The Triple Helix

Gene, Organism, and Environment

Richard Lewontin is Alexander Agassiz Research Professor at the Museum of Comparative Zoology, Harvard University. His many books include Biology and Ideology, Not in Our Genes, and Human Diversity

One of our most brilliant evolutionary biologists, Richard Lewontin has also been a leading critic of those--scientists and non-scientists alike--who would misuse the science to which he has contributed so much. In The Triple Helix, Lewontin the scientist and Lewontin the critic come together to provide a concise, accessible account of what his work has taught him about biology and about its relevance to human affairs. In the process, he exposes some of the common and troubling misconceptions that misdirect and stall our understanding of biology and evolution.

The central message of this book is that we will never fully understand living things if we continue to think of genes, organisms, and environments as separate entities, each with its distinct role to play in the history and operation of organic processes. Here Lewontin shows that an organism is a unique consequence of both genes and environment, of both internal and external features. Rejecting the notion that genes determine the organism, which then adapts to the environment, he explains that organisms, influenced in their development by their circumstances, in turn create, modify, and choose the environment in which they live.

The Triple Helix is vintage Lewontin: brilliant, eloquent, passionate, and deeply critical. But it is neither a manifesto for a radical new methodology nor a brief for a new theory. It is instead a primer on the complexity of biological processes, a reminder to all of us that living things are never as simple as they may seem.

The Way of the Cell

Molecules, Organisms, and the Order of Life

Franklin M. Harold is Emeritus Professor of Biochemistry and Molecular Biology at Colorado State University.

Description
What is life? Fifty years after physicist Erwin Schrodinger posed this question in his celebrated and inspiring book, the answer remains elusive. In The Way of the Cell , one of the world's most respected microbiologists draws on his wide knowledge of contemporary science to provide fresh insight into this intriguing and all-important question.

What is the relationship of living things to the inanimate realm of chemistry and physics? How do lifeless but special chemicals come together to form those intricate dynamic ensembles that we recognize as life? To shed light on these questions, Franklin Harold focuses here on microorganisms--in particular, the supremely well-researched bacterium E. coli --because the cell is the simplest level of organization that manifests all the features of the phenomenon of life. Harold shows that as simple as they appear when compared to ourselves, every cell displays a dynamic pattern in space and time, orders of magnitude richer than its elements. It integrates the writhings and couplings of billions of molecules into a coherent whole, draws matter and energy into itself, constructs and reproduces its own order, and persists in this manner for numberless generations while continuously adapting to a changing world.

