhere’’ that is not marred by ideology or personal preferences. That is a lofty ideal toward which perhaps it makes sense to strive, but it is hardly the reality. This collection of thirteen essays assembled by Denis R. Alexander and Ronald L. Numbers ought to give much pause to scientists and the public at large, though historians, sociologists and philosophers of science will hardly be surprised by the material covered here

    The Extended (Evolutionary) Synthesis Debate: Where Science Meets Philosophy

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    Recent debates between proponents of the modern evolutionary synthesis (the standard model in evolutionary biology) and those of a possible extended synthesis are a good example of the fascinating tangle among empirical, theoretical, and conceptual or philosophical matters that is the practice of evolutionary biology. In this essay, we briefly discuss two case studies from this debate, highlighting the relevance of philosophical thinking to evolutionary biologists in the hope of spurring further constructive cross-pollination between the two fields

    A benign juvenile environment reduces the strength of antagonistic pleiotropy and genetic variation in the rate of senescence

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    The environment can play an important role in the evolution of senescence because the optimal allocation between somatic maintenance and reproduction depends on external factors influencing life expectancy. The aims of this study were to experimentally test whether environmental conditions during early life can shape senescence schedules, and if so, to examine whether variation among individuals or genotypes with respect to the degree of ageing differs across environments. We tested life-history plasticity and quantified genetic effects on the pattern of senescence across different environments within a reaction norm framework by using an experiment on the three-spined stickleback (Gasterosteus aculeatus, Linnaeus) in which F1 families originating from a wild annual population experienced different temperature regimes. Male sticklebacks that had experienced a more benign environment earlier in life subsequently reduced their investment in carotenoid-based sexual signals early in the breeding season, and consequently senesced at a slower rate later in the season, compared to those that had developed under harsher conditions. This plasticity of ageing was genetically determined. Both antagonistic pleiotropy and genetic variation in the rate of senescence were evident only in the individuals raised in the harsher environment. The experimental demonstration of genotype-by-environment interactions influencing the rate of reproductive senescence provides interesting insights into the role of the environment in the evolution of life histories. The results suggest that benign conditions weaken the scope for senescence to evolve and that the dependence on the environment may maintain genetic variation under selection

    Vindicating science – by bringing it down

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    Science, in the classical view, is the epitome of a rational endeavor, untrammeled by social and cultural influences. It strives to reflect the way the world really is, and is elevated above our petty human lives. Social explanations come into view only when science goes astray – when it stops being science. In recent decades, radical sociologists and other science bashers have tried to wrestle away science from the hands of those upholding the classical view, bringing science down to the level of other human endeavors. Science, they maintain, is social to the bone, and scientific knowledge is nothing but a tissue social constructions. In turn, this radicalism has fueled suspicions among science advocates about any naturalized conception of science: science should be free from the contamination of social influences. Both parties in the dispute, as we argue in this chapter, buy into an intuitive view that characterizes much of our everyday reasoning about the causes of belief: a stark opposition between the rational and the social. Wherever social influences hold sway, reason takes the hindmost. And wherever reason reigns, there is no need for social explanations. This opposition harks back to an even more basic intuition: true and justified beliefs don’t require a causal explanation. They are just self-evident. We grapple for causal explanations (social or otherwise) only when rationality fails. This assumption, handy though it is as a heuristic and first approximation, does not survive careful scrutiny, and needs to be abandoned. A rich causal account of science, including the constitutive role of the social, in no way detracts from its epistemic credentials. Science, after all, is the concerted effort of many human brains. If we want a non-miraculous explanation of science’s successes, we had better be able to account for them in social terms

    Weighing the evidence in evolutionary biology

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    The joke among scientists is that ‘philosopher’ is the last stage of one’s scien- tific career, to be arrived at when one can no longer get grants funded or graduate stu- dents to advise. Despite the fact that some of the greatest minds in evolutionary biology (from Darwin to Ernst Mayr) were very much interested in the philosophical aspects of what they were doing, the bad joke persists in the halls of academia

    Plasticity to wind is modular and genetically variable in Arabidopsis thaliana

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    Thigmomorphogenesis, the characteristic phenotypic changes by which plants react to mechanical stress, is a widespread and probably adaptive type of phenotypic plasticity. However, little is known about its genetic basis and population variation. Here, we examine genetic variation for thigmomorphogenesis within and among natural populations of the model system Arabidopsis thaliana. Offspring from 17 field-collected European populations was subjected to three levels of mechanical stress exerted by wind. Overall, plants were remarkably tolerant to mechanical stress. Even high wind speed did not significantly alter the correlation structure among phenotypic traits. However, wind significantly affected plant growth and phenology, and there was genetic variation for some aspects of plasticity to wind among A. thaliana populations. Our most interesting finding was that phenotypic traits were organized into three distinct and to a large degree statistically independent covariance modules associated with plant size, phenology, and growth form, respectively. These phenotypic modules differed in their responsiveness to wind, in the degree of genetic variability for plasticity, and in the extent to which plasticity affected fitness. It is likely, therefore, that thigmomorphogenesis in this species evolves quasi-independently in different phenotypic module

