According to a classical narrative, early geneticists, failing to see how Mendelism provides the missing pieces of Darwin’s theory, rejected gradual changes and advocated an implausible yet briefly popular view of evolution-by-mutation; after decades of delay (in which synthesis was prevented by personal conflicts, disciplinary rivalries, and anti-Darwinian animus), Darwinism emerged on a new Mendelian basis. Based on the works of four influential early geneticists – Bateson, de Vries, Morgan and Punnett –, and drawing on recent scholarship, we offer (...) an alternative that turns the classical view on its head. For early geneticists, embracing discrete inheritance and the mutation theory (for the origin of hereditary variation) did not entail rejection of selection, but rejection of Darwin’s non-Mendelian views of heredity and variation, his doctrine of natura non facit saltum, and his conception of “natural selection” as a creative force that shapes features out of masses of infinitesimal differences. We find no evidence of a delay in synthesizing mutation, rules of discrete inheritance, and selection in a Mendelian-Mutationist Synthesis. Instead, before 1918, early geneticists had conceptualized allelic selection, the Hardy–Weinberg equilibrium, the evolution of a quantitative trait under selection, the probability of fixation of a new mutation, and other key innovations. Contemporary evolutionary thinking seems closer to their more ecumenical view than to the restrictive mid-twentieth-century consensus known as the Modern Synthesis. (shrink)

Philosophers have proposed various kinds of relations between Mendelian genetics and molecular biology: reduction, replacement, explanatory extension. This paper argues that the two fields are best characterized as investigating different, serially integrated, hereditary mechanisms. The mechanisms operate at different times and contain different working entities. The working entities of the mechanisms of Mendelian heredity are chromosomes, whose movements serve to segregate alleles and independently assort genes in different linkage groups. The working entities of numerous mechanisms of molecular biology (...) are larger and smaller segments of DNA plus related molecules. Discovery of molecular DNA mechanisms filled black boxes that were noted, but unilluminated, by Mendelian genetics. (shrink)

Clustered regularly interspaced short palindromic repeats genome editing has already reinvented the direction of genetic and stem cell research. For more complex diseases it allows scientists to simultaneously create multiple genetic changes to a single cell. Technologies for correcting multiple mutations in an in vivo system are already in development. On the surface, the advent and use of gene editing technologies is a powerful tool to reduce human suffering by eradicating complex disease that has a genetic etiology. Gene drives are (...) CRISPR mediated alterations to genes that allow them to be passed on to subsequent populations at rates that approach one hundred per cent transmission. Therefore, from an anticipatory biomedical ethics perspective, it is possible to conceive gene drive being used with CRISPR to permanently ameliorate aberrant genes from wild-type populations containing mutations. However, there are also a number of possible side effects that could develop as the result of combining gene editing and gene drive technologies in an effort to eradicate complex diseases. In this paper, we critically analyse the hypothesis that the combination of CRISPR and gene drive will have a deleterious effect on human populations from an ethical perspective by developing an anticipatory ethical analysis of the implications for the use of CRISPR together with gene drive in humans. (shrink)

