Organization figures centrally in the understanding of biological systems advanced by both new mechanists and proponents of the autonomy framework. The new mechanists focus on how components of mechanisms are organized to produce a phenomenon and emphasize productive continuity between these components. The autonomy framework focuses on how the components of a biological system are organized in such a way that they contribute to the maintenance of the organisms that produce them. In this paper we analyze and compare these two (...) accounts of organization and argue that understanding biological organisms as cohesively integrated systems benefits from insights from both. To bring together the two accounts, we focus on the notions of control and regulation as bridge concepts. We start from a characterization of biological mechanisms in terms of constraints and focus on a specific type of mechanism, control mechanisms, that operate on other mechanisms on the basis of measurements of variables in the system and its environment. Control mechanisms are characterized by their own set of constraints that enable them to sense conditions, convey signals, and effect changes on constraints in the controlled mechanism. They thereby allow living organisms to adapt to internal and external variations and to coordinate their parts in such a manner as to maintain viability. Because living organisms contain a vast number of control mechanisms, a central challenge is to understand how they are themselves organized. With the support of examples from both unicellular and multicellular systems we argue that control mechanisms are organized heterarchically, and we discuss how this type of control architecture can, without invoking top-down and centralized forms of organizations, succeed in coordinating internal activities of organisms. (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)

Functional robustness refers to a system’s ability to maintain a function in the face of perturbations to the causal structures that support performance of that function. Modularity, a crucial element of standard methods of causal inference and difference-making accounts of causation, refers to the independent manipulability of causal relationships within a system. Functional robustness appears to be at odds with modularity. If a function is maintained despite manipulation of some causal structure that supports that function, then the relationship between that (...) structure and function fails to be manipulable independent of other causal relationships within the system. Contrary to this line of reasoning, I argue that functional robustness often attends feedback control, rather than failures of modularity. Feedback control poses its own challenges to causal explanation and inference, but those challenges do not undermine modularity—and indeed, modularity is crucial to grappling with them. (shrink)

This article demonstrates that non-mechanistic, dynamical explanations are a viable approach to explanation in the special sciences. The claim that dynamical models can be explanatory without reference to mechanisms has previously been met with three lines of criticism from mechanists: the causal relevance concern, the genuine laws concern, and the charge of predictivism. I argue, however, that these mechanist criticisms fail to defeat non-mechanistic, dynamical explanation. Using the examples of Haken et al.’s model of bimanual coordination, and Thelen et al.’s (...) dynamical field model of infant perseverative reaching, I show how each mechanist criticism fails once the standards of Woodward’s interventionist framework are applied to dynamical models. An even-handed application of Woodwardian interventionism reveals that dynamical models are capable of producing genuine explanations without appealing to underlying mechanistic details. 1Introduction2Interventionism and Mechanistic Explanation 2.1Causal relevance and ideal interventions2.2Invariance2.3Explanation3Covering-Laws and Dynamical Explanation 3.1Dynamical models3.2Covering-law explanation3.3Prediction4Causal Relevance 4.1The causal relevance concern4.2Intervening on dynamical models4.3Test case I: The Haken–Kelso–Bunz model4.4Test case II: Dynamical field model5Genuine Laws 5.1The genuine laws concern5.2Using invariance in place of laws5.3Test case I: The Haken–Kelso–Bunz model5.4Test case II: Dynamical field model6Prediction 6.1Predictivism6.2Crude and invariant prediction7Interventionist Criticism of the Haken–Kelso–Bunz Model8Dynamical Explanation8Conclusion. (shrink)

I propose a dynamic causal approach to characterizing the notion of a mechanism. Levy and Bechtel, among others, have pointed out several critical limitations of the new mechanical philosophy, and pointed in a new direction to extend this philosophy. Nevertheless, they have not fully fleshed out what that extended philosophy would look like. Based on a closer look at neuroscientific practice, I propose that a mechanism is a dynamic causal system that involves various components interacting, typically nonlinearly, with one another (...) to produce a phenomenon of interest. (shrink)

