We describe an approach to measuring biological information where ‘information’ is understood in the sense found in Francis Crick’s foundational contributions to molecular biology. Genes contain information in this sense, but so do epigenetic factors, as many biologists have recognized. The term ‘epigenetic’ is ambiguous, and we introduce a distinction between epigenetic and exogenetic inheritance to clarify one aspect of this ambiguity. These three heredity systems play complementary roles in supplying information for development. -/- We then consider the evolutionary significance (...) of the three inheritance systems. Whilst the genetic inheritance system was the key innovation in the evolution of heredity, in modern organisms the three systems each play important and complementary roles in heredity and evolution. -/- Our focus in the earlier part of the paper is on ‘proximate biology’, where information is a substantial causal factor that causes organisms to develop and causes offspring to resemble their parents. But much philosophical work has focused on information in ‘ultimate biology’. Ultimate information is a way of talking about the evolutionary design of the mechanisms of development and inheritance. We conclude by clarifying the relationship between the two. Ultimate information is not a causal factor that acts in development or heredity, but it can help to explain the evolution of proximate information, which is. (shrink)

Griffiths et al. (2015) have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.

The discovery of RNA interference in 1998 has made a lasting impact on biological research. Identifying the regulatory role of small RNAs changed the modes of molecular biological inquiry as well as biologists' understanding of genetic regulation. This article examines the early years of small RNA biology's success story. I query which factors had to come together so that small RNA research came into life in the blink of an eye. I primarily look at scientific repertoires as facilitators of rapid (...) scientific change. I show that for a short period of time, between the years 1998 and 2002, different model organism communities, investigative strategies, technological innovations, and research interests could be successfully aligned to take small RNA research off the ground. I discuss how the keystone discoveries were situated in specific experimental traditions and what strategies were employed to establish these discoveries as more general phenomena. Providing thus a practice-based approach of rapid scientific change, I ask how to relate the change in propositional bits of scientific knowledge with changes in scientific practice. (shrink)

A central idea of developmental systems theory is ‘parity’ or ‘symmetry’ between genes and non-genetic factors of development. The precise content of this idea remains controversial, with different authors stressing different aspects and little explicit comparisons among the various interpretations. Here I characterise and assess several influential versions of parity.

The philosophy of biology literature offers several arguments aimed at showing that information theory is conceptually unsuited to capture the informational talk in molecular biology. Such arguments led to the consensus that, if the informational talk in biology can be defended and explained at all, we need a different strategy. The debate, in fact, developed mostly along this line. However, recent contributions seem to (and even claim to) challenge the consensus and thus to vindicate the role and relevance of information (...) theory to this particular debate. In this paper, I examine the main arguments leading to such a consensus and I analyze the extent to which those recent accounts actually succeed in vindicating the invocation of information theory. I argue that these attempts fail to vindicate the information-theoretic strategy and, therefore, the consensus remains unaffected by them. (shrink)

Recent philosophical work on causation has focused on distinctions across types of causal relationships. This paper argues for another distinction that has yet to receive attention in this work. This distinction has to do with whether causal relationships have “material continuity,” which refers to the reliable movement of material from cause to effect. This paper provides an analysis of material continuity and argues that causal relationships with this feature are associated with a unique explanatory perspective, are studied with distinct causal (...) investigative methods, and provide different types of causal control over their effects. (shrink)

The status of genes as bearers of semantic content remains very much in dispute among philosophers of biology. In a series of papers, Nicholas Shea has argued that his ‘infotel’ theory of semantics vindicates the claim that genes carry semantic content. On Shea’s account, each organism is associated with a ‘developmental system’ that takes genetic representations as inputs and produces whole-organism traits as outputs. Moreover, at least in his most recent work on the topic, Shea is explicit in claiming that (...) these genetic representations are ‘read in ontogenetic time, in the course of individual development’. Here I argue that a close examination of the process of reading, in Shea’s sense, reveals that acts of reading do not actually occur over the course of developmental time at all. To make this vivid, I contrast the process of reading for Shea with another type of developmental process that is widely seen as a form of reading directed on inherited genes, and which certainly does occur over the course of developmental time, namely, gene expression. I suggest that this error in Shea’s thinking can be traced back to an equivocation on Shea’s part in the meaning of ‘reads’, and also to a reliance on an invalid principle regarding the transference of representational content from one token gene to another. The issues at play are bound up with questions about causation and in particular about causation over time. Thus, having first presented my arguments in a way that doesn’t depend on any particular theory of causation, I then make use of Kenneth Waters’ framework of difference-making causation to conceptually sharpen and shed further light on matters. I conclude by discussing a consequence of the fact that acts of reading do not occur in development. 1 Introduction2 Reading for Shea3 Gene Expression as Reading4 Are Genetic Representations Read in Development? Part 15 The Manipulability Theory of Causation and Difference-Making Causation6 Are Genetic Representations Read in Development? Part 27 Conclusion. (shrink)

