We reconstruct genetic determinism as a reductionist thesis to the effect that the molecular properties of cells can be accounted for to a great extent by their genetic outfit. The non-reductionist arguments offered at this molecular level often use the relationship between structure and function as their point of departure. By contrast, we develop a non-reductionist argument that is confined to the structural characteristics of biomolecules; no appeal to functions is made. We raise two kinds of objections against the reducibility (...) claim underlying genetic determinism. First, some conceptual distinctions at the protein level cannot be captured on a genetic basis. A one-to-many relationship between DNA sequences and proteins emerges from them. Second, the relationship between genes and proteins is characterized by explanatory loops or reciprocal explanatory dependence. The presence of proteins is explained by the transcription from corresponding DNA sequences, and the latter is in turn accounted for by the action of proteins. By contrast, a reductive account requires a unidirectional explanatory dependence. (shrink)

Whereas an inference (deductive as well as inductive) is usually viewed as being valid in virtue of its argument form, the present paper argues that scientific reasoning is material inference, i.e., justified in virtue of its content. A material inference is licensed by the empirical content embodied in the concepts contained in the premises and conclusion. Understanding scientific reasoning as material inference has the advantage of combining different aspects of scientific reasoning, such as confirmation, discovery, and explanation. This approach explains (...) why these different aspects (including discovery) can be rational without conforming to formal schemes, and why scientific reasoning is local, i.e., justified only in certain domains and contingent on particular empirical facts. The notion of material inference also fruitfully interacts with accounts of conceptual change and psychological theories of concepts. (shrink)

This essay analyzes and develops recent views about explanation in biology. Philosophers of biology have parted with the received deductive-nomological model of scientific explanation primarily by attempting to capture actual biological theorizing and practice. This includes an endorsement of different kinds of explanation (e.g., mathematical and causal-mechanistic), a joint study of discovery and explanation, and an abandonment of models of theory reduction in favor of accounts of explanatory reduction. Of particular current interest are philosophical accounts of complex explanations that appeal (...) to different levels of organismal organization and use contributions from different biological disciplines. The essay lays out one model that views explanatory integration across different disciplines as being structured by scientific problems. I emphasize the philosophical need to take the explanatory aims pursued by different groups of scientists into account, as explanatory aims determine whether different explanations are competing or complementary and govern the dynamics of scientific practice, including interdisciplinary research. I distinguish different kinds of pluralism that philosophers have endorsed in the context of explanation in biology, and draw several implications for science education, especially the need to teach science as an interdisciplinary and dynamic practice guided by scientific problems and explanatory aims. (shrink)

Heritability is routinely interpreted causally. Yet, what such an interpretation amounts to is often unclear. Here, I provide a causal interpretation of this concept in terms of range of causal influence, one of several causal dimensions proposed within the interventionist account of causation. An information-theoretic measure of range of causal influence has recently been put forward in the literature. Starting from this formalization and relying upon Woodward’s analysis, I show that an important problem associated with interpreting heritability causally, namely the (...) locality problem, amounts, at least partly, to a low invariance and low stability between the genotype/environment and the phenotype of individuals. In light of this, I plead for a causal interpretation of heritability that takes the notions of Woodward’s invariance and stability into consideration. In doing so, I defuse naive causal interpretations of heritability. (shrink)

Okasha, in Evolution and the Levels of Selection, convincingly argues that two rival statistical decompositions of covariance, namely contextual analysis and the neighbour approach, are better causal decompositions than the hierarchical Price approach. However, he claims that this result cannot be generalized in the special case of soft selection and argues that the Price approach represents in this case a better option. He provides several arguments to substantiate this claim. In this paper, I demonstrate that these arguments are flawed and (...) argue that neither the Price equation nor the contextual and neighbour partitionings sensu Okasha are adequate causal decompositions in cases of soft selection. The Price partitioning is generally unable to detect cross-level by-products and this naturally also applies to soft selection. Both contextual and neighbour partitionings violate the fundamental principle of determinism that the same cause always produces the same effect. I argue that a fourth partitioning widely used in the contemporary social sciences, under the generic term of ‘hierarchical linear model’ and related to contextual analysis understood broadly, addresses the shortcomings of the three other partitionings and thus represents a better causal decomposition. I then defend this model against the argument that because it predicts that there is some organismal selection in some specific cases of segregation distortion then it should be rejected. I show that cases of segregation distortion that intuitively seem to contradict the conclusion drawn from the hierarchical linear model are in fact cases of multilevel selection 2 while the assessment of the different partitionings are restricted to multilevel selection 1. (shrink)

