A crucial question for a process view of life is how to identify a process and how to follow it through time. The genidentity view can contribute decisively to this project. It says that the identity through time of an entity X is given by a well-identified series of continuous states of affairs. Genidentity helps address the problem of diachronic identity in the living world. This chapter describes the centrality of the concept of genidentity for David Hull and proposes an (...) extension of Hull’s view to the ubiquitous phenomenon of symbiosis. Finally, using immunology as a key example, it shows that the genidentity view suggests that the main interest of a process approach is epistemological rather than ontological and that its principal claim is one of priority, namely that processes precede and define things, and not vice versa. (shrink)

Waddington’s experiments on genetic assimilation showed that selection on environmentally induced phenotypic variants can cause inherited evolutionary changes in the phenotype. We have recently extended this work by demonstrating that it is possible to select for a polyphenism in a monophenic species . We found that a mutation in the juvenile hormone regulatory pathway in Manduca sexta enabled heat stress to reveal a hidden reaction norm of larval coloration. Artificial selection for increased color change in response to heat-shock resulted in (...) the genetic accommodation of a black/green larval color polyphenism, caused by an environment-sensitive threshold switch mediated by the endocrine system. (shrink)

A new etiological model is proposed for schizophrenia that combines variability‐enhancing nonspecific factors acting during development with more specific risk factors. This model is better suited than the current etiological models of schizophrenia, based on the risk factors paradigm, for predicting and/or explaining several important findings about schizophrenia: high co‐morbidity rates, low specificity of many risk factors, and persistence in the population of the associated genetic polymorphisms. Compared with similar models, e.g., de‐canalization, common psychopathology factor, sexual‐selection, or differential sensitivity to (...) the environment, this proposal is more general and integrative. Recently developed research methods have proven the existence of genetic and environmental factors that enhance developmental variability. Applying such methods to newly collected or already available data can allow for testing the hypotheses upon which this model is built. If validated, this model may change the understanding of the etiology of schizophrenia, the research models, and preventionbrk paradigms. (shrink)

Many scientists and philosophers of science are troubled by the relative isolation of developmental from evolutionary biology. Reconciling the science of development with the science of heredity preoccupied a minority of biologists for much of the twentieth century, but these efforts were not corporately successful. Mainly in the past fifteen years, however, these previously dispersed integrating programmes have been themselves synthesized and so reinvigorated. Two of these more recent synthesizing endeavours are evolutionary developmental biology and developmental systems theory. While the (...) former is a bourgeoning and scientifically well-respected biological discipline, the same cannot be said of DST, which is virtually unknown among biologists. In this review, we provide overviews of DST and EDB, summarize their key tenets, examine how they relate to one another and to the study of epigenetics, and survey the impact that DST and EDB have had on biological theory and practice. (shrink)

There is a tendency in both scientific and humanistic disciplines to think of biological evolution in humans as significantly impeded if not completely overwhelmed by the robust cultural and technological capabilities of the species. The aim of this article is to make sense of and evaluate this claim. In Section 2 , I flesh out the argument that humans are ‘insulated’ from ordinary evolutionary mechanisms in terms of our contemporary biological understandings of phenotypic plasticity, niche construction, and cultural transmission. In (...) Section 3 , I consider two obvious objections to the above argument based on the growing literatures related to gene-culture coevolution and recent positive selection on the human genome, as well as a pair of less common objections relating to the connection between plasticity, population size and evolvability. In Section 4 , I argue that both the ‘human evolutionary stasis argument’ and its various detractor theories are premised on a fundamental conceptual flaw: they take evolutionary stasis for granted, since they fail to conceive of stabilizing selection as a type of evolution and drift as a universal tendency that dominates in the absence of selection. Without the continued operation of natural selection, the very properties that are purported to reduce the evolutionary response to selection in humans would themselves drift into non-functionality. I conclude that properly conceived, biological evolution is a permanent and ineradicable fixture of any species, including Homo sapiens. (shrink)