We may now ask the question: In what historical perspective should we place the work of Richard Goldschmidt? There is no doubt that in the period 1910–1950 Goldschmidt was an important and prolific figure in the history of biology in general, and of genetics in particular. His textbook on physiological genetics, published in 1938, was an amazing compendium of ideas put forward in the previous half-century about how genes influence physiology and development. His earlier studies on the genetic and geographic (...) distribution of the various species and races of Lymantria contributed soundly to an understanding of the inheritance and development of sex, as well as the genetics of speciation. He was a curious mixture of the experimentalist, empiricist, and theorizer, who could grasp both the large and the small at once and wrap them into the same integrated and coherent package.In insisting on trying to relate genetics to development, Goldschmidt was continually forced to speculate and to forsake experimental fact for generalized theory. In refusing to reconcile a physiological and developmental conception with a corpuscular theory of the gene, he forced himself to substitute for a large body of experimentally verified evidence, vague and general speculations which did not lead in any precise direction. L. C. Dunn summarizes succinctly the effect of Goldschmidt's thinking on the development of genetic theory: Although Goldschmidt's ideas had a considerable influence in directing attention to the developmental processes intervening between genes and characters, they did not lead to the establishment of a general theory of development in genetical terms. In fact, at the end of the period, as signalized by Goldschmidt's book of 1938 [Physiological Gentics] doubt remained whether there was a field with a defined problem which could be identified as developmental genetics.Yet the frequency with which Goldschmidt is cited by later writers suggests that there is a more positive side to his contribution than this. The early Mendelians had recognized the genic constitution of organisms and the Drosophila workers had uncovered in detail the chromosomal mechanism of heredity. These great discoveries were of classical character, solidly based on a multitude of well established facts. By themselves, however, they would not have been sufficient to place genetics in the central position within biology which it was to assume. Beyond the “static” analysis of gene transmission an insight was needed into the dynamic role of genes in cellular physiology, biochemistry, and development. Goldschmidt recognized this aspect and outlined in brilliant generalizations a physiological theory of genetics. Necessarily the prophetic nature of this achievement — romantic in the sense of Ostwald's classification of great scientists and their discoveries — transcended its factual basis. It was the audacity of the theoretician unimpeded by the still scanty data which gave a new focus to biological thought.Some have called Goldschmidt an “obstructionist” in the history of genetics—one whose efforts were largely directed toward useless and continual criticism — challenge for the sake of challenge. As this line of argument goes, time wasted answering Goldschmidt's poorly conceived criticisms could have been better used to pursue new lines of thought within the classical gene theory. Sometimes historians are upbraided for studying the work of such “obstructionists,” or even the work of those whose ideas have later proved to be inadequate. This argument misses the point of history and the lessons which it can teach. Perhaps Goldschmidt did take the time of a number of the classical geneticists who tried to answer his objections to the gene theory; and perhaps many of his own ideas about genes were, by today's view, “wrong.” These are always easier judgments to make by hindsight than at the moment. But that is not the point. Goldschmidt had a considerable influence on his contemporaries, and to dismiss him as an obstructionist because his opponents later proved to be more nearly right, distorts history and obscures significant questions which we might well be asking. It might be valuable to know why Goldschmidt felt compelled to be an iconoclast —and how that impulse, psychological in orgin, led him to overlook critical items of evidence which his opponents considered more carefully. It might also be valuable to try and understand how a contemporary of Goldschmidt or. Morgan really viewed the gene theory — what were its strong and weak point? Such questions are not readily answered by studying the work of only those men who were correct by later standards.Answers to some of the above questions can be gleaned from this study of Goldschmidt — though the first, and most psychologically oriented, question is largely untouched here.On the one hand, Goldschmidt forced classical geneticists to reexamine the foundation of their ideas about the nature, inviolability, and even physical dimensions of genes. He also kept alive the very real problems of gene physiology and its relations to development — a relationship that was given less attention by the Drosophila school in their pursuit of the transmission process. On a broader level he emphasized to the biological community a principle that was in danger of being lost in the enthusiasm surrounding the expansion of the Mendelian-chromosome theory. The point was that all theories in science are transient, logical constructs which should not be held as sacred. Time and again, as the history of science has shown, theories become rigid structures which retard new modes of thought. From Goldschmidt's perspective, the gene theory was in danger of performing just that function, for it was preventing workers from viewing the gene in a functional as well as a structural light.On the other hand, examining the work of critics (or even of outright “obstructionists”) gives the historian an opportunity to observe how the more established community of scholars at some point in time reacts to challenges of its cherished ideas. The fact that many workers in his own day (such as Beadle, Luria, Delbruck, Sturtevant, Bridges, and others), as well as most geneticists today, saw Goldschmidt as having been largely “obstructionist” is useful historical (and/or sociological) data. Clearly, as this paper has tried to show, Goldschmidt's ideas were not all obstructionist, and his viewpoint that genes must be considered functionally was one which was clearly valid, premature as it may have been from an experimental and technique point of view. Perhaps Goldschmidt's major fault was that he developed alternative theories which were not easily testable. Nonetheless, his challenge to a fundamental and established idea brought forth a reaction from many members of the genetic community which indicates how unwilling they were to reconsider the formalized theory on which their work was based. While many of Goldschmidt's criticisms — and particularly his way of making them — arose out of his own idiosyncrasies, they were also a product of his times. His view of the nature of theory-construction, and his rejection of old-style reductionism and mechanism, were part of a growing awareness within the world scientific community that explanations based on reducing complex phenomena to ultimate particles or units were clearly inadequate. The success of the Mendelian-chromosome theory had obscured that fact for many geneticists, but to Goldschmidt it was a point that could not be allowed to pass unnoticed. (shrink)

The target article by Charney on behavior genetics/genomics discusses how numerous molecular factors can inform heritability estimations and genetic association studies. These factors find application in the search for genes for behavioral phenotypes, including neuropsychiatric disorders. We elaborate upon how single causal factors can generate multiple phenotypes, and discuss how multiple causal factors may converge on common neurodevelopmental mechanisms.