Mechanistic models in molecular systems biology are generally mathematical models of the action of networks of biochemical reactions, involving metabolism, signal transduction, and/or gene expression. They can be either simulated numerically or analyzed analytically. Systems biology integrates quantitative molecular data acquisition with mathematical models to design new experiments, discriminate between alternative mechanisms and explain the molecular basis of cellular properties. At the heart of this approach are mechanistic models of molecular networks. We focus on the articulation and development of mechanistic (...) models, identifying five constraints which guide the articulation of models in molecular systems biology. These constraints are not independent of one another, with the result that modeling becomes an iterative process. We illustrate the use of these constraints in the modeling of the mechanism for bistability in the lac operon. (shrink)

In the fall of 2018 Jiankui He shocked the international community with the following announcement: two female babies, “Lulu” and “Nana,” whose germlines had been modified by the cutting edge, yet profoundly unsafe CRISPR-Cas9 technology had been born. This event galvanized policy makers and scientists to advocate for more explicit and firm regulation of human germline gene editing. Recent policy proposals attempt to integrate safety considerations and public input to identify specific types of diseases that may be safe targets for (...) human GGE. This paper argues these policy proposals are inadequate in different ways. While Sarkar intends to incorporate input from the disability community for the purpose of deciding the value of human GGE, I argue that his strategy for doing so is inadequate. I’ll argue that an iterative, deliberative process is a more appropriate framework for allowing the disability community to inform policy on human GGE. Further policy proposals have been framed in terms of monogenetic or single-gene diseases. I argue that this way of conceptualizing disease is not what matters for deciding which disorders are viable candidates for human GGE. Instead, what matters is that the disease in question must have genes that have a high degree of causal control with respect to the disease and alternative nucleic acid sequences variants that are likely to produce traits deemed desirable must be identified. Previous policy proposals leave unspecified. What conditions must be met for satisfying condition should not be left to individual scientists to decide for themselves. The present proposal offers some guidance on this issue. (shrink)

In this article, we use the theory of Information Ethics to argue that deceased people have a prima facie moral right to privacy in the context of health data research, and that this should be reflected in regulation and guidelines. After death, people are no longer biological subjects but continue to exist as informational entities which can still be harmed/damaged. We find that while the instrumental value of recognising post-mortem privacy lies in the preservation of the social contract for health (...) research, its intrinsic value is grounded in respect for the dignity of the post-mortem informational entity. However, existing guidance on post-mortem data protection is available only in the context of genetic studies. In comparing the characteristics of genetic data and other health-related data, we identify two features of DNA often given as arguments for this genetic exceptionalism: relationality and embodiment. We use these concepts to show that at the appropriate Level of Abstraction, there is no morally relevant distinction between posthumous genetic and other health data. Thus, genetic data should not automatically receive special moral status after death. Instead we make a plea for ‘contextual exceptionalism’. Our analysis concludes by reflecting on a real-world case and providing suggestions for contextual factors that researchers and oversight bodies should take into account when designing and evaluating research projects with health data from deceased subjects. (shrink)

Fisher’s ‘fundamental theorem of natural selection’ is notoriously abstract, and, no less notoriously, many take it to be false. In this paper, I explicate the theorem, examine the role that it played in Fisher’s general project for biology, and analyze why it was so very fundamental for Fisher. I defend Ewens (1989) and Lessard (1997) in the view that the theorem is in fact a true theorem if, as Fisher claimed, ‘the terms employed’ are ‘used strictly as defined’ (1930, p. (...) 38). Finally, I explain the role that projects such as Fisher’s play in the progress of scientific inquiry. (shrink)

This paper addresses the topic of determinism in contemporary microbiome research. I distinguish two types of deterministic claims about the microbiome, and I show evidence that both types of claims are present in the contemporary literature. First, the idea that the host genetics determines the composition of the microbiome which I call “host-microbiome determinism”. Second, the idea that the genetics of the holobiont (the individual unit composed by a host plus its microbiome) determines the expression of certain phenotypic traits, which (...) I call “microbiome-phenotype determinism”. Drawing on the stability of traits conception of individuality (Suárez in Hist Philos Life Sci 42:11, 2020) I argue that none of these deterministic hypotheses is grounded on our current knowledge of how the holobiont is transgenerationally assembled, nor how it expresses its phenotypic traits. (shrink)

These preprints were automatically compiled into a PDF from the collection of papers deposited in PhilSci-Archive in conjunction with the PSA 2018.