Mechanistic explanations are often said to explain because they reveal the causal structure of the world. Conversely, dynamical models supposedly lack explanatory power because they do not describe causal structure. The only way for dynamical models to produce causal explanations is via the 3M criterion: the model must be mapped onto a mechanism. This framing of the situation has become the received view around the viability of dynamical explanation. In this paper, I argue against this position and show that dynamical (...) models can themselves reveal causal structure and consequently produce nonmechanistic, dynamical explanations. Taking the example of cell fates from systems biology, I show how dynamical models, and specifically the attractor landscapes they describe, identify the causes of cell differentiation and explain why cells select particular fates. These dynamical features of the system better fit Woodward’s (2010, 2018) criteria of specificity and proportionality and make them the best candidate causes of cell fates than mechanisms. I also show how these causes are irreducible and inaccessible to mechanistic models, making 3M unworkable and counterproductive in this case. Dynamical models can reveal dynamical causes and thereby provide causal explanations. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge of the (...) counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (shrink)

Life scientists increasingly rely upon abstraction-based modeling and reasoning strategies for understanding biological phenomena. We introduce the notion of constraint-based reasoning as a fruitful tool for conceptualizing some of these developments. One important role of mathematical abstractions is to impose formal constraints on a search space for possible hypotheses and thereby guide the search for plausible causal models. Formal constraints are, however, not only tools for biological explanations but can be explanatory by virtue of clarifying general dependency-relations and patterning between (...) functions and structures. We describe such situations as constraint-based explanations and argue that these differ from mechanistic strategies in important respects. While mechanistic explanations emphasize change-relating causal features, constraint-based explanations emphasize formal dependencies and generic organizational features that are relatively independent of lower-level changes in causal details. Our distinction between mechanistic and constraint-based explanations is pragmatically motivated by the wish to understand scientific practice. We contend that delineating the affordances and assumptions of different explanatory questions and strategies helps to clarify tensions between diverging scientific practices and the innovative potentials in their combination. Moreover, we show how constraint-based explanation integrates several features shared by otherwise different philosophical accounts of abstract explanatory strategies in biology. (shrink)

We outline a framework of multilevel neurocognitive mechanisms that incorporates representation and computation. We argue that paradigmatic explanations in cognitive neuroscience fit this framework and thus that cognitive neuroscience constitutes a revolutionary break from traditional cognitive science. Whereas traditional cognitive scientific explanations were supposed to be distinct and autonomous from mechanistic explanations, neurocognitive explanations aim to be mechanistic through and through. Neurocognitive explanations aim to integrate computational and representational functions and structures across multiple levels of organization in order to explain (...) cognition. To a large extent, practicing cognitive neuroscientists have already accepted this shift, but philosophical theory has not fully acknowledged and appreciated its significance. As a result, the explanatory framework underlying cognitive neuroscience has remained largely implicit. We explicate this framework and demonstrate its contrast with previous approaches. (shrink)

Functional decomposition is an important goal in the life sciences, and is central to mechanistic explanation and explanatory reduction. A growing literature in philosophy of science, however, has challenged decomposition-based notions of explanation. ‘Holists’ posit that complex systems exhibit context-sensitivity, dynamic interaction, and network dependence, and that these properties undermine decomposition. They then infer from the failure of decomposition to the failure of mechanistic explanation and reduction. I argue that complexity, so construed, is only incompatible with one notion of decomposition, (...) which I call ‘atomism’, and not with decomposition writ large. Atomism posits that function ascriptions must be made to parts with minimal reference to the surrounding system. Complexity does indeed falsify atomism, but I contend that there is a weaker, ‘contextualist’ notion of decomposition that is fully compatible with the properties that holists cite. Contextualism suggests that the function of parts can shift with external context, and that interactions with other parts might help determine their context-appropriate functions. This still admits of functional decomposition within a given context. I will give examples based on the notion of oscillatory multiplexing in systems neuroscience. If contextualism is feasible, then holist inferences are faulty—one cannot infer from the presence of complexity to the failure of decomposition, mechanism, and reductionism. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge of the (...) counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (shrink)