Adaptation by means of natural selection depends on the ability of populations to maintain variation in heritable traits. According to the Modern Synthesis this variation is sustained by mutations and genetic drift. Epigenetics, evodevo, niche construction and cultural factors have more recently been shown to contribute to heritable variation, however, leading an increasing number of biologists to call for an extended view of speciation and evolution. An additional common feature across the animal kingdom is learning, defined as the ability to (...) change behavior according to novel experiences or skills. Learning constitutes an additional source for phenotypic variation, and change in behavior may induce long lasting shifts in fitness, and hence favor evolutionary novelties. Based on published studies, I demonstrate how learning about food, mate choice and habitats has contributed substantially to speciation in the canonical story of Darwin’s finches on the Galapagos Islands. Learning cannot be reduced to genetics, because it demands decisions, which requires a subject. Evolutionary novelties may hence emerge both from shifts in allelic frequencies and from shifts in learned, subject driven behavior. The existence of two principally different sources of variation also prevents the Modern Synthesis from self-referring explanations. (shrink)

Since Darwin, there has been a long and arduous struggle to understand the source and maintenance of natural genetic variation and its relationship to phenotype. The reason that this task is so difficult is that it requires integration of detailed, and as yet incomplete, knowledge from several biological disciplines, including evolutionary, population, and developmental genetics. In this ‘post‐genomic’ era, it is relatively easy to identify differences in the DNA sequence between individuals. However, the task remains to delineate how this abundant (...) genetic diversity actually contributes to phenotypic diversity. This necessitates tackling the problem of hidden genetic variation. Genetic polymorphisms can be conditionally cryptic, but have the potential to contribute to phenotypic variation in particular genetic backgrounds or under specific environmental conditions. A recent paper by Lauter and Doebley highlights the contribution of hidden genetic variation to traits characterizing the morphological evolution of modern maize from its wild grass‐like progenitor teosinte.1 This work is the first to demonstrate hidden variance for selected (agronomically ‘adaptive’) traits in a well‐characterized model for morphological evolution. BioEssays 24:685–689, 2002. © 2002 Wiley Periodicals, Inc. (shrink)

The vast majority (> 95%) of single-gene mutations in yeast affect not only the expression of the mutant gene, but also the expression of many other genes. These data suggest the presence of a previously uncharacterized ‘gene expression network’—a set of interactions between genes which dictate gene expression in the native cell environment. Here, we quantitatively analyze the gene expression network revealed by microarray expression data from 273 different yeast gene deletion mutants.(1) We find that gene expression interactions form a (...) robust, error-tolerant ‘scale-free’ network, similar to metabolic pathways(2) and artificial networks such as power grids and the internet.(3-5) Because the connectivity between genes in the gene expression network is unevenly distributed, a scale-free organization helps make organisms resistant to the deleterious effects of mutation, and is thus highly adaptive. The existence of a gene expression network poses practical considerations for the study of gene function, since most mutant phenotypes are the result of changes in the expression of many genes. Using principles of scale-free network topology, we propose that fragmenting the gene expression network via ‘genome-engineering’ may be a viable and practical approach to isolating gene function. BioEssays 24:267–274, 2002. © 2002 Wiley Periodicals, Inc.; DOI 10.1002/bies.10054. (shrink)

Darwin’s claim that Natural Selection, through optimization of fitness, explains complex biological design has not yet been properly formalized. Alan Grafen’s Formal Darwinism Project aims at providing such a formalization and at demonstrating that fitness maximization is coherent with results from Population Genetics, usually interpreted as denying it. We suggest that Grafen’s proposal suffers from some limitations linked to its concept of design as optimized fitness. In order to overcome these limitations, we propose a classification of evolutionary facts based on (...) a bi-dimensional complexity space, which adds robustness to fitness as measure of the quality of a design. In this space, each point represents an organismic architecture, and movement between two points would be an evolutionary fact. Natural Selection explains movement along the fitness axis, while non-selective mechanisms explain movement on the robustness axis. Moreover, we propose a thermodynamic metaphor to draw parallelisms between notions of fitness and entropy, robustness and energy, and movement in this space and reversible and irreversible cycles. We argue that this metaphor illustrates different evolutionary processes usually overlooked by proposals of formalization of Darwinian theory, such Grafen’s Formal Darwinism Project. (shrink)