    Experimental alteration of DNA methylation affects the phenotypic plasticity of ecologically relevant traits in Arabidopsis thaliana

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    Heritable phenotypic variation in plants can be caused not only by underlying genetic differences, but also by variation in epigenetic modifications such as DNA methylation. However, we still know very little about how relevant such epigenetic variation is to the ecology and evolution of natural populations. We conducted a greenhouse experiment in which we treated a set of natural genotypes of Arabidopsis thaliana with the demethylating agent 5-azacytidine and examined the consequences of this treatment for plant traits and their phenotypic plasticity. Experimental demethylation strongly reduced the growth and fitness of plants and delayed their flowering, but the degree of this response varied significantly among genotypes. Differences in genotypes' responses to demethylation were only weakly related to their genetic relatedness, which is consistent with the idea that natural epigenetic variation is independent of genetic variation. Demethylation also altered patterns of phenotypic plasticity, as well as the amount of phenotypic variation observed among plant individuals and genotype means. We have demonstrated that epigenetic variation can have a dramatic impact on ecologically important plant traits and their variability, as well as on the fitness of plants and their ecological interactions. Epigenetic variation may thus be an overlooked factor in the evolutionary ecology of plant population

    Natural selection. II. Developmental variability and evolutionary rate

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    In classical evolutionary theory, genetic variation provides the source of heritable phenotypic variation on which natural selection acts. Against this classical view, several theories have emphasized that developmental variability and learning enhance nonheritable phenotypic variation, which in turn can accelerate evolutionary response. In this paper, I show how developmental variability alters evolutionary dynamics by smoothing the landscape that relates genotype to fitness. In a fitness landscape with multiple peaks and valleys, developmental variability can smooth the landscape to provide a directly increasing path of fitness to the highest peak. Developmental variability also allows initial survival of a genotype in response to novel or extreme environmental challenge, providing an opportunity for subsequent adaptation. This initial survival advantage arises from the way in which developmental variability smooths and broadens the fitness landscape. Ultimately, the synergism between developmental processes and genetic variation sets evolutionary rate

    Phenotypic robustness can increase phenotypic variability after non-genetic perturbations in gene regulatory circuits

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    Non-genetic perturbations, such as environmental change or developmental noise, can induce novel phenotypes. If an induced phenotype confers a fitness advantage, selection may promote its genetic stabilization. Non-genetic perturbations can thus initiate evolutionary innovation. Genetic variation that is not usually phenotypically visible may play an important role in this process. Populations under stabilizing selection on a phenotype that is robust to mutations can accumulate such variation. After non-genetic perturbations, this variation can become a source of new phenotypes. We here study the relationship between a phenotype's robustness to mutations and a population's potential to generate novel phenotypic variation. To this end, we use a well-studied model of transcriptional regulation circuits. Such circuits are important in many evolutionary innovations. We find that phenotypic robustness promotes phenotypic variability in response to non-genetic perturbations, but not in response to mutation. Our work suggests that non-genetic perturbations may initiate innovation more frequently in mutationally robust gene expression traits.Comment: 11 pages, 5 figure

    The emerging structure of the Extended Evolutionary Synthesis: where does Evo-Devo fit in?

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    The Extended Evolutionary Synthesis (EES) debate is gaining ground in contemporary evolutionary biology. In parallel, a number of philosophical standpoints have emerged in an attempt to clarify what exactly is represented by the EES. For Massimo Pigliucci, we are in the wake of the newest instantiation of a persisting Kuhnian paradigm; in contrast, Telmo Pievani has contended that the transition to an EES could be best represented as a progressive reformation of a prior Lakatosian scientific research program, with the extension of its Neo-Darwinian core and the addition of a brand-new protective belt of assumptions and auxiliary hypotheses. Here, we argue that those philosophical vantage points are not the only ways to interpret what current proposals to ‘extend’ the Modern Synthesis-derived ‘standard evolutionary theory’ (SET) entail in terms of theoretical change in evolutionary biology. We specifically propose the image of the emergent EES as a vast network of models and interweaved representations that, instantiated in diverse practices, are connected and related in multiple ways. Under that assumption, the EES could be articulated around a paraconsistent network of evolutionary theories (including some elements of the SET), as well as models, practices and representation systems of contemporary evolutionary biology, with edges and nodes that change their position and centrality as a consequence of the co-construction and stabilization of facts and historical discussions revolving around the epistemic goals of this area of the life sciences. We then critically examine the purported structure of the EES—published by Laland and collaborators in 2015—in light of our own network-based proposal. Finally, we consider which epistemic units of Evo-Devo are present or still missing from the EES, in preparation for further analyses of the topic of explanatory integration in this conceptual framework
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