International Society for History, Philosophy, and Social Studies of Biology

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TUESDAY, JULY 7  /  15:30 - 17:00  /  DS-R520
Organized session / standard talks
Thinking about cells (2): How do cells work?

Jane Maienschein (Arizona State University, United States); Karl Matlin (University of Chicago, United States)

These two coordinated sessions look at what cells are and how they work, in parallel with consideration of epistemological questions about how we know. The first session examines the evolving understanding of what cells are, including an overview of early concepts and close examination of studies in protozoa and in stem cells. Throughout, we ask about the methods and assumptions involved. The second session turns to questions about how cells work. This includes a look at explorations of cytoplasmic streaming within cells, at the understanding of cell death, and at intersections of form and function through study of mitochondria and oxidative phosphorylation. Here issues of methods, metaphor, and the heuristic use of form in order to inform mechanical explanations of function play important roles. The sessions work together to get at historical, philosophical, and biological questions about cells.

Explaining the “pulse of protoplasm”: The search for molecular mechanisms of protoplasmic streaming

Michael Dietrich (Dartmouth College, United States)

Explanations for protoplasmic streaming began with appeals to contraction in the eighteenth century and ended with appeals to contraction in the twentieth. During the intervening years, biologists proposed a diverse array of mechanisms for streaming motions. This paper focuses on the re-emergence of contraction among the molecular mechanisms proposed for protoplasmic streaming during the twentieth century. The revival of contraction is a result of a broader transition from colloidal chemistry to a macromolecular approach to the chemistry of proteins, the recognition of the phenomena of shuttle streaming and the pulse of protoplasm, and the influential analogy between protoplasmic streaming and muscle contraction.

Regulating cell death

Andrew Reynolds (Cape Breton University, Canada)

Since the 1970s cell death has been classified into two chief forms: necrosis, an accidental death due to injury, and apoptosis, a genetically regulated form of cell death associated with normal development and tissue homeostasis. This distinction was based on morphological features of dying cells observed with light and electron microscopy. Apoptosis soon became synonymous with the earlier described phenomenon of programmed cell death, first observed in the context of animal development. Increased attention to cell death led to an expanding catalog of descriptions of novel variations of apoptosis and necrosis with overlapping morphologies. The Nomenclature Committee on Cell Death (NCCD), created in 2005 to provide guidance on the classification and description of cell death, has increasingly recommended eschewing morphological criteria in favor of more precise, quantitative biochemical and genetic criteria associated with causal mechanisms. In its 4th and latest report (published online 19 Sept. 2014) the NCCD recommends a new classification distinguishing ‘accidental cell death’ and ‘regulated cell death’, the latter now defined by the ability of researchers to successfully pre-empt cell death through pharmacologic or genetic intervention. This shift away from morphological criteria suggests not only a clinical focus, but also the success of molecular biology at intervening in the regular life of cells. Talk of ‘rewiring’ and ‘reprogramming’ cell ‘circuits’ to alter the outcomes of various ‘subroutines’ of regulated cell death suggests a heavy influence of computer engineering metaphors. Do these metaphors promote the assumption that any regular causal sequence of events (a ‘mechanism’) in the cell is part of an adaptive and functional ‘program’?, and should we be asking “How much of the interactions between proteins and other molecules within a cell are more closely analogous to ‘weather’ than to subroutines of a computer program?”

Mitochondrial form and the search for the mechanism of oxidative phosphorylation

Karl Matlin (University of Chicago, United States)

In the 1950s a group of enzymologists in the United States and Europe proposed and attempted to prove the "chemical hypothesis" of oxidative phosphorylation postulating the existence of mitochondrial high-energy intermediates required for production of ATP. These efforts were, in the end, unsuccessful, and the chemical hypothesis was displaced beginning in 1961 by Peter Mitchell's "chemiosmotic" hypothesis, shown in subsequent years to be essentially correct. In the same period, cell biologists, led mainly by George Palade, described the intricate structure of mitochondria using electron microscopy. While the controversies surrounding biochemical aspects of the competing chemical and chemiosmotic hypotheses have received significant attention, less historical scholarship has focused on the intersection between biochemical studies and the discovery of mitochondrial structure. This paper explores how mitochondrial form as described by Palade figured in the experiments of these scientists, finding that mitochondrial compartmentalization was adopted by Mitchell as a key element of his chemiosmotic hypothesis, but was overlooked or misunderstood by enzymologists investigating the chemical hypothesis. These historical events are interpreted in terms of a more general approach to explanation of cellular phenomena that utilizes morphology heuristically as a constraint on possible explanatory models.