We reconsider the Nagelian theory of reduction and argue that, contrary to a widely held view, it is the right analysis of intertheoretic reduction. The alleged difficulties of the theory either vanish upon closer inspection or turn out to be substantive philosophical questions rather than knock-down arguments.

Reduction and reductionism have been central philosophical topics in analytic philosophy of science for more than six decades. Together they encompass a diversity of issues from metaphysics and epistemology. This article provides an introduction to the topic that illuminates how contemporary epistemological discussions took their shape historically and limns the contours of concrete cases of reduction in specific natural sciences. The unity of science and the impulse to accomplish compositional reduction in accord with a layer-cake vision of the sciences, the (...) seminal contributions of Ernest Nagel on theory reduction and how they strongly conditioned subsequent philosophical discussions, and the detailed issues pertaining to different accounts of reduction that arise in both physical and biological science (e.g., limit-case and part-whole reduction in physics, the difference-making principle in genetics, and mechanisms in molecular biology) are explored. The conclusion argues that the epistemological heterogeneity and patchwork organization of the natural sciences encourages a pluralist stance about reduction. (shrink)

Schaffner’s model of theory reduction has played an important role in philosophy of science and philosophy of biology. Here, the model is found to be problematic because of an internal tension. Indeed, standard antireductionist external criticisms concerning reduction functions and laws in biology do not provide a full picture of the limits of Schaffner’s model. However, despite the internal tension, his model usefully highlights the importance of regulative ideals associated with the search for derivational, and embedding, deductive relations among mathematical (...) structures in theoretical biology. A reconstructed Schaffnerian model could therefore shed light on mathematical theory development in the biological sciences and on the epistemology of mathematical practices more generally. *Received November 2006; revised March 2009. †To contact the author, please write to: Philosophy Department, University of California, Santa Cruz, 1156 High St., Santa Cruz, CA 95064; e‐mail: [email protected]. (shrink)

Selectionist evolutionary theory has often been faulted for not making novel predictions that are surprising, risky, and correct. I argue that it in fact exhibits the theoretical virtue of predictive capacity in addition to two other virtues: explanatory unification and model fitting. Two case studies show the predictive capacity of selectionist evolutionary theory: parallel evolutionary change in E. coli, and the origin of eukaryotic cells through endosymbiosis.

Methodological reductionists practice ‘wannabe reductionism’. They claim that one should pursue reductionism, but never propose how. I integrate two strains in prior work to do so. Three kinds of activities are pursued as “reductionist”. “Successional reduction” and inter-level mechanistic explanation are legitimate and powerful strategies. Eliminativism is generally ill-conceived. Specific problem-solving heuristics for constructing inter-level mechanistic explanations show why and when they can provide powerful and fruitful tools and insights, but sometimes lead to erroneous results. I show how traditional metaphysical (...) approaches fail to engage how science is done. The methods used do so, and support a pragmatic and non-eliminativist realism. (shrink)

Richard Levins’ distinction between aggregate, composed and evolved systems acquires new significance as we recognize the importance of mechanistic explanation. Criteria for aggregativity provide limiting cases for absence of organization, so through their failure, can provide rich detectors for organizational properties. I explore the use of failures of aggregativity for the analysis of mechanistic systems in diverse contexts. Aggregativity appears theoretically desireable, but we are easily fooled. It may be exaggerated through approximation, conditions of derivation, and extrapolating from some conditions (...) of decomposition illegtimately to others. Evolved systems particularly may require analyses under alternative complementary decompositions. Exploring these conditions helps us to better understand the strengths and limits of reductionistic methods. (shrink)