It is argued that once biological systems reach a certain level of complexity, mechanistic explanations provide an inadequate account of many relevant phenomena. In this article, I evaluate such claims with respect to a representative programme in systems biological research: the study of regulatory networks within single-celled organisms. I argue that these networks are amenable to mechanistic philosophy without need to appeal to some alternate form of explanation. In particular, I claim that we can understand the mathematical modelling techniques of (...) systems biologists as part of a broader practice of constructing and evaluating mechanism schemas. This argument is elaborated by considering the case of bacterial chemotactic networks, where some research has been interpreted as explaining phenomena by means of abstract design principles. (shrink)

Epigenetics investigates the dynamics of gene expression in various cells, and the signals from the internal and external environment affecting these dynamics. Neuroepigenetics extends this research into neurons and glia cells. Environmental-induced changes in gene expression are not only associated with the emerging structure and function of the nervous system during ontogeny, but are also fundamental to the wiring of neural circuitries responsible for learning and memory. Yet philosophers of science and neuroscience have so far paid little attention to these (...) findings. In this article, we describe some recent experimental work on the neuroepigenetics of fear and stress responses in rodents, its ingenious experimental translation into humans, and how this work seems not to be accurately described by popular “mechanist” accounts. Our final goal is to motivate broader philosophical attention to neuroepigenetics practices and findings, especially for how it considers environmentally driven and developmental plasticity in psychological explanations. (shrink)

In this essay I propose that what design principles in systems biology and systems neuroscience do is to present abstract characterizations of mechanisms, and thereby facilitate mechanistic explanation. To show this, one design principle in systems neuroscience, i.e., the multilayer perceptron, is examined. However, Braillard contends that design principles provide a sort of non-mechanistic explanation due to two related reasons: they are very general and describe non-causal dependence relationships. In response to this, I argue that, on the one hand, all (...) mechanisms are more or less general, and on the other, many design principles are causal systems. (shrink)

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)

I argue (1) that what (ontic) New Mechanistic philosophers of science call mechanisms would be material Gestalten, and (2) that Merleau-Ponty’s engagement with Gestalt theory can help us frame a standing challenge against ontic conceptions of mechanisms. In short, until the (ontic) New Mechanist can provide us with a plausible account of the organization of mechanisms as an objective feature of mind-independent ontic structures in the world which we might discover – and no ontic Mechanist has done so – it (...) is more conservative to claim that mechanistic organization is instead a mind-dependent aspect of our epistemic strategies of mechanistic explanation. (shrink)

In this article, I discuss the concept of robustness in neuroscience. Various mechanisms for making systems robust have been discussed across biology and neuroscience. Many of these notions originate from engineering. I argue that concepts borrowed from engineering aid neuroscientists in operationalizing robustness, formulating hypotheses about mechanisms for robustness, and quantifying robustness. Furthermore, I argue that the significant disanalogies between brains and engineered artifacts raise important questions about the applicability of the engineering framework. I argue that the use of such (...) concepts should be understood as a kind of simplifying idealization. (shrink)

We contend that diagrams are tools not only for communication but also for supporting the reasoning of biologists. In the mechanistic research that is characteristic of biology, diagrams delineate the phenomenon to be explained, display explanatory relations, and show the organized parts and operations of the mechanism proposed as responsible for the phenomenon. Both phenomenon diagrams and explanatory relations diagrams, employing graphs or other formats, facilitate applying visual processing to the detection of relevant patterns. Mechanism diagrams guide reasoning about how (...) the parts and operations work together to produce the phenomenon and what experiments need to be done to improve on the existing account. We examine how these functions are served by diagrams in circadian rhythm research. (shrink)

The Linda paradox is a key topic in current debates on the rationality of human reasoning and its limitations. We present a novel analysis of this paradox, based on the notion of verisimilitude as studied in the philosophy of science. The comparison with an alternative analysis based on probabilistic confirmation suggests how to overcome some problems of our account by introducing an adequately defined notion of verisimilitudinarian confirmation.

