The evolutionary web of life

Published on December 2, 2014   30 min

Other Talks in the Series: Evolution and Medicine

0:00
The title of this talk is "The Evolutionary Web of Life." My name is John Torday. I'm a Professor of Pediatrics and Obstetrics and I also am in the Evolutionary Medicine Program at University of California-Los Angeles.
0:14
The rationale for this presentation is rather unconventional in that I'm using homeostasis as the selection pressure for evolution. So I'm going to go through that rationale. Homeostasis is the mechanistic basis for physiology. Homeostasis be traced all the way back to unicellular organisms. Unicellular organisms are the bauplan, or the blueprint for metazoans, or multicellular organisms. And homeostasis is a mechanism for monitoring of the environment, both internal, that is, physiology, and external, which is the physical environment. Homeostatic set-points can be changed through cellular-molecular remodeling, providing a mechanism for structural/functional change in adaptation to the environment. Or, as we recognize it, evolution.
0:60
So a historic perspective is of use here for this homeostatic approach. The concept of homeostasis was first formulated by Claude Bernard in the 19th Century. And then, a term was coined by Walter Canon in the 20th Century. Homeostasis is not part of the evolutionary biology domain per se, but probably because it was focused on fossilized material as the ultimate evidence for its relevance. The agents that mediate homeostasis do not fossilize, though it may be argued that their remains are embedded in molecular structure and function. For example, Conrad Bloch, the discoverer of cholesterol synthesis, reasoned that since it took 6 oxygen molecules to generate 1 cholesterol molecule, that cholesterol was actually a molecular fossil. We've extended that concept by reducing complex physiologic principles to molecular phenotypes, and then reverse-engineered their evolutionary history using their ontogeny, phylogeny, and pathophysiology as algorithms to understand their forward and reverse histories.
2:02
I've focused on lung biology. First of all, because I've been a scientist in lung biology for almost 50 years now and I understand that biology well. And furthermore, my own research at the cellular-molecular level has actually been the reason that I've focused on its evolution because of insights gained by doing so. So I'm showing the process of vertebrate lung evolution starting from the swim bladder of fish and then progressing to the skin of land vertebrates such as frogs as amphibians, reptiles, and mammals as a continuum. And in that legend, I show that the rationale here is that the alveoli of the lung actually have gotten progressively smaller in diameter in order to accommodate gas exchange. So the decrease in the surface area of the alveoli actually increases the gas exchange efficiency over evolutionary time. And I also showed two icons, one for myofibroblasts in pink, and for lipofibroblasts in white, which is important because those two cell types have been the way in which the lung from a structural/functional standpoint has accommodated this decrease in alveolar diameter and the concomitant increase in lung surfactant production. So surfactant is a soapy material that's produced by the alveoli. It's shown at the left as the y-axis, and on the x-axis, I've regressed that against our Thyroid Hormone-related Protein, or PTHrP. PTHrP receptor signaling because that is the mechanism by which the surfactant has become progressively more efficient in its production biogenetically and also developmentally. The conventional way of thinking about this process is the relationship between ventilation and perfusion, or V/Q matching. That's the conventional physiologic perspective. What I'm showing is a breakdown in the cellular-molecular mechanisms that underpin lung evolutionary trends. First of all, again the decrease in alveolar diameter being accommodated by the surfactant production. And the reason for that is because as the diameter of the alveolus decreases, by the law of Laplace, the surface tension increases. So in order to facilitate that, the system has evolved a progressively better way of producing lung surfactant in order to prevent alveolar collapse that would have occurred because of increased surface tension. So the myofibroblasts and the lipofibroblasts were key in this cellular evolutionary process, as well as the synthesis of matrix proteins, particularly type IV collagen, which I'm showing at the bottom of that legend as the green highlighted alveolar structure. Type IV collagen is a natural barrier in that it prevents the exudation of fluids from the micro-circulation of the alveoli, and it, too, has accommodated lung evolution. And at the very bottom, I'm showing both phylogeny and ontogeny as one in the same process. So ontogeny, the short-term history of the organism developmentally and phylogeny being the long-term history, both of which function through the same cellular-molecular mechanisms. Shown schematically starting at the far left as a structure that's more akin to the swim bladder of fish or the amphibian lung being a muscle-lined structure with epithelial cells at the air's surface. And then as you progress from left to right, you see that there's a progressive decrease in the size of the alveolar structure. And in association with a transition from the pink myofibroblasts to the white lipofibroblasts. And as I will explain as I go through this lecture, that process, that transition from the pink to the white cell types, fibroblasts, actually is what's facilitated surfactant production and the evolution of the gas exchange unit for efficient oxygenation to meet the metabolic demands of vertebrates as they emerged from water onto land.
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The evolutionary web of life

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