In this paper, I wish to challenge theory-biased approaches to scientific knowledge, by arguing for a study of theorizing, as a cognitive activity, rather than of theories, as abstract structures independent from the agents’ understanding of them. Such a study implies taking into account scientists’ reasoning processes, and their representational practices. Here, I analyze the representational practices of geneticists in the 1910s, as a means of shedding light on the content of classical genetics. Most philosophical accounts of classical genetics fail (...) to distinguish between the purely genetic, or Mendelian level, and the cytological one. I distinguish between them by characterizing them in terms of their respective associated representational practices. I then present how the two levels were articulated within Morgan’s theory of crossing-over, and I describe the representational technique of linkage mapping, which embodies the “merging” of the Mendelian and cytological levels. I propose an analysis of the mapping scheme, as a means of enlightening the conceptual articulation of Mendelian and cytological hypotheses within classical genetics. Finally, I present the respective views of three opponents to Morgan in the 1910s, who had a different understanding of the articulation of cytology and Mendelism, and entertained different views concerning the role and proper interpretation of maps. I propose to consider these diverging perspectives as instantiating what I call different “versions” of classical genetics. (shrink)

The presence of gene–environment statistical interaction and correlation in biological development has led both practitioners and philosophers of science to question the legitimacy of heritability estimates. The paper offers a novel approach to assess the impact of GxE and rGE on the way genetic and environmental causation can be partitioned. A probabilistic framework is developed, based on a quantitative genetic model that incorporates GxE and rGE, offering a rigorous way of interpreting heritability estimates. Specifically, given an estimate of heritability and (...) the variance components associated with estimates of GxE and rGE, I arrive at a probabilistic account of the relative effect of genes and environment. (shrink)

Can a heritability value tell us something about the weight of genetic versus environmental causes that have acted in the development of a particular individual? Two possible questions arise. Q1: what portion of the phenotype of X is due to its genes and what portion to its environment? Q2: what portion of X’s phenotypic deviation from the mean is a result of its genetic deviation and what portion a result of its environmental deviation? An answer to Q1 provides the full (...) information about X’s development, while an answer to Q2 leaves out a large portion unexplained—that portion which corresponds to the phenotypic mean. Q1 is unanswerable, but I show it is nevertheless legitimate under certain quantitative genetics models. With regard to Q2, opinions in the philosophical and biological literature differ as to its legitimacy. I argue that not only is it legitimate, but in particular, under a few simplifying assumptions, it allows for a quantitative probabilistic answer: for normally distributed quantitative traits with no G-E correlation or statistical G × E interaction, we can assess the probability that X’s genes had a greater effect than its environment on its deviation from the mean population value. This probability is expressed as a function the heritability and the individual’s phenotypic value; we can also provide a quantitative probabilistic answer to Q2 for an arbitrary individual where the probability is a function only of heritability. (shrink)

This essay examines the origin of genotype-environment interaction, or G×E. "Origin" and not "the origin" because the thesis is that there were actually two distinct concepts of G×E at this beginning: a biometric concept, or \[G \times E_B\], and a developmental concept, or \[G \times E_D \]. R. A. Fisher, one of the founders of population genetics and the creator of the statistical analysis of variance, introduced the biometric concept as he attempted to resolve one of the main problems in (...) the biometric tradition of biology - partitioning the relative contributions of nature and nurture responsible for variation in a population. Lancelot Hogben, an experimental embryologist and also a statistician, introduced the developmental concept as he attempted to resolve one of the main problems in the developmental tradition of biology - determining the role that developmental relationships between genotype and environment played in the generation of variation. To argue for this thesis, I outline Fisher and Hogben's separate routes to their respective concepts of G × E; then these separate interpretations of G × E are drawn on to explicate a debate between Fisher and Hogben over the importance of G × E, the first installment of a persistent controversy. Finally, Fisher's \[G \times E_B\] and Hogben's \[G \times E_D \] are traced beyond their own work into mid-2Oth century population and developmental genetics, and then into the infamous IQ Controversy of the 1970s. (shrink)

Philosophers of science have developed an account of causal-mechanical explanation that captures regularity, but this account neglects variation. In this article I amend the philosophy of mechanisms to capture variation. The task is to explicate the relationship between regular causal mechanisms responsible for individual development and causes of variation responsible for variation in populations. As it turns out, disputes over this relationship have rested at the heart of the nature–nurture debate. Thus, an explication of the relationship between regular causal mechanisms (...) and causes of variation and between individual development and variation offers both the necessary amendment to the philosophy of mechanisms and the resources to mediate the dispute. (shrink)

