Evolution of cultural communication systems: the coevolution of cultural signals and genes encoding learning preferences

In several communication systems that rely on social learning, such as bird song, and possibly human language, the range of signals that can be learned is limited by perceptual biases--predispositions--that are presumably based on genes. In this paper, we examine the coevolution of such genes with the culturally transmitted communication traits themselves, using deterministic population genetic models. We argue that examining how restrictive genetic predispositions are is a useful way of examining the evolutionary origin and maintenance of learning. Under neutral cultural evolution, where no cultural trait has any inherent advantage over another, there is selection in favour of less restrictive genes (genes that allow a wider range of signals to recognized). In contrast, cultural conformity (where the most common cultural trait is favoured) leads to selection in favour of more restrictive genes.     

Animal morality: What is the debate about?

Empirical studies of the social lives of non-human primates, cetaceans, and other social animals have prompted scientists and philosophers to debate the question of whether morality and moral cognition exists in non-human animals. Some researchers have argued that morality does exist in several animal species, others that these species may possess various evolutionary building blocks or precursors to morality, but not quite the genuine article, while some have argued that nothing remotely resembling morality can be found in any non-human species. However, these different positions on animal morality generally appear to be motivated more by different conceptions of how the term “morality” is to be defined than by empirical disagreements about animal social behaviour and psychology. After delving deeper into the goals and methodologies of various of the protagonists, I argue that, despite appearances, there are actually two importantly distinct debates over animal morality going on, corresponding to two quite different ways of thinking about what it is to define “morality”, “moral cognition”, and associated notions. Several apparent skirmishes in the literature are thus cases of researchers simply talking past each other. I then focus on what I take to be the core debate over animal morality, which is concerned with understanding the nature and phylogenetic distribution of morality conceived as a psychological natural kind. I argue that this debate is in fact largely terminological and non-substantive. Finally, I reflect on how this core debate might best be re-framed.     

Mitochondrial medicine

After reviewing the history of mitochondrial diseases, I follow a genetic classification to discuss new developments and old conundrums. In the field of mitochondrial DNA (mtDNA) mutations, I argue that we are not yet scraping the bottom of the barrel because: (i) new mtDNA mutations are still being discovered, especially in protein-coding genes; (ii) the pathogenicity of homoplasmic mutations is being revisited; (iii) some genetic dogmas are chipped but not broken; (iv) mtDNA haplotypes are gaining interest in human pathology; (v) pathogenesis is still largely enigmatic. In the field of nuclear DNA (nDNA) mutations, there has been good progress in our understanding of disorders due to faulty intergenomic communication. Of the genes responsible for multiple deletions and depletion of mtDNA, mutations in POLG have been associated with a great variety of clinical phenotypes in humans and to precocious aging in mice. Novel pathogenetic mechanisms include alterations in the lipid milieu of the inner mitochondrial membrane and mutations in genes controlling mitochondrial motility, fission, and fusion.     

Do the evolutionary origins of our moral beliefs undermine moral knowledge?

According to some recent arguments, (Joyce in The evolution of morality, MIT Press, Cambridge, 2006; Ruse and Wilson in Conceptual issues in evolutionary biology, MIT Press, Cambridge, 1995; Street in Philos Studies 127: 109–166, 2006) if our moral beliefs are products of natural selection, then we do not have moral knowledge. In defense of this inference, its proponents argue that natural selection is a process that fails to track moral facts. In this paper, I argue that our having moral knowledge is consistent with, (a) the hypothesis that our moral beliefs are products of natural selection, and (b) the claim (or a certain interpretation of the claim) that natural selection fails to track moral facts. I also argue that natural selection is a process that could track moral facts, albeit imperfectly. I do not argue that we do have moral knowledge. I argue instead that Darwinian considerations provide us with no reason to doubt that we do, and with some reasons to suppose that we might.     

