The sensorimotor theory of vision and visual consciousness is often described as a radical alternative to the computational and connectionist orthodoxy in the study of visual perception. However, it is far from clear whether the theory represents a significant departure from orthodox approaches or whether it is an enrichment of it. In this study, I tackle this issue by focusing on the explanatory structure of the sensorimotor theory. I argue that the standard formulation of the theory subscribes to the same (...) theses of the dynamical hypothesis and that it affords covering-law explanations. This however exposes the theory to the mere description worry and generates a puzzle about the role of representations. I then argue that the sensorimotor theory is compatible with a mechanistic framework, and show how this can overcome the mere description worry and solve the problem of the explanatory role of representations. By doing so, it will be shown that the theory should be understood as an enrichment of the orthodoxy, rather than an alternative. (shrink)

An underlying assumption in computational approaches in cognitive and brain sciences is that the nervous system is an input–output model of the world: Its input–output functions mirror certain relations in the target domains. I argue that the input–output modelling assumption plays distinct methodological and explanatory roles. Methodologically, input–output modelling serves to discover the computed function from environmental cues. Explanatorily, input–output modelling serves to account for the appropriateness of the computed function to the explanandum information-processing task. I compare very briefly the (...) modelling explanation to mechanistic and optimality explanations, noting that in both cases the explanations can be seen as complementary rather than contrastive or competing. (shrink)

When does a developing human being acquire moral status? I outline three different positions based on substance ontology that attempt to solve the question by locating some morally salient event in the process of human development question. In the second section, I consider some specific empirical objections to one of these positions, refute them, and then show how similar objections and responses would generalize to the other substance-based positions on the question. The crucial finding is that all the attempts to (...) answer the question that involve substance ontology need to appeal to dispositions. (shrink)

Philosophical discussions of systems biology have enriched the notion of mechanistic explanation by pointing to the role of mathematical modeling. However, such accounts still focus on explanation in terms of tracking a mechanism's operation across time (by means of mental or computational simulation). My contention is that there are explanations of molecular systems where the explanatory understanding does not consist in tracking a mechanism's operation and productive continuity. I make this case by a discussion of bifurcation analysis in dynamical systems, (...) articulating the distinctive way in which explanatory understanding is provided, especially about the reversibility or irreversibility of molecular processes. (shrink)

A survey of models in immunology is conducted and distinct kinds of models are characterized based on whether models are material or conceptual, the distinctiveness of their epistemic purpose, and the criteria for evaluating the goodness of a model relative to its intended purpose. I argue that the diversity of models in interdisciplinary fields such as immunology reflects the fact that information about the phenomena of interest is gathered from different sources using multiple methods of investigation. To each model is (...) attached a description specifying how information about a phenomenon of interest has been acquired, highlighting points of commonality and difference between the methodological and epistemic histories of the information encapsulated in different models. These points of commonality and difference allow investigators to integrate findings from different models into more comprehensive explanatory accounts, as well as to troubleshoot anomalies and faulty accounts by going back to the original building blocks. (shrink)

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)

The paper discusses how systems biology is working toward complex accounts that integrate explanation in terms of mechanisms and explanation by mathematical models—which some philosophers have viewed as rival models of explanation. Systems biology is an integrative approach, and it strongly relies on mathematical modeling. Philosophical accounts of mechanisms capture integrative in the sense of multilevel and multifield explanations, yet accounts of mechanistic explanation have failed to address how a mathematical model could contribute to such explanations. I discuss how mathematical (...) equations can be explanatorily relevant. Several cases from systems biology are discussed to illustrate the interplay between mechanistic research and mathematical modeling, and I point to questions about qualitative phenomena, where quantitative models are still indispensable to the explanation. Systems biology shows that a broader philosophical conception of mechanisms is needed, which takes into account functional-dynamical aspects, interaction in complex networks with feedback loops, system-wide functional properties such as distributed functionality and robustness, and a mechanism’s ability to respond to perturbations. I offer general conclusions for philosophical accounts of explanation. (shrink)

Explanation in terms of gene regulatory networks has become standard practice in evolutionary developmental biology. In this paper, we argue that GRNs fail to provide a robust, mechanistic, and dynamic understanding of the developmental processes underlying the genotype–phenotype map. Explanations based on GRNs are limited by three main problems: the problem of genetic determinism, the problem of correspondence between network structure and function, and the problem of diachronicity, as in the unfolding of causal interactions over time. Overcoming these problems requires (...) dynamic mechanistic explanations, which rely not only on mechanistic decomposition, but also on dynamic modeling to reconstitute the causal chain of events underlying the process of development. We illustrate the power and potential of this type of explanation with a number of biological case studies that integrate empirical investigations with mathematical modeling and analysis. We conclude with general considerations on the relation between mechanism and process in evo-devo. (shrink)

Multilevel research strategies characterize contemporary molecular inquiry into biological systems. We outline conceptual, methodological, and explanatory dimensions of these multilevel strategies in microbial ecology, systems biology, protein research, and developmental biology. This review of emerging lines of inquiry in these fields suggests that multilevel research in molecular life sciences has significant implications for philosophical understandings of explanation, modeling, and representation.