Pluralism is often put forth as a counter-position to reductionism. In this essay, I argue that reductionism and pluralism are in fact consistent. I propose that there are several potential goals for reductions and that the proper form of a reduction should be considered in tandem with the goal that it aims to achieve. This insight provides a basis for clarifying what version of reductionism are currently defended, for explicating the notion of a fundamental level of explanation, and for showing (...) how one can be both a reductionist and a pluralist. (shrink)

Research in pharmacogenomics and precision medicine has recently introduced the concept of Polygenic Scores (PGSs), namely, indexes that aggregate the effects that many genetic variants are predicted to have on individual disease risk. The popularity of PGSs is increasing rapidly, but surprisingly little attention has been paid to the idealisations they make about phenotypic development. Indeed, PGSs rely on quantitative genetics models and methods, which involve considerable theoretical assumptions that have been questioned on various grounds. This comes with epistemological and (...) ethical concerns about the use of PGSs in clinical decision-making. In this paper, I investigate to what extent idealisations in genetics models can impact the data gathering and clinical interpretation of genomics findings, particularly the calculation and predictive accuracy of PGSs. Although idealisations are considered ineliminable components of scientific models, they may be legitimate or not depending on the epistemic aims of a model. I thus analyse how various idealisations have been introduced in classical models and progressively readapted throughout the history of genetic theorising. Notably, this process involved important changes in the epistemic purpose of such idealisations, which raises the question of whether they are legitimate in the context of contemporary genomics. (shrink)

This paper discusses the individuation of characters for the use asunits by geneticists at the beginning of the 20th century. Thediscussion involves the Presence and Absence Hypothesis as a case study. It issuggested that the gap between conceptual consideration and etiological factorsof individuating of characters is being handled by way of mutual adjustment.Confrontation of a suggested morphological unit character with experimentresults molded the final boundaries of it.

This article is a systematic critical survey of work done in the philosophy of biology within the logical empiricist tradition, beginning in the 1930s and until the end of the 1950s. It challenges a popular view that the logical empiricists either ignored biology altogether or produced analyses of little value. The earliest work on the philosophy of biology within the logical empiricist corpus was that of Philipp Frank, Ludwig von Bertalanffy, and Felix Mainx. Mainx, in particular, provided a detailed analysis (...) of biology in the 1930s and 1940s in his contribution to the logical empiricists’ Encyclopedia of Unified Science. However, the most important contributions to the philosophy of biology were those of Joseph Henry Woodger and Ernest Nagel. Woodger is primarily remembered for deploying the axiomatic method in biology but he also used semiformal methods for the analysis of many biological problems. While Woodger’s axiomatic work was often derided by some later philosophers of biology (e.g., David Hull and Michael Ruse), this article defends both the biological and the philosophical significance of some of that work, for instance, those aspects that led to the recognition of the conceptual complexity of mereology and temporal identity in biological systems. Woodger’s semiformal analyses were even more important, for instance, his explication of the concepts of the Bauplan and of innateness. Nagel’s importance lies in his analyses of reduction and emergence in the context of all empirical sciences and his use of these analyses in a careful exploration of biological problems. While Nagel’s model of reduction was generally rejected by philosophers of science in the 1970s and 1980s, particularly for biological contexts, it has recently been sympathetically reconstructed by many commentators; this article defends its continued relevance for the philosophy of biology. (shrink)

Since the late 1990s, the characterization of complete DNA sequences for a large and taxonomically diverse set of species has continued to gain in speed and accuracy. Sequence analyses have indicated a strikingly baroque structure for most eukaryotic genomes, with multiple repeats of DNA sequences and with very little of the DNA specifying proteins. Much of the DNA in these genomes has no known function. These results have generated strong interest in the factors that govern the evolution of genome architecture. (...) While adaptationist ‘just so’ stories have been offered, recent theoretical analyses based on mathematical population genetics strongly suggest that non-adaptive processes dominate genome architecture evolution. This article critically synthesizes and develops these arguments, explicating a core argument along with several variants. It provides a critical assessment of the evidence that supports these arguments’ premises. It also analyses adaptationist responses to these arguments and notes potential problems with the core argument. These theoretical analyses continue the molecular reinterpretation of evolution initiated by the neutral theory in 1968. The article ends by noting that some of these arguments can also be extended to evolution at higher levels of organization which raises questions about adaptationism in general. This remains a puzzle because there is probably little reason to doubt that many organismic features are genuine adaptations. 1 Introduction2 Preliminaries: Senses of Adaptationism3 Genome Architecture3.1 Surprises of early eukaryotic genetics3.2 Genome structure, post-20014 The Case against Adaptationism4.1 Just so stories versus population genetics4.2 The core argument4.3 Three variants of the core argument4.4 Examples: Non-adaptive features of the genome5 Adaptationist Responses6 Concluding Remarks. (shrink)