SummaryIt is argued that Hugo de Vries's conversion to Mendelism did not agree with his previous theoretical framework. De Vries regarded the number of offspring expressing a certain character as a hereditary quality, intrinsic to the state of the pangene involved. His was a shortlived conversion since after the ‘rediscovery’ he failed to unify his older views with Mendelism. De Vries was never very much of a Mendelian. The usual stories of the Dutch ‘rediscovery’ need, therefore, a considerable reshaping.

Summary In 1979, Robert C. Olby published an article titled ?Mendel no Mendelian??, in which he questioned commonly held views that Gregor Mendel (1822?1884) laid the foundations for modern genetics. According to Olby, and other historians of science who have since followed him, Mendel worked within the tradition of so-called hybridists, who were interested in the evolutionary role of hybrids rather than in laws of inheritance. We propose instead to view the hybridist tradition as an experimental programme characterized by (...) a dynamic development that inadvertently led to a focus on the inheritance of individual traits. Through a careful analysis of publications on hybridization by Carl Linnaeus (1707?1778), Joseph Gottlieb Koelreuter (1733?1806), Carl Friedrich Gärtner (1772?1850), and finally Mendel himself, we will show that this development consisted in repeated reclassifications of hybrids to accommodate anomalies, which in the end allowed Mendel to draw analogies between whole organisms, individual traits, and ?elements? contained in reproductive cells. Mendel's achievement was a product of normal science, and yet a revolutionary step forward. This also explains why, in 1900, when the report he gave on his experiments was ?rediscovered?, Mendel could be read as a ?Mendelian? (shrink)

Mendelian Inheritance in Man, a computerized catalogue of human genetic disorders authored and maintained by cardiologist and medical genetics pioneer Victor A. McKusick, played a major part in demarcating between a novel biomedical science and the eugenic projects of racial betterment which existed prior to its emergence. Nonetheless, it built upon prior efforts to systematize genetic knowledge tied to individuals and institutions invested in eugenics. By unpacking the process of digitizing a homespun cataloguing project and charting its development into (...) an online database, this article aims to illuminate how the institution-building efforts of one individual created an ‘information order’ for accessing genetic information that tacitly shaped the norms and priorities of the field toward the pursuit of specific genes associated with discernible genetic disorders. This was not by design, but rather arose through negotiation with the catalogue's users; it accommodated further changes as biomedical research displaced the Mendelian paradigm. While great effort was expended toward making sequence data available to investigators during the Human Genome Project, MIM was largely taken for granted as a ‘legacy system’, McKusick's own labour of love. Drawing on recent histories of biomedical data, the article suggests that the bibliographical work of curation and translation is a central feature of value production in the life sciences meriting attention in its own right. (shrink)

The precise 1:1 segregation of Mendelian heredity is ordinarily taken for granted, yet there are numerous examples of ‘cheating’ genes that perpetuate themselves in the population by biasing the Mendelian process in their favor. One example is the Segregation Distortion system of Drosophila melanogaster, in which the distorting gene causes its homologous chromosome to produce a nonfunctional sperm. This system depends on three closely linked components, whose molecular basis is beginning to be understood.The system is characterized by numerous (...) modifiers changing the degree of distortion. Mathematical theory shows that unlinked modifiers that change the degree of distortion in the direction of Mendelism always increase in the population. This provides a mechanism for removing cheaters and preserving the honesty of the Mendelian gene‐shuffle. (shrink)

Almost every human disease has both a genetic and an environmental component. Even a classical inherited condition such as hemophilia can be influenced by external factors—in fact, most of the pathogenic effects of the mutation can be avoided by judicious injections of clotting factor, leading to a nearly normal life expectancy. For infectious diseases, often considered as essentially environmental, there are well-documented inherited differences in susceptibility, one of the most striking being the resistance to HIV infection of homozygous carriers of (...) the delta-32 mutation in the CCR5 gene (Dragic et al. 1996). Nevertheless, a number of conditions are “mostly genetic,” others “mostly environmental,” while many .. (shrink)