Overexpression of AGAMOUS-LIKE 28 (AGL28) promotes flowering by upregulating expression of floral promoters within the autonomous pathway

MADS box genes are known to perform important functions in the development of various plant organs. Although the functions of many MADS box genes have previously been elucidated, the biological function of the type I MADS box genes remains poorly understood. In order to understand the function and regulation of the type I MADS box genes, we conducted molecular genetic analyses of AGL28, a member of the Malpha class of type I genes. AGL28 was expressed in vegetative tissues in a photoperiod-independent manner, but not within the reproductive apex. This indicates that AGL28 plays a role in the vegetative phase. Overexpression of AGL28 caused precocious flowering via the upregulation of the expression of FCA and LUMINIDEPENDENS (LD), both floral promoters within the autonomous pathway. However, the loss of AGL28 function did not result in any obvious flowering time phenotype, which suggests that AGL28 may perform a redundant function. Collectively, our data suggest that AGL28 is a positive regulator of known floral promoters within the autonomous pathway in Arabidopsis.     

Ruse's Darwinian meta-ethics: A critique

Michael Ruse, in Taking Darwin Seriously seeks to establish that taking Darwin seriously requires us to treat morality as subjective and naturalistic. I argue that, if morality is not objective, then we have no good reason for being moral if we can avoid detection and punishment. As a consequence, we will only continue to behave morally as long as we remain ignorant of Ruse's theory, that is, as long as the cat is not let out of the bag. Ruse offers a number of arguments to show that his theory can overcome such problems. I argue that they all fail. Ruse also argues that he can offer a naturalistic account of ethics which steps around the naturalistic fallacy and avoids the confusion of reasons with causes. His principal argument for this view is an analogy between spiritualism and morality. I argue that this analogy fails.     

Developmental capacitance, genetic accommodation, and adaptive evolution

The concept of genetic accommodation remains controversial, in part because it remains unclear whether evolution by genetic accommodation forces a revolution, or merely a shift in emphasis, in our understanding of how evolution produces adaptive new traits. Here I outline a perspective that largely favors the latter view. I argue that evolution by genetic accommodation can easily be integrated into traditional evolutionary concepts. At the same time, evolution by genetic accommodation invites novel empirical and theoretical approaches that may allow biologists to push the boundaries of our current understanding of the process of evolution and to solve some long-standing controversies. Specifically, I discuss the role of developmental mechanisms as natural, and likely ubiquitous, capacitors of cryptic genetic variation, and the role of environmental perturbations as mechanisms by which such variation can become visible to selection on an individual to population-wide scale. I argue that in combination, developmental capacitance and large-scale environmental perturbations have the potential to facilitate rapid evolution including the origin of novel adaptive features while circumventing otherwise powerful genetic and population-biological constraints on adaptive evolution. I end by highlighting several promising avenues for future empirical research to explore the mechanisms and significance of evolution by genetic accommodation.     

Stocking the Genetic Supermarket: Reproductive Genetic Technologies and Collective Action Problems

Reproductive genetic technologies (RGTs) allow parents to decide whether their future children will have or lack certain genetic predispositions. A popular model that has been proposed for regulating access to RGTs is the ‘genetic supermarket’. In the genetic supermarket, parents are free to make decisions about which genes to select for their children with little state interference. One possible consequence of the genetic supermarket is that collective action problems will arise: if rational individuals use the genetic supermarket in isolation from one another, this may have a negative effect on society as a whole, including future generations. In this article we argue that RGTs targeting height, innate immunity, and certain cognitive traits could lead to collective action problems. We then discuss whether this risk could in principle justify state intervention in the genetic supermarket. We argue that there is a plausible prima facie case for the view that such state intervention would be justified and respond to a number of arguments that might be adduced against that view.     