Biological processes are often explained by identifying the underlying mechanisms that generate a phenomenon of interest. I characterize a basic account of mechanistic explanation and then present three challenges to this account, illustrated with examples from molecular biology. The basic mechanistic account is insufficient for explaining nonsequential and nonlinear dynamic processes, is insufficient for explaining the inherently stochastic nature of many biological mechanisms, and fails to give a proper framework for analyzing organization. I suggest that biological processes are best approached (...) as a multidimensional gradient—with some processes being paradigmatic cases of mechanisms and some being marginal cases. (shrink)

We explore the crucial role of diagrams in scientific reasoning, especially reasoning directed at developing mechanistic explanations of biological phenomena. We offer a case study focusing on one research project that resulted in a published paper advancing a new understanding of the mechanism by which the central circadian oscillator in Synechococcus elongatus controls gene expression. By examining how the diagrams prepared for the paper developed over the course of multiple drafts, we show how the process of generating a new explanation (...) vitally involved the development and integration of multiple versions of different types of diagrams, and how reasoning about the mechanism proceeded in tandem with the development of the diagrams used to represent it. (shrink)

This paper employs an interventionist framework to elucidate some issues having to do with explanation in neurobiology and with the differences between mechanistic and non-mechanistic explanations.

Mechanistic accounts of explanation have recently found popularity within philosophy of science. Presently, we introduce the idea of an extended mechanistic explanation, which makes explicit room for the role of environment in explanation. After delineating Craver and Bechtel’s account, we argue this suggestion is not sufficiently robust when we take seriously the mechanistic environment and modeling practices involved in studying contemporary complex biological systems. Our goal is to extend the already profitable mechanistic picture by pointing out the importance of the (...) mechanistic environment. It is our belief that extended mechanistic explanations, or mechanisms that take into consideration the temporal sequencing of the interplay between the mechanism and the environment, allow for mechanistic explanations regarding a broader group of scientific phenomena. (shrink)

Since cognitive neuroscience aims at giving an integrated account of mind and brain, its ontology should include both neural and cognitive entities and specify their relations. According to what we call the standard ontological framework of cognitive neuroscience, the aim of cognitive neuroscience should be to establish one-to-one mappings between neural and cognitive entities. Where such entities do not yet closely align, this can be achieved by reforming the cognitive ontology, the neural ontology, or both. In order to assess the (...) limits and the possibilities of the SOFCN, we will examine a paradigmatic case study: the concept of Broca’s area, which indicates an alleged mapping between the left inferofrontal gyrus and the production of language. We review evidence showing that such a mapping does not hold, thus calling into question either the status of Broca’s area or the validity of the SOFCN. We then propose some strategies for addressing the issue and suggest that it may be solved within the SOFCN by adopting both of the following strategies: first, more accurately defining the relevant neural structures and second, switching the focus of neural ontology from structures to events, individuated by a where conjoint with a how. (shrink)

This paper is aimed at identifying how a model’s explanatory power is constructed and identified, particularly in the practice of template-based modeling (Humphreys, Philos Sci 69:1–11, 2002; Extending ourselves: computational science, empiricism, and scientific method, 2004), and what kinds of explanations models constructed in this way can provide. In particular, this paper offers an account of non-causal structural explanation that forms an alternative to causal–mechanical accounts of model explanation that are currently popular in philosophy of biology and cognitive science. Clearly, (...) defences of non-causal explanation are far from new (e.g. Batterman, Br J Philos Sci 53:21–38, 2002a; The devil in the details: asymptotic reasoning in explanation, reduction, and emergence, 2002b; Pincock, Noûs 41:253–275, 2007; Mathematics and scientific representation 2012; Rice, Noûs. doi:10.1111/nous.12042, 2013; Biol Philos 27:685–703, 2012), so the targets here are focused on a particular type of robust phenomenon and how strong invariance to interventions can block a range of causal explanations. By focusing on a common form of model construction, the paper also ties functional or computational style explanations found in cognitive science and biology more firmly with explanatory practices across model-based science in general. (shrink)