This paper analyzes the development of evolutionary theory in the period from 1918 to 1932. It argues that: (i) Fisher's work in 1918 constituted a not fully satisfactory reduction of biometry to Mendelism; (ii) there was a synthesis in the 1920s but that this synthesis was mainly one of classical genetics with population genetics, with Haldane's The Causes of Evolution being its founding document; (iii) the most important achievement of the models of theoretical population genetics was to show that natural (...) selection sufficed as a mechanism for evolution; and (iv) Haldane formulated a prospective evolutionary theory in the 1920s whereas Fisher and Wright formulated retrospective theories of evolutionary history. (shrink)

This paper analyzes the concept of biodiversity in conservation biology and assesses potential methods for its measurement.

On the basis of distinctions between those properties of entities that can be defined without reference to other entities and those that (in different ways) cannot, this note argues that non-trivial forms of frequency-dependent selection of entities should be interpreted as selection occurring at a level higher than that of those entities. It points out that, except in degenerately simple cases, evolutionary game-theoretic models of selection are not models of individual selection. Similarly, models of genotypic selection such as heterosis cannot (...) be legitimately interpreted as models of genic selection. The analysis presented here supports the views that: (i) selection should be viewed as a multi-level process; (ii) upper-level selection is ubiquitous; (iii) kin selection should be viewed as a type of group selection rather than individual selection; and (iv) inclusive fitness is not an individual property. (shrink)

This is a critical notice of Evolution's Eye by Susan Oyama, focusing on developmental systems theory primarily in relation to the nature-nurture debates and the explanation of behaviour.

The goal of forming a science of intentional behavior requires a more richly detailed account of symbolic systems than is assumed by the authors. Cultural systems are not simply the equivalent in the ideational domain of culture of the purported Baldwin Effect in the genetic domain. © 2014 Cambridge University Press.

Griffiths and Stotz’s Genetics and Philosophy: An Introduction offers a very good overview of scientific and philosophical issues raised by present-day genetics. Examining, in particular, the questions of how a “gene” should be defined and what a gene does from a causal point of view, the authors explore the different domains of the life sciences in which genetics has come to play a decisive role, from Mendelian genetics to molecular genetics, behavioural genetics, and evolution. In this review, I highlight what (...) I consider as the two main theses of the book, namely: genes are better conceived as tools; genes become causes only in a context. I situate these two theses in the wider perspective of developmental systems theory. This leads me to emphasize that Griffiths and Stotz reflect very well an on going process in genetics, which I call the “epigenetization” of genetics, i.e., the growing interest in the complex processes by which gene activation is regulated. I then make a factual objection, which is that Griffiths and Stotz have almost entirely neglected the perspective of ecological developmental biology, and more precisely recent work on developmental symbioses, and I suggest that this omission is unfortunate in so far as an examination of developmental symbioses would have considerably strengthened Griffiths and Stotz’s own conclusions. (shrink)

Fisher’s ‘fundamental theorem of natural selection’ is notoriously abstract, and, no less notoriously, many take it to be false. In this paper, I explicate the theorem, examine the role that it played in Fisher’s general project for biology, and analyze why it was so very fundamental for Fisher. I defend Ewens and Lessard in the view that the theorem is in fact a true theorem if, as Fisher claimed, ‘the terms employed’ are ‘used strictly as defined’. Finally, I explain the (...) role that projects such as Fisher’s play in the progress of scientific inquiry. (shrink)