This paper examines the process that led to the identification of chromosomes as carriers of genes. It focuses on the role played by explanations in theory construction and analyzes the status given to the entities and processes introduced through such explanations. I argue that the theory of the gene was a functional explanation that, as such, could not offer decisive support for the existence of genes. However, I maintain that functional explanations set the conditions of identification needed to discover the (...) physical structure that has a certain function in a given system. In this case, the theory of the gene helped to select the chromosomes as the physical structure responsible for the Mendelian segregation of genes. In its turn, the theory of chromosome inheritance helped to reduce the permissive character of the theory of the gene, regulating its further development. (shrink)

Cytogenetics was born of the confluence of two so-far independent fields: cytological studies and breeding studies, which merged through the identification of genes with chromosomes. In this paper I argue that genes were introduced as functional entities. Functional explanations are presented here as a subclass of inferences to the best explanation and I argue that abductive arguments do not offer conclusive proof for the existence of the entities postulated through them. However, functional explanations usually follow a scheme laid out by (...) Fodor (1968): there is a first phase where hypothetical entities are postulated and individuated through their effects; there is a second phase where the physical structures responsible for these effects are sought. I analyze the development of both phases in the construction of the chromosome theory of Mendelian inheritance. I will argue that first-phase theories are important to set conditions of identification for the functions played by a certain structure in a given containing system. (shrink)

The Genotype-Phenotype (G-P) distinction was proposed in the context of Mendelian genetics, in the wake of late 19th century studies about heredity. In this paper, we provide a conceptual analysis that highlights that the G-P distinction was grounded on three pillars: observability, transmissibility, and causality. Originally, the genotype is the non-observable and transmissible cause of the phenotype, which is its observable and non-transmissible effect. We argue that the current developments of biology have called the validity of such pillars into (...) question. First, molecular biology has unveiled the putative material substrate of the genotype (qua DNA), making it an observable object. Second, numerous findings on nongenetic heredity suggest that some phenotypic traits can be directly transmitted. Third, recent organicist approaches to biological phenomena have emphasized the reciprocal causality between parts of a biological system, which notably applies to the relations between genotypes and phenotypes. As a consequence, we submit that the G-P distinction has lost its general validity, although it can still apply to specific situations. This calls for forging new frameworks and concepts to better describe heredity and development. (shrink)

This article offers a close examination of a small selection of pedigrees taken from German Mendelian and eugenic scholarship of the 1920s and 1930s. It examines the procedures that became customary for presenting data on human inherited pathologies, as well as the frequent changes in the information content of those charts. Relevant biographical and genealogical data was removed, and important indications regarding the diagnostic methods applied by the investigating scholar were lost, as soon as a pedigree was charted or (...) reproduced. Data on healthy individuals was condensed, leading to an emphasis on the hereditary burden of pathological traits. At times, healthy individuals were entirely omitted, as were exogenous martial partners. These modifications paved the way for further theoretical amendments, including the addition of ‘carrier’ status to chosen individuals along the pedigree. With this addition, these pedigrees changed their ontological status, from empirical records of human reproduction to partially hypothetical illustrations of Mendelian theory itself. This process was complemented by the representation of theoretical genetic models in the format of a human pedigree. A comparison to practices of charting pedigrees still common today suggests that the processes hereby revealed are far from exceptional. In line with the ideas put forward by Ludwik Fleck, they are interpreted as germane to the way scientific ideas are communicated and propagated and to the scientific culture of genetics. The article also offers a refinement to Fleck’s analysis of textbook construction, which highlights the extent to which textbook examples differ from the original data on which they are based. (shrink)

Laudan's thesis that conceptual problem solving is at least as important as empirical problem solving in scientific research is given support by a study of the relation between the chromosome theory and the Mendelian research program. It will be shown that there existed a conceptual tension between the chromosome theory and the Mendelian program. This tension was to be resolved by changing the constraints of the Mendelian program. The relation between the chromosome theory and the Mendelian (...) program is shown to be a good illustration of the influence of science itself on the rational standards governing scientific development. (shrink)

This innovative book focuses on the development of the gene theory as a case study in scientific creativity.