The distinction between perception and cognition has always had a firm footing in both cognitive science and folk psychology. However, there is little agreement as to how the distinction should be drawn. In fact, a number of theorists have recently argued that, given the ubiquity of top-down influences, we should jettison the distinction altogether. I reject this approach, and defend a pluralist account of the distinction. At the heart of my account is the claim that each legitimate way of marking (...) a border between perception and cognition deploys a notion I call ‘stimulus-control.’ Thus, rather than being a grab bag of unrelated kinds, the various categories of the perceptual are unified into a superordinate natural kind. (shrink)

I argue that we can visually perceive others as seeing agents. I start by characterizing perceptual processes as those that are causally controlled by proximal stimuli. I then distinguish between various forms of visual perspective-taking, before presenting evidence that most of them come in perceptual varieties. In doing so, I clarify and defend the view that some forms of visual perspective-taking are “automatic”—a view that has been marshalled in support of dual-process accounts of mindreading.

Perceptual processes differ from cognitive, this paper argues, in functioning to be causally controlled by proximal stimuli, and being modular, at least in a modest sense that excludes their being isotropic in Jerry Fodor's sense. This claim agrees with such theorists as Jacob Beck and Ben Phillips that a function of stimulus-control is needed for perceptual status. In support of this necessity claim, I argue, inter alia, that E.J. Green's recent architectural account misclassifies processes deploying knowledge of grammar as perceptual. (...) _Pace_ Beck and Phillips, however, I argue a function of stimulus-control is insufficient for perceptual as opposed to cognitive status. One consideration in favour of such insufficiency, noted but (I argue) not convincingly rebutted by these theorists, concerns perpetually grounded demonstrative thought. Two other considerations trade on the fact that a function of stimulus-control can arise not from blind nature but intentional design or social institutions, where so-functioning processes may but need not be perceptual. I offer two cases where such processes are cognitive, viz. skilful play-by-play announcing of ongoing events, and voluntary visualizing of ongoing events under the guidance of apt play-by-play announcements, dubbed announcement-driven visualizing (ADV). The cognitive status of these three diverse phenomena cannot be explained by an absence of a perception-like representational format or content (for ADV has such) or by a presence of personal-level mental states causally mediating between stimuli and outputs (for perception has such). A bettter explanation invokes, I argue, the non-modular character of the generating process. (shrink)

Minimal genetic pre-formationism is defended, in that primacy is ascribed to DNA in the structuring of molecules through molecular codes. This together with the importance of such codes for stability and variation in living systems makes DNA categorically different from other causal factors. It is argued that post-transcriptional and post-translational processing in protein synthesis does not rob DNA of this structuring role. Notions of structuring causal powers that may vary in degree, of arbitrary molecular codes that are more or less (...) realized, of partial templating and of genetic information as a subspecies of mechanistic information are brought in to support this and to rival causal and semantic notions of information. It is concluded that the primacy of genes in their structuring of molecules goes together with parity between genes and non-genetic causal factors in regulation of living systems. This is seen to hold independently of the radical reconceptualization of organism cum environment that has been suggested in developmental systems theory. (shrink)

This article considers the popular thesis that a more proportional relationship between a cause and its effect yields a more abstract causal explanation of that effect, which in turn produces a deeper explanation. This thesis is taken to have important implications for choosing the optimal granularity of explanation for a given explanandum. In this article, I argue that this thesis is not generally true of probabilistic causal relationships. In light of this finding, I propose a pragmatic, interest-relative measure of explanatory (...) depth. This measure uses a decision-theoretic model of information pricing to determine the optimal granularity of explanation for a given explanandum, agent, and decision problem. (shrink)

In cases in which many causes together bring about an effect, it is common to select some as particularly important. Philosophers since Mill have been pessimistic about analyzing this reasoning because of its variability and the multifarious causal and pragmatic details of how it works. I argue Mill was right to think these details matter but wrong that they preclude philosophical analysis of causal selection. I show that analyzing the pragmatic details of scientific debates about the important causes of the (...) Bhopal Gas Tragedy can illuminate causal reasoning about disasters and shed new light on causality and causal selection. (shrink)

Even though complexity is a concept that is ubiquitously used by biologists and philosophers of biology, it is rarely made precise. I argue that a clarification of the concept is neither trivial nor unachievable, and I propose a unifying framework based on the technical notion of “effective complexity” that allows me to do justice to conflicting intuitions about biological complexity, while taking into account several distinctions in the usage of the concept that are often overlooked. In particular, I propose a (...) distinction between two kinds of complexity, “mechanical” and “emergent”, which can be understood as different ways of relating the effective complexity of mechanisms and of behaviors in biological explanations. I illustrate the adequacy of this framework by discussing different attempts to understand intracellular organization in terms of pathways and networks. My framework provides a different way of thinking about recent philosophical debates, for example, on the difference between mechanistic and topological explanations and about the concept of emergence. Moreover, it can contribute to a proper assessment of metascientific arguments that invoke biological complexity. (shrink)

The interventionist account of causal explanation, in the version presented by Jim Woodward, has been recently claimed capable of buttressing the widely felt—though poorly understood—hunch that high-level, relatively abstract explanations, of the sort provided by sciences like biology, psychology and economics, are in some cases explanatorily optimal. It is the aim of this paper to show that this is mistaken. Due to a lack of effective constraints on the causal variables at the heart of the interventionist causal-explanatory scheme, as presently (...) formulated it is either unable to prefer high-level explanations to low, or systematically overshoots, recommending explanations at so high of a level as to be virtually vacuous. (shrink)

The concept of causal specificity is drawing considerable attention from philosophers of biology. It became the rationale for rejecting (and occasionally, accepting) a thesis of causal parity of developmental factors. This literature assumes that attributing specificity to causal relations is at least in principle a straightforward (if not systematic) task. However, the parity debate in philosophy of biology seems to be stuck at a point where it is not the biological details that will help move forward. In this paper, I (...) take a step back to reexamine the very idea of causal specificity and its intended role in the parity dispute in philosophy of biology. I contend that the idea of causal specificity across variations as currently discussed in the literature is irreducibly twofold in nature: it is about two independent components that are not mutually entailed. I show this to be the source of prior complications with the notion of specificity itself that ultimately affect the purposes for which it is often invoked, notably to settle the parity dispute. (shrink)

This article reconsiders the theoretical role of the genetic code. By drawing on published and unpublished sources from the 1950s, I analyse how the code metaphor was actually employed by the scientists who first promoted its use. The analysis shows that the term ‘code’ picked out mechanism sketches, consisting of more or less detailed descriptions of ordinary molecular components, processes, and structural properties of the mechanism of protein synthesis. The sketches provided how-possibly explanations for the ordering of amino acids by (...) nucleic acids. I argue that employing the code metaphor was justified in virtue of its descriptive-denotational and explanatory roles, and because it highlighted a similarity with conventional codes that was particularly salient at the time. 1 Introduction2 Coding Schemes in the 1950s2.1 The research problem: Determining amino acid sequences2.2 The solution: Mapping schemes or ‘codes’3 The Code Metaphor Played Descriptive and Explanatory Roles4 Theness of Codes and the Expendability of the Code Metaphor5 The Role of Arbitrariness6 Conclusions. (shrink)

The concept of regulation pervades biology, for example in models of genetic regulatory networks and the endocrine system. Regulation has a normative opposite, dysregulation, which figures prominently in biomedical models of disease. The use of normative concepts in biology, however, has been thought to present some challenges for the physicalist view of the world, and various resolutions have been proposed. Up to now the problem of biological normativity has been debated largely in connection with the concept of biological information. In (...) this paper we shift focus to the concept of biological regulation, proposing that it provides a promising new approach to these issues. Models of regulatory systems have several features: they are causal, but they do not deal with the energy exchanges and transformations covered by physics and chemistry; further, and entirely connected, regulatory systems can break down, and this is because they and their causal-regulatory properties are dependent on fragile molecular structures. Biological regulatory systems exhibit normativity, because they are not determined by physical and chemical laws, but their close relationship with physical laws and physicalist ontology is transparent. (shrink)

According to the proponents of Developmental Systems Theory and the Causal Parity Thesis, the privileging of the genome as “first among equals” with respect to the development of phenotypic traits is more a reflection of our own heuristic prejudice than of ontology - the underlying causal structures responsible for that specified development no more single out the genome as primary than they do other broadly “environmental” factors. Parting with the methodology of the popular responses to the Thesis, this paper offers (...) a novel criterion for ‘causal primacy’, one that is grounded in the ontology of the unique causal role of dispositional properties. This paper argues that, if the genome is conceptualised as realising dispositional properties that are “directed toward” phenotypic traits, the parity of ‘causal roles’ between genetic and extra-genetic factors is no longer apparent, and further, that the causal primacy of the genome is both plausible and defensible. (shrink)

The biological sciences have always proven a fertile ground for philosophical analysis, one from which has grown a rich tradition stemming from Aristotle and flowering with Darwin. And although contemporary philosophy is increasingly becoming conceptually entwined with the study of the empirical sciences with the data of the latter now being regularly utilised in the establishment and defence of the frameworks of the former, a practice especially prominent in the philosophy of physics, the development of that tradition hasn’t received the (...) wider attention it so thoroughly deserves. This review will briefly introduce some recent significant topics of debate within the philosophy of biology, focusing on those whose metaphysical themes (in everything from composition to causation) are likely to be of wide-reaching, cross-disciplinary interest. (shrink)

Both biosemiotics and evolutionary epistemology are concerned with how knowledge evolves. (Applied) Evolutionary Epistemology thereby focuses on identifying the units, levels, and mechanisms or processes that underlie the evolutionary development of knowing and knowledge, while biosemiotics places emphasis on the study of how signs underlie the development of meaning. We compare the two schools of thought and analyze how in delineating their research program, biosemiotics runs into several problems that are overcome by evolutionary epistemologists. For one, by emphasizing signs, biosemiotics (...) needs to delineate a semiotic threshold, which is a problem not encountered by evolutionary epistemologists. Instead, the latter recognizes that all organisms are knowers that evolve knowledge, which they recognize to extend toward phenomena produced by organisms such as behavior, cognition, language, culture, science, and technology. Secondly, biosemiotics attempts at continuing adaptationist notions on how organisms relate to their environment, while especially Applied Evolutionary Epistemology comes to redefine the nature of the organism–environment relationship in such a way that it recognizes the spatiotemporal boundedness of existence, which in turn makes adaptationist accounts obsolete. (shrink)

This PhD dissertation examines the conceptual and theoretical foundations of the most general and most widely used framework for understanding social evolution, W. D. Hamilton's theory of kin selection. While the core idea is intuitive enough (when organisms share genes, they sometimes have an evolutionary incentive to help one another), its apparent simplicity masks a host of conceptual subtleties, and the theory has proved a perennial source of controversy in evolutionary biology. To move towards a resolution of these controversies, we (...) need a careful and rigorous analysis of the philosophical foundations of the theory. My aim in this work is to provide such an analysis. I begin with an examination of the concepts behavioural ecologists employ to describe and classify types of social behaviour. I stress the need to distinguish concepts that are often conflated: for example, we need to distinguish simple cooperation from collaboration in collective tasks, behaviours from strategies, and control from manipulation and coercion. I proceed from here to the formal representation of kin selection via George R. Price’s covariance selection mathematics. I address a number of interpretative issues the Price formalism raises, including the vexed question of whether kin selection theory is ‘formally equivalent’ to multi-level selection theory. In the second half of the dissertation, I assess the uses and limits of Hamilton’s rule for the evolution of social behaviour; I provide a precise statement of the conditions under which the rival neighbour-modulated fitness and inclusive fitness approaches in contemporary kin selection theory are equivalent (and describe cases in which they are not); and I criticize recent formal attempts to establish the controversial claim that kin selection leads to organisms behaving as if maximizing their inclusive fitness. (shrink)

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. This paper is (...) concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

This dissertation aims to determine the optimal level of granularity for the variables used in probabilistic causal models. These causal models are useful for generating explanations in a number of scientific contexts. In Chapter 1, I argue that there is rarely a unique level of granularity at which a given phenomenon can be causally explained, thereby rejecting various causal exclusion arguments. In Chapter 2, I consider several recent proposals for measuring the explanatory power of causal explanations, and show that these (...) measures fail to track the comparative depth of explanations given at different levels of granularity. In Chapter 3, I offer a pragmatic account of how to partition the measure space of a causal variable so as to optimally explain its effect. My account uses the decision-theoretic notion of value of information, and indexes the relative depth of an explanation to a particular agent faced with a particular decision problem. Chapter 4 applies this same decisiontheoretic framework to answer the epistemic question of how to discover constitutive relationships in nature. In Chapter 5, I describe the formal details of the relationship between random variables that are meant to be coarse-grained and fine-grained representations of the same type of phenomenon. I use this formal framework to rebut a popular argument for the view that special science probabilities can be objective chances. Chapter 6 discusses challenges related to the causal interpretation of Bayes nets that use imprecise rather than precise probabilities. (shrink)

We propose a novel account of the distinction between innate and acquired biological traits: biological traits are innate to the degree that they are caused by factors intrinsic to the organism at the time of its origin; they are acquired to the degree that they are caused by factors extrinsic to the organism. This account borrows from recent work on causation in order to make rigorous the notion of quantitative contributions to traits by different factors in development. We avoid the (...) pitfalls of previous accounts and argue that the distinction between innate and acquired traits is scientifically useful. We therefore address not only previous accounts of innateness but also skeptics about any account. The two are linked, in that a better account of innateness also enables us better to address the skeptics. (shrink)

Griffiths et al. have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.