In 1878 evolutionary theoretician Edward D. Cope published an eight-page paper filled with prescient ideas that clearly anticipated theoretical evolutionary topics that are actively being debated some 145 years later. An examination of these ideas and their modern counterparts is the primary objective of this essay. A proposal is also made to provide an answer to Cope’s Puzzle concerning the sequences of events involved in the evolution of adaptive animal structures. This article revisits Cope’s “The Relation of Animal Motion to (...) Animal Evolution” (published in _The American Naturalist_, volume 12, number 1, January 1878, pp. 40–48) for _Biological Theory_’s “Classics in Biological Theory” collection; Cope’s original paper is available as supplementary material in the online version of this article. (shrink)

Biological agency has received much attention in recent philosophy of biology. But what is the motivation for introducing talk of agency into biology and what is meant by “agent”? Two distinct motivations can be discerned. The first is that thinking of organisms as agents helps to articulate what is distinctive about organisms vis-à-vis other biological entities. The second is that treating organisms as agent-like is a useful heuristic for understanding their evolved behavior. The concept of agent itself may be understood (...) in at least four different ways: minimal agent, intelligent agent, rational agent, and intentional agent. Which understanding is most appropriate depends on which of the two motivations we are concerned with. (shrink)

The first part of this essay relates a minimal and primordial concept of agency to be found in science and technology studies to an overall ontology of liveliness. The second part explores the relation between minimal and higher-level conceptions of agency concerning goal-orientedness and adaptation, and moves towards specifically biological concerns via a discussion of cybernetic machines.

The dual role of microbial communities as either beneficial/functional or harmful/pathogenic involves two issues concerning causality in physiology and medicine, etiology of disease, and the notion of function in biology. Causal explanation formulated by the germ theory of disease and the Koch postulates connects the existence of a specifically identified microbe to disease by the isolation and identification of a pathogen from an organism with the disease and the successful infection of a healthy individual. Similarly, microbiome research in medicine centers (...) on taxonomic composition in correlation with physiological conditions and germ-free mice experimentations to establish causal connections. However, because the microbiome is an ecological community, it lacks the specificity of identification assumed in the germ theory. Furthermore, the ecological aspects within and between microbiomes such as background conditions, microbial interactions, and interdependence, are treated as confounding. Looking at ecological studies, the causal explanations are less specific regarding complex systems with their processes of interactions. This article makes the following two points: One is that microbiome causality in the host should be understood similarly to the microbiome causality in an ecosystem. The second is that if considering a microbiome’s causality in the host as an ecosystem, its etiological explanation needs to be revisited to include a heterogeneous and mutual notion of interactions. Finally, according to the second point, the notion of function in ecology with its relevant notion of causality should be considered accordingly. (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)

The theory of biological autonomy provides a naturalized characterization of agency, understood as a general biological phenomenon that extends beyond the domain of intentionality and causation by mental states. Agency refers to the capacity of autonomous living beings (roughly speaking: organisms) to purposively and functionally control the interactions with the environment, and to adaptively modulate their own self-determining organization and behavior so as to maintain their own existence, construed as their intrinsic telos. We mention some crucial strengths of the autonomist (...) conception of agency, and some interesting challenges that it faces. Among the latter, we focus on the intertwined relationships between agency and evolution, as well as on the transition between agency and cognition. (shrink)

In this essay we aim to present some considerations regarding a minimal but concrete notion of agency and goal-directed behavior that are useful for characterizing biological systems at different scales. These considerations are a particular perspective, bringing together concepts from dynamical systems, combinatorial problem-solving, and connectionist learning with an emphasis on the relationship between parts and wholes. This perspective affords some ways to think about agents that are concrete and quantifiable, and relevant to some important biological issues. Instead of advocating (...) for a strict definition of minimally agential characteristics, we focus on how (even for a modest notion of agency) the agency of a system can be more than the sum of the agency of its parts. We quantify this in terms of the problem-solving competency of a system with respect to resolution of the frustrations between its parts. This requires goal-directed behavior in the sense of delayed gratification, i.e., taking dynamical trajectories that forego short-term gains (or sustain short-term stress or frustration) in favor of long-term gains. In order for this competency to belong to the system (rather than to its parts or given by its construction or design), it can involve distributed systemic knowledge that is acquired through experience, i.e., changes in the organization of the relationships among its parts (without presupposing a system-level reward function for such changes). This conception of agency helps us think about the ways in which cells, organisms, and perhaps other biological scales, can be agential (i.e., more agential than their parts) in a quantifiable sense, without denying that the behavior of the whole depends on the behaviors of the parts in their current organization. (shrink)