Advocates of “Mendelism” early on stressed the usefulness of Mendelian principles for breeders. Ever since, that usefulness—and the favourable opinion of Mendelism it supposedly engendered among breeders—has featured in explanations of the rapid rise of Mendelian genetics. An important counter-tradition of commentary, however, has emphasized the ways in which early Mendelian theory in fact fell short of breeders’ needs. Attention to intellectual property, narrowly and broadly construed, makes possible an approach that takes both the tradition and the (...) counter-tradition seriously, by enabling a more complete description of the theory-reality shortfall and a better understanding of how changing practices, on and off the Mendelians’ experimental farms, functioned to render that shortfall unproblematic. In the case of plant breeding in Britain, a perennial source of lost profits and disputes over ownership was the appearance of individual plants departing from their varietal types—so-called “rogues.” Mendelian plant varieties acquired a reputation for being rogue-free, and so for demonstrating the correctness of Mendelian principles , at a time when Mendelians were gradually taking control of the means for distributing their varieties. Mendelian breeders protected their products physically from rogue-inducing contamination in such a way that when rogues did appear, the default explanation—that contamination had somehow occurred—ensured that there was no threat to Mendelian principles. (shrink)

One of the lecture plates in the collection of the Museum of the University of Amsterdam, generally believed to be used by the Dutch botanist Hugo de Vries, has aroused much discussion in relation to the question of whether or not de Vries knew Mendel's laws before he published his rediscovery of them in 1900. The plate suggests that de Vries observed Mendelian segregation ratios in 1895 and 1896 in the progeny of a cross of two varieties of Papaver (...) with different flower colour. According to his own account, it was through this cross that he first deduced the laws of Mendel in 1896. Some researchers have accepted the lecture plate as proof for this claim. My conclusion is that the plate was not made before 1900 but in 1904 for a lecture course in the USA and, as a consequence, that it is not a contemporary piece of evidence. A closer look at the descriptions of the depicted experiment in de Vries' publications revealed that its original goal was not to investigate segregation but to transfer a monstrosity. The segregation of the flower colour was a accidental event. No research notes of the experiment have survived, but a note on an experiment with Veronica, performed in the same successive years as the Papaver experiment and definitely intended to investigate the segregation of flower colour, shows that this experiment was interpreted in a theoretically conceived, more or less Mendelian way. Because of a sloppy performance, no firm conclusions could be drawn from the experiment, but de Vries clearly had the idea of Mendelian segregation in 1896. That he never brought it up before 1900 suggests that he could not establish the general validity of segregation rules, as is shown in the case of Veronica. The reading of Mendel's paper in 1900 immediately put an end to de Vries' doubts. He scrapped the failures and kept the successes, proudly presenting these to the public as proof for the laws of segregation and, at the same time, of the independence of his discovery. (shrink)

Summary Long-standing claims have been made for nearly the entire twentieth century that the biometrician, Karl Pearson, and his colleague, W. F. R. Weldon, rejected Mendelism as a theory of inheritance. It is shown that at the end of the nineteenth century Pearson considered various theories of inheritance (including Francis Galton's law of ancestral heredity for characters underpinned by continuous variation), and by 1904 he ?accepted the fundamental idea of Mendel? as a theory of inheritance for discontinuous variation. Moreover, in (...) 1909, he suggested a synthesis of biometry and Mendelism. Despite the many attempts made by a number of geneticists (including R. A. Fisher in 1936) to use Pearson's chi-square (X 2, P) goodness-of-fit test on Mendel's data, which produced results that were ?too good to be true?, Weldon reached the same conclusion in 1902, but his results were never acknowledged. The geneticist and arch-rival of the biometricians, Williams Bateson, was instead exceptionally critical of this work and interpreted this as Weldon's rejection of Mendelism. Whilst scholarship on Mendel, by historians of science in the last 18 years, has led to a balanced perspective of Mendel, it is suggested that a better balanced and more rounded view of the hereditarian-statistical work of Pearson, Weldon, and the biometricians is long overdue. (shrink)

The increasing attention which has been given to social history of science and to the sociological analysis of scientific activity has resulted in a renewed interest in scientific controversies. Furthermore, the rejection of the presentist view of history, according to which those contestants who took what we can identify, with the benefit of modern knowledge, as the ‘right’ stand in a controversy, were right and their opponents were ‘wrong’, left the subject of scientific controversies with many questions. What determines their (...) emergence, course and resolution? When Froggatt and Nevin wrote on the Bio-metric-Mendelian controversy in 1971 they called their article ‘descriptive rather than interpretative’, so they avoided the very questions we would like to ask. Provine, in the same year, concentrated on the strong personalities of the contestants, their clashes, and the scientific arguments in play. But in 1975 Mackenzie and Barnes argued that the controversy could not be accounted for unless recourse was had to sociological factors. Their view has become widely known and figured prominently in 1982 in Steven Shapin's recital of the empirical achievements of the application of the sociological approach. I have returned to this subject because I do not yet feel altogether convinced by Mackenzie and Barnes' analysis. Even if their analysis of the controversy between Pearson and Bateson be accepted, it is not so obvious how effectively it can be used to explain the controversy between Weldon and Bateson, and I am not confident that it is adequate for an understanding of the evolution of their differing views of the mechanism of evolution. (shrink)