There have been two different schools of thought on the evolution of dominance. On the one hand, followers of Wright [Wright S. 1929. Am. Nat. 63: 274–279, Evolution: Selected Papers by Sewall Wright, University of Chicago Press, Chicago; 1934. Am. Nat. 68: 25–53, Evolution: Selected Papers by Sewall Wright, University of Chicago Press, Chicago; Haldane J.B.S. 1930. Am. Nat. 64: 87–90; 1939. J. Genet. 37: 365–374; Kacser H. and Burns J.A. 1981. Genetics 97: 639–666] have defended the view that dominance (...) is a product of non-linearities in gene expression. On the other hand, followers of Fisher [Fisher R.A. 1928a. Am. Nat. 62: 15–126; 1928b. Am. Nat. 62: 571–574; Bürger R. 1983a. Math. Biosci. 67: 125–143; 1983b. J. Math. Biol. 16: 269–280; Wagner G. and Burger R. 1985. J. Theor. Biol. 113: 475–500; Mayo O. and Reinhard B. 1997. Biol. Rev. 72: 97–110] have argued that dominance evolved via selection on modifier genes. Some have called these “physiological” versus “selectionist,” or more recently [Falk R. 2001. Biol. Philos. 16: 285–323], “functional,” versus “structural” explanations of dominance. This paper argues, however, that one need not treat these explanations as exclusive. While one can disagree about the most likely evolutionary explanation of dominance, as Wright and Fisher did, offering a “physiological” or developmental explanation of dominance does not render dominance “epiphenomenal,” nor show that evolutionary considerations are irrelevant to the maintenance of dominance, as some [Kacser H. and Burns J.A. 1981. Genetics 97: 639–666] have argued. Recent work [Gilchrist M.A. and Nijhout H.F. 2001. Genetics 159: 423–432] illustrates how biological explanation is a multi-level task, requiring both a “top-down” approach to understanding how a pattern of inheritance or trait might be maintained in populations, as well as “bottom-up” modeling of the dynamics of gene expression. (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)

It has been argued that implicit biases are operative in philosophy and lead to significant epistemic costs in the field. Philosophers working on this issue have focussed mainly on implicit gender and race biases. They have overlooked ideological bias, which targets political orientations. Psychologists have found ideological bias in their field and have argued that it has negative epistemic effects on scientific research. I relate this debate to the field of philosophy and argue that if, as some studies suggest, the (...) same bias also exists in philosophy then it will lead to hitherto unrecognised epistemic hazards in the field. Furthermore, the bias is epistemically different from the more familiar biases in respects that are important for epistemology, ethics, and metaphilosophy. (shrink)

This chapter contains sections titled: Highlights of Past Literature Current Work Future Work.

In this paper I argue that the ontological interpretation of the concepts of reduction and emergence is often misleading in the philosophy of science and should nearly always be eschewed in favor of an epistemological interpretation. As a paradigm case, an example is drawn from the philosophy of chemistry to illustrate the drawbacks of “ontological reduction” and “ontological emergence,” and the virtues of an epistemological interpretation of these concepts.

According to the received view of evolution, only genes are inherited. From this view it follows that only genetically-caused phenotypic variation is selectable and, thereby, that all selection is at bottom genetic selection. This paper argues that the received view is wrong. In many species, there are intergenerationally-stable phenotypic differences due to environmental differences. Natural selection can act on these nongenetically-caused phenotypic differences in the same way it acts on genetically-caused phenotypic differences. Some selection is at bottom nongenetic selection. The (...) argument against the received view involves a reformulation of the concepts of inheritance and heritability. Inherited factors are all those developmental factors responsible for parent–offspring similarity; some inherited factors are genetic and some are not. Heritable variation is intergenerationally-stable phenotypic variation; some such variation is genetically-caused and some is not. The received view and its critics The possibility of nongenetic selection (the lucky butterfly) The reality of nongenetic selection 3.1 Imprinting mechanisms 3.2 Other learning mechanisms 3.3 Other nongenetic mechanisms Genetic and nongenetic inheritance mechanisms Genetic and nongenetic inherited factors Genetic and nongenetic heritability Conclusions + Current address: Dr Matteo Mameli, Research Fellow, King's College, Cambridge, CB2 1ST, United Kingdom, matteo.mameli{at}kings.cam.ac.uk' + u + '@' + d + ''//-->. (shrink)