Causal Control and Genetic Causation (original) (raw)
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Code or cause? Genetic information as influence
The notion of biological “information” has been at the center of a vivacious debate in which different tools coming from various disciplines (linguistics, semiotics, information theory) have been used in order to make sense of a family of intuitions concerning biological heredity, species-specificity and sexual reproduction. The connection between the concept of information and genes has been inaugurated by Francis Crick with his formulation of the so called “Central Dogma” and the “Sequence Hypothesis”. However, historically the use of the term “information” in biology traces back to Weismann (Maynard Smith; 2000:181-182) and is also present in the work of scientist-philosophers such as Erwin Schroedinger and Jacques Monod. The actual philosophical debate around the adequacy of the information paradigm in representing genetic phenomena focuses on its epistemological status (metaphor, model or description of the real state of affairs) as well as on its heuristic validity. Beyond detractors and supporters of the notion of information in biology, there are however scholars assuming a somewhat intermediate position which legitimates only some notions of the term information in connection to biology, while others consider any notion legitimate as long as it is used consistently (Godfrey-Smith 2007, Godfrey-Smith and Sterelny, 2008). Whereas in physics the notion of information tends to be ontologically committed (see for instance its role in the debate on the time-arrow: Progogine and Stengers, 1988), philosophers of biology are increasingly proposing deflationary accounts of biological/genetic information in that they reduce it to causality (Boniolo, 2008, Boniolo 2003, Wilkins forthcoming, Weber 2006, Šustar 2007). The purpose of this paper is to test the explanatory power of the deflationary accounts of the notion of information in biology in order to verify whether they succeed in their attempt and, if so, whether some of them fares better than the others and why. As it will come out, a simple reduction of the concept of information to that of causal efficiency is little more illuminating, if at all, than the idea of information itself. Instead, the notion of causation as influence, developed by David Lewis (2000) and recruited by contemporary philosophers of science such as Ken Waters (2007) and Jim Woodward (2010), succeeds in providing a non-trivial reductionist account of the notion of genetic information with a relevant explanatory power.
Genes, Causation and Intentionality
History and Philosophy of the Life Sciences, 2005
I want to exhibit the deeper metaphysical reasons why some common ways of describing the causal role of genes in development and evolution are problematic. Specifically, I show why using the concept of information in an intentional sense in genetics is inappropriate, even given a naturalistic account of intentionality. Furthermore, I argue that descriptions that use notions such as programming, directing or orchestrating are problematic not for empirical reasons, but because they are not strictly causal. They are intentional. By contrast, other notions that are part of the received view in genetics and evolutionary theory are defensible if understood correctly, in particular the idea that genes are the main replicators in evolution.
On Gene's Action and Reciprocal Causation
Foundation of Science, 2011
Advancing the reductionist conviction that biology must be in agreement with the assumptions of reductive physicalism (the upward hierarchy of causal powers, the upward fixing of facts concerning biological levels) A. Rosenberg argues that downward causation is ontologically incoherent and that it comes into play only when we are ignorant of the details of biological phenomena. Moreover, in his view, a careful look at relevant details of biological explanations will reveal the basic molecular level that characterizes biological systems, defined by wholly physical properties, e.g., geometrical structures of molecular aggregates (cells). In response, we argue that contrary to his expectations one cannot infer reductionist assumptions even from detailed biological explanations that invoke the molecular level, as interlevel causal reciprocity is essential to these explanations. Recent very detailed explanations that concern the structure and function of chromatin—the intricacies of supposedly basic molecular level—demonstrate this. They show that what seem to be basic physical parameters extend into a more general biological context, thus rendering elusive the concepts of the basic level and causal hierarchy postulated by the reductionists. In fact, relevant phenomena are defined across levels by entangled, extended parameters. Nor can the biological context be explained away by basic physical parameters defining molecular level shaped by evolution as a physical process. Reductionists claim otherwise only because they overlook the evolutionary significance of initial conditions best defined in terms of extended biological parameters. Perhaps the reductionist assumptions (as well as assumptions that postulate any particular levels as causally fundamental) cannot be inferred from biological explanations because biology aims at manipulating organisms rather than producing explanations that meet the coherence requirements of general ontological models. Or possibly the assumptions of an ontology not based on the concept of causal powers stratified across levels can be inferred from biological explanations. The incoherence of downward causation is inevitable,
Forthcoming in: C. Kenneth Waters and James Woodward (eds.), Philosophical Perspectives on Causal Reasoning in Biology. Minnesota Studies in the Philosophy of Science Vol. XXI. Minneapolis: University of Minnesota Press, 2013
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.