Philosophers now treat the relationship between Classical Mendelian Genetics and molecular biology as a paradigm of nonreduction and this example is playing an increasingly prominent role in debates about the reducibility of theories ranging from macrosocial science to folk psychology. Patricia Churchland (1986), for example, draws an analogy between the alleged elimination of the “causal mainstay” of classical genetics and her view that today’s psychological theory will be eliminated by neuroscience. Patricia Kitcher takes an autonomous rather than eliminativist view (...) of the reported nonreduction in genetics and reasons that psychology will retain a similar autonomy from lower level sciences (1980 and 1982). Although Churchland and Kitcher offer different interpretations of the apparent failure of molecular biology to reduce classical genetics, they agree that this failure will help illuminate theoretical relations between psychology and lower level sciences. The appearance of the Mendelian example along side the usual ones from physics and chemistry marks a turning point in philosophy of science. (shrink)

Laudan's thesis that conceptual problem solving is at least as important as empirical problem solving in scientific research is given support by a study of the relation between the chromosome theory and the Mendelian research program. It will be shown that there existed a conceptual tension between the chromosome theory and the Mendelian program. This tension was to be resolved by changing the constraints of the Mendelian program. The relation between the chromosome theory and the Mendelian (...) program is shown to be a good illustration of the influence of science itself on the rational standards governing scientific development. (shrink)

Cultural effects can influence the results of causal genetic analyses, such as Mendelian randomisation, but the potential influences of culture on genotype–phenotype associations are not currently well understood. Different genetic variants could be associated with different phenotypes in different populations, or culture could confound or influence the direction of the association between genotypes and phenotypes in different populations.

In our commentary we ask whether we should ultimately endeavour to find the deep causes of behaviours? Then we discuss two extensions of the proposed framework: (1) Mendelian randomisation and (2) hypothesis-free gene–environment interaction (leveraging heterogeneity in genetic associations). These complementary methods help move us towards second-generation causal knowledge, ultimately understanding mechanistic pathways and identifying more effective intervention targets.

The bitterness and protracted character of the biometrician–Mendelian debate has long aroused the interest of historians of biology. In this paper, we focus on another and much less discussed facet of the controversy: competing interpretations of the inheritance of mental defect. Today, the views of the early Mendelians, such as Charles B. Davenport and Henry H. Goddard, are universally seen to be mistaken. Some historians assume that the Mendelians' errors were exposed by advances in the science of genetics. Others (...) believe that their mistakes could have been identified by contemporaries. Neither interpretation takes account of the fact that the lapses for which the Mendelian eugenicists are now notorious were, in fact, mostly identified at the time by the biometricians David Heron and Karl Pearson. In this paper we ask why their objections had so little impact. We think the answer illustrates an important general point about the social prerequisites for effective scientific critique. (shrink)

Philosophers now treat the relationship between classical genetics and molecular biology as a paradigm of nonreduction and this example is playing an increasingly prominent role in debates about the reducibility of theories in other sciences. This paper shows that the anti-reductionist consensus about genetics will not withstand serious scrutiny. In addition to defusing the main anti-reductionist objections, this critical analysis uncovers tell-tale signs of a significant reduction in progress. It also identifies philosophical issues relevant to gaining a better understanding of (...) what is now happening in genetics and of what we might expect to happen in other sciences. (shrink)

Philosophers now treat the relationship between classical genetics and molecular biology as a paradigm of nonreduction and this example is playing an increasingly prominent role in debates about the reducibility of theories in other sciences. This paper shows that the anti-reductionist consensus about genetics will not withstand serious scrutiny. In addition to defusing the main anti-reductionist objections, this critical analysis uncovers tell-tale signs of a significant reduction in progress. It also identifies philosophical issues relevant to gaining a better understanding of (...) what is now happening in genetics and of what we might expect to happen in other sciences. (shrink)