Orphaned at conception: the uncanny offspring of embryos

A number of advances in assisted reproduction have been greeted by the accusation that they would produce children 'without parents'. In this paper I will argue that while to date these accusations have been false, there is a limited but important sense in which they would be true of children born of a reproductive technology that is now on the horizon. If our genetic parents are those individuals from whom we have inherited 50% of our genes, then, unlike in any other reproductive scenario, children who were conceived from gametes derived from stem cell lines derived from discarded IVF embryos would have no genetic parents! This paper defends this claim and investigates its ethical implications. I argue that there are reasons to think that the creation of such embryos might be morally superior to the existing alternatives in an important set of circumstances.     

Selecting potential children and unconditional parental love

For now, the best way to select a child's genes is to select a potential child who has those genes, using genetic testing and either selective abortion, sperm and egg donors, or selecting embryos for implantation. Some people even wish to select against genes that are only mildly undesirable, or to select for superior genes. I call this selection drift – the standard for acceptable children is creeping upwards. The President's Council on Bioethics and others have raised the parental love objection : Just as we should love existing children unconditionally, so we should unconditionally accept whatever child we get in the natural course of things. If we set conditions on which child we get, we are setting conditions on our love for whatever child we get. Although this objection was prompted by selection drift, it also seems to cover selecting against genes for severe impairments.
I argue that selection drift is not inconsistent with the ideal of unconditional parental love and, moreover, that the latter actually implies that we should practise selection drift – in other words, we should try to select potential children with the best genetic endowments. My endowment argument for the second claim works from an analogy between arranging an endowment prior to conception to fund a future child's education, and arranging a genetic endowment by selecting a potential child who already has it, where in both cases the child would not have existed without the endowment. I conclude with some programmatic remarks about the nonidentity problem.     

Quantitative integration of genetic factors in the learning and production of canary song

Learned bird song is influenced by inherited predispositions. The canary is a model system for the interaction of genes and learning on behaviour, especially because some strains have undergone artificial selection for song. In this study, roller canaries (bred for low-pitched songs) and border canaries (whose song is higher pitched, similar to the wild-type) were interbred and backcrossed to produce 58 males that sorted into seven genetically distinct groups. All males were tutored with the same set of songs, which included both low- and high-pitched syllables. Individuals were consistent within genetic groups but differed between groups in the proportion of low- versus high-pitched syllables they learned and sang. Both sex-linked and autosomal factors affected song learning and song production, in an additive manner. Dominant Z-chromosome factors facilitated high-pitched syllable learning and production, whereas the sex-linked alleles associated with the switch to low-pitched syllables under artificial selection were largely recessive. With respect to autosomal effects, the most surprising result is that males in the same genetic group had almost identical repertoires. This result challenges two common preconceptions: that genetic changes at different loci lead to distinct phenotypic changes, and that genetic predispositions affect learning in simple and general ways. Rather, different combinations of genetic changes can be associated with the same phenotypic effect; and predispositions can be remarkably specific, such as a tendency to learn and sing one song element rather than another.     

A blueprint for vocal learning: auditory predispositions from brains to genomes

Memorizing and producing complex strings of sound are requirements for spoken human language. We share these behaviours with likely more than 4000 species of songbirds, making birds our primary model for studying the cognitive basis of vocal learning and, more generally, an important model for how memories are encoded in the brain. In songbirds, as in humans, the sounds that a juvenile learns later in life depend on auditory memories formed early in development. Experiments on a wide variety of songbird species suggest that the formation and lability of these auditory memories, in turn, depend on auditory predispositions that stimulate learning when a juvenile hears relevant, species-typical sounds. We review evidence that variation in key features of these auditory predispositions are determined by variation in genes underlying the development of the auditory system. We argue that increased investigation of the neuronal basis of auditory predispositions expressed early in life in combination with modern comparative genomic approaches may provide insights into the evolution of vocal learning.     

Functional conservation and divergence of FVE genes that control flowering time and cold response in rice and Arabidopsis

Recent molecular and genetic studies in rice, a short-day plant, have elucidated both conservation and divergence of photoperiod pathway genes and their regulators. However, the biological roles of rice genes that act within the autonomous pathway are still largely unknown. In order to better understand the function of the autonomous pathway genes in rice, we conducted molecular genetic analyses of OsFVE, a rice gene homologous to Arabidopsis FVE. OsFVE was found to be ubiquitously expressed in vegetative and reproductive organs. Overexpression of OsFVE could rescue the flowering time phenotype of the Arabidopsis fve mutants by up-regulating expression of the SUPPRESSOR OF OVEREXPRESSION OF CO1 (SOC1) and down-regulating FLOWERING LOCUS C (FLC) expression. These results suggest that there may be a conserved function between OsFVE and FVE in the control of flowering time. However, OsFVE overexpression in the fve mutants did not rescue the flowering time phenotype in in relation to the response to intermittent cold treatment.     

Cultural transmission and the evolution of human behaviour: a general approach based on the Price equation

Transmitted culture can be viewed as an inheritance system somewhat independent of genes that is subject to processes of descent with modification in its own right. Although many authors have conceptualized cultural change as a Darwinian process, there is no generally agreed formal framework for defining key concepts such as natural selection, fitness, relatedness and altruism for the cultural case. Here, we present and explore such a framework using the Price equation. Assuming an isolated, independently measurable culturally transmitted trait, we show that cultural natural selection maximizes cultural fitness, a distinct quantity from genetic fitness, and also that cultural relatedness and cultural altruism are not reducible to or necessarily related to their genetic counterparts. We show that antagonistic coevolution will occur between genes and culture whenever cultural fitness is not perfectly aligned with genetic fitness, as genetic selection will shape psychological mechanisms to avoid susceptibility to cultural traits that bear a genetic fitness cost. We discuss the difficulties with conceptualizing cultural change using the framework of evolutionary theory, the degree to which cultural evolution is autonomous from genetic evolution, and the extent to which cultural change should be seen as a Darwinian process. We argue that the nonselection components of evolutionary change are much more important for culture than for genes, and that this and other important differences from the genetic case mean that different approaches and emphases are needed for cultural than genetic processes.     

Developmental objections to evolutionary modularity

Evolutionary psychologists argue that selective pressures in our ancestral environment yield a highly specialized set of modular cognitive capacities. However, recent papers in developmental psychology and neuroscience claim that evolutionary accounts of modularity are incompatible with the flexibility and plasticity of the developing brain. Instead, they propose cortical and neuronal brain structures are fixed through interactions with our developmental environment. Buller and Gray Hardcastle contend that evolutionary accounts of cognitive development are unacceptably rigid in light of evidence of cortical plasticity. The developing structure of the brain is both too random and too sensitive to external stimuli to be the product of a fixed genetic mechanism. They also claim that the complexity of the human brain cannot be explained in terms of our meager genetic endowment. There simply are not enough genes to program the intricate neuronal structures that are essential to cognition. I argue that neither of these arguments are persuasive. Small numbers of genes can function to determine diverse phenotypical outcomes through evolutionarily selected developmental systems. Similarly, theories of modularity do not rule out the possibility that innate cognitive systems exploit environmental regularities to guide the developing structure of the brain. Consequently, the anti-adaptionist consequences of these positions should be rejected.     

Might there be a medical conscience?

I defend the feasibility of a medical conscience in the following sense: a medical professional can object to the prevailing medical norms because they are incorrect as medical norms. In other words, I provide an account of conscientious objection that makes use of the idea that the conscience can issue true normative claims, but the claims in question are claims about medical norms rather than about general moral norms. I further argue that in order for this line of reasoning to succeed, there needs to be an internal morality of medicine that determines what medical professionals ought to do qua medical professionals. I utilize a constructivist approach to the internal morality of medicine and argue that medical professionals can conscientiously object to providing treatment X, if providing treatment X is not in accordance with norms that would have been constructed, in light of the end of medicine, by the appropriate agents under the appropriate conditions.     

Mad2 and spindle assembly checkpoint function during meiosis I in mammalian oocytes

During mammalian mitosis, a proofreading network called the spindle assembly checkpoint (SAC) is indispensable for ensuring the fidelity of chromosome segregation. An inhibitory SAC signal is deputed to inhibits mitotic cell-cycle progression in response to misaligned chromosomes until such imperfections are rectified thereby ensuring equitable chromosome partitioning to daughter cells. Amongst the cast of SAC proteins, mitotic arrest deficient 2 (Mad2) plays a leading role in transducing the SAC signal. The aneuploidy and cancer predispositions of individuals who harbour genetic mutations in SAC genes emphasise the in vivo significance of this surveillance mechanism. In humans, congenital aneuploidies such as Down's syndrome demonstrate an exponential increase with advancing female age. Although largely the result of female meiosis I errors, the molecular entities that succumb with age in oocytes remain elusive. Declining oocyte SAC function could plausibly contribute to such errors. Until recently however, convincing evidence for a functional SAC in mammalian oocytes during meiosis I was unforthcoming. Here I review the evidence regarding the SAC in female mammalian meiosis I and how our understanding of this system has evolved in recent years. This review will focus on Mad2 as this is the SAC protein that has been most comprehensively investigated.     

Adaptation and Moral Realism

Conventional wisdom has it that evolution makes a sham of morality, even if morality is an adaptation. I disagree. I argue that our best current adaptationist theory of meaning offers objective truth conditionsfor signaling systems of all sorts. The objectivity is, however, relative to species – specifically to the adaptive history of the signaling system in question. While evolution may not provide the kind of species independent objective standards that (e.g.) Kantians desire, this should be enough for the practical work of justifying our confidence in the objectivity of moral standards. If you believe morality is an adaptation, you should be a moral realist.     

Agential autonomy and biological individuality

What is a biological individual? How are biological individuals individuated? How can we tell how many individuals there are in a given assemblage of biological entities? The individuation and differentiation of biological individuals are central to the scientific understanding of living beings. I propose a novel criterion of biological individuality according to which biological individuals are autonomous agents. First, I articulate an ecological–dynamical account of natural agency according to which, agency is the gross dynamical capacity of a goal-directed system to bias its repertoire to respond to its conditions as affordances. Then, I argue that agents or agential dynamical systems can be agentially dependent on, or agentially autonomous from, other agents and that this agential dependence/autonomy can be symmetrical or asymmetrical, strong or weak. Biological individuals, I propose, are all and only those agential dynamical systems that are strongly agentially autonomous. So, to determine how many individuals there are in a given multiagent aggregate, such as multicellular organism, a colony, symbiosis, or a swarm, we first have to identify how many agential dynamical systems there are, and then what their relations of agential dependence/autonomy are. I argue that this criterion is adequate to the extent that it vindicates the paradigmatic cases, and explains why the paradigmatic cases are paradigmatic, and why the problematic cases are problematic. Finally, I argue for the importance of distinguishing between agential and causal dependence and show the relevance of agential autonomy for understanding the explanatory structure of evolutionary developmental biology.     

Kant on epigenesis, monogenesis and human nature: the biological premises of anthropology

The aim of this paper is to show that for Kant, a combination of epigenesis and monogenesis is the condition of possibility of anthropology as he conceives of it and that moreover, this has crucial implications for the biological dimension of his account of human nature. More precisely, I begin by arguing that Kant's conception of mankind as a natural species is based on two premises: firstly the biological unity of the human species (monogenesis of the human races); and secondly the existence of 'seeds' which may or may not develop depending on the environment (epigenesis of human natural predispositions). I then turn to Kant's account of man's natural predispositions and show that far from being limited to the issue of races, it encompasses unexpected human features such as gender, temperaments and nations. These predispositions, I argue, are means to the realisation of Nature's overall purpose for the human species. This allows me to conclude that man's biological determinism leads to the species' preservation, cultivation and civilisation.