Causal Specificity, Biological Possibility and Non-parity about Genetic Causes
Several authors have used the notion of causal specificity in order to defend non-parity about genetic causes (Waters 2007, Woodward 2010, Weber 2017, forthcoming). Non-parity in this context is the idea that DNA and some other biomolecules that are often described as information-bearers by biologists play a unique role in life processes, an idea that has been challenged by Developmental Systems Theory (e.g., Oyama 2000). Indeed, it has proven to be quite difficult to state clearly what the alleged special role of genetic causes consists in. In this paper, I show that the set of biomolecules that are normally considered to be information-bearers (DNA, mRNA) can be shown to be the most specific causes of protein primary structure, provided that causal specificity is measured over a relevant space of biological possibilities, disregarding physical as well as logically possible states of the causal variables.
Rethinking the Meaning of Biological Information
2010
We are grateful to the commentators for taking the time to respond to our article. Too many interesting and important points have been raised for us to tackle them all in this response, and so in the below we have sought to draw out the major themes. These include problems with both the term 'ultimate causation' and the proximate-ultimate causation dichotomy more generally, clarification of the meaning of reciprocal causation, discussion of issues related to the nature of development and phenotypic plasticity and their roles in evolution, and consideration of the need for an extended evolutionary synthesis.
Griffiths and Stotz’s Genetics and Philosophy: An Introduction offers a very good overview of scientific and philosophical issues raised by present-day genetics. Examining, in particular, the questions of how a “gene” should be defined and what a gene does from a causal point of view, the authors explore the different domains of the life sciences in which genetics has come to play a decisive role, from Mendelian genetics to molecular genetics, behavioural genetics, and evolution. In this review, I highlight what I consider as the two main theses of the book, namely: i) genes are better conceived as tools; ii) genes become causes only in a context. I situate these two theses in the wider perspective of developmental systems theory (DST). This leads me to emphasize that Griffiths and Stotz reflect very well an on going process in genetics, which I call the “epigenetization” of genetics, i.e., the growing interest in the complex processes by which gene activation is regulated. I then make a factual objection, which is that Griffiths and Stotz have almost entirely neglected the perspective of ecological developmental biology, and more precisely recent work on developmental symbioses, and I suggest that this omission is unfortunate in so far as an examination of developmental symbioses would have considerably strengthened Griffiths and Stotz’s own conclusions.
Biological functions are causes, not effects: A critique of selected effects theories
Studies in History and Philosophy of Science, 2024
The theory of Selected Effects (SE) is currently the most widely accepted etiological account of function in biology. It argues that the function of any trait is the effect that past traits of that type produced that contributed to its current existence. Its proper or etiological function is whatever effect was favoured by natural selection irrespective of the trait's current effects. By defining function with respect to the effects of natural selection, the theory claims to eschew the problem of backwards causality and to ground functional normativity on differential reproduction or differential persistence. Traditionally, many have criticised the theory for its inability to envisage any function talk outside selective reproduction, for failing to account for the introduction of new functions, and for treating function as epiphenomenal. This article unveils four additional critiques of the SE theory that highlight the source of its critical problems. These critiques follow from the fact that natural selection is not a form of work, but a passive filter that merely blocks or permits prior functioning traits to be reproduced. Natural selection necessarily assumes the causal efficacy of prior organism work to produce the excess functional traits and offspring from which only the best fitted will be preserved. This leads to four new incapacities of the SE theory, which will be here analysed: (i) it provides no criterion for determining what distinguishes a proper from an incidental function; (ii) it cannot distinguish between neutral, incidental, and malfunctioning traits, thus treating organism benefit as irrelevant; (iii) it fails to account for the physical work that makes persistence and reproduction possible, and (iv) in so doing, it falls into a vicious regress. We conclude by suggesting that, inspired by Mills and Beatty's propensity interpretation, the aporia of backward causation implicit in anticipatory accounts of function can also be avoided by a dispositional approach that defines function in terms of work that synchronously counters the ubiquitous tendency for organism entropy to increase in the context of far-fromequilibrium thermodynamics.
From Biological Determination to Entangled Causation
Acta Biotheoretica, regular article, 2019
Biologists and philosophers often use the language of determination in order to describe the nature of developmental phenomena. Accounts in terms of determination have often been reductionist. One common idea is that DNA is supposed to play a special explanatory role in developmental explanations, namely, that DNA is a developmental determinant. In this article we try to make sense of determination claims in developmental biology. Adopting a manipulationist approach, we shall first argue that the notion of developmental determinant is causal. We suggest that two different theses concerning developmental determination can be articulated: determination of occurrence and structural determination. We shall argue that, while the first thesis is problematic, the second, opportunely qualified, is feasible. Finally, we shall argue that an analysis of biological causation in terms of determination cannot account for entangled dynamics. Characterising causal entanglement as a particular kind of interactive causation whereby difference-making causes ascribable to different levels of biological organisation influence a particular ontogenetic outcome, we shall, via two illustrative examples, diagnose some potential limits of a reductionist, molecular and intra-level understanding of biological causation.