An important strategy in the discovery of biological mechanisms involves the piecing together of experimental results from interventions. However, if mechanisms are investigated by means of ideal interventions, as defined by James Woodward and others, then the kind of information revealed is insufficient to discriminate between modular and non-modular causal contributions. Ideal interventions suffice for constructing webs of causal dependencies that can be used to make some predictions about experimental outcomes, but tell us little about how causally relevant factors are (...) organized together and how they interact with each other in order to produce a phenomenon. I argue that lab research relies on more elaborated types of interventions targeting in a controlled fashion multiple variables at the same time in order to probe the temporal organization of causally-relevant factors along distinct causal pathways and to test for non-modular interaction effects, thus providing crucial spatial-temporal constraints guiding the formulation of more detailed mechanistic explanations. (shrink)

Philosophers of science diverge on the question what drives the growth of scientific knowledge. Most of the twentieth century was dominated by the notion that theories propel that growth whereas experiments play secondary roles of operating within the theoretical framework or testing theoretical predictions. New experimentalism, a school of thought pioneered by Ian Hacking in the early 1980s, challenged this view by arguing that theory-free exploratory experimentation may in many cases effectively probe nature and potentially spawn higher evidence-based theories. Because (...) theories are often powerless to envisage workings of complex biological systems, theory-independent experimentation is common in the life sciences. Some such experiments are triggered by compelling observation, others are prompted by innovative techniques or instruments, whereas different investigations query big data to identify regularities and underlying organizing principles. A distinct fourth type of experiments is motivated by a major question. Here I describe two question-guided experimental discoveries in biochemistry: the cyclic adenosine monophosphate mediator of hormone action and the ubiquitin-mediated system of protein degradation. Lacking underlying theories, antecedent data bases, or new techniques, the sole guides of the two discoveries were respective substantial questions. Both research projects were similarly instigated by theory-free exploratory experimentation and continued in alternating phases of results-based interim working hypotheses, their examination by experiment, provisional hypotheses again, and so on. These two cases designate theory-free, question-guided, stepwise biochemical investigations as a distinct subtype of the new experimentalism mode of scientific enquiry. (shrink)

This paper argues against the view that the standard explanation of phase transitions in statistical mechanics may be considered a causal explanation, a distortion that can nevertheless successfully represent causal relations.

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)

Dynamical systems play a central role in explanations in cognitive neuroscience. The grounds for these explanations are hotly debated and generally fall under two approaches: non-mechanistic and mechanistic. In this paper, I first outline a neurodynamical explanatory schema that highlights the role of dynamical systems in cognitive phenomena. I next explore the mechanistic status of such neurodynamical explanations. I argue that these explanations satisfy only some of the constraints on mechanistic explanation and should be considered pseudomechanistic explanations. I defend this (...) argument against three alternative interpretations of the neurodynamical explanatory schema. The independent interpretation holds that neurodynamical explanations and mechanisms are independent. The constitutive interpretation holds that neurodynamical explanations are constitutive but otherwise non-mechanistic. Both the independent and constitutive interpretations fail to account for all the features of neurodynamical explanations. The partial interpretation assumes that the targets of dynamical systems models are mechanisms and so holds that neurodynamical explanations are incomplete because they lack mechanistic details. I contend instead that the targets of those models are dynamical systems distinct from mechanisms and defend this claim against several objections. I conclude with a defense of the pseudomechanistic interpretation and a discussion of the source of their explanatory power in relation to a causal-mechanical description of the world. (shrink)

We address the question of whether and to what extent explanatory and modelling strategies in systems biology are mechanistic. After showing how dynamic mathematical models are actually required for mechanistic explanations of complex systems, we caution readers against expecting all systems biology to be about mechanistic explanations. Instead, the aim may be to generate topological explanations that are not standardly mechanistic, or to arrive at design principles that explain system organization and behaviour in general, but not specific mechanisms. These abstraction (...) strategies serve various aims, including prediction and control, that are central to understanding the epistemic diversity of systems biology. (shrink)

Mechanisms consist of component parts and processes organized in a specific way to produce changes that may give rise to one or more phenomena. I aim to examine the generative mechanism of generative material models in the production of new material models. A generative material model in biology is a living material model that is capable of generating new material models. I contend that generative mechanisms of a generative material model are not to be conflated with biological mechanisms: the former (...) is a mechanism manipulated and altered by the modeler while the latter is a naturally occurring mechanism. I examine the ways in which idealization may contribute to the generative mechanism in generating new model organisms. I articulate that the component parts and activities in a generative mechanism are to a large extent shaped by idealization in generative material modeling. Although biological mechanisms do have a role to play in the generation of model organisms, I propose that we shall view the generative mechanism as a hybrid of biological mechanisms and modeling activities. I shall argue that the notion of generative mechanisms as hybrid mechanisms is different from the extant conceptions of mechanisms in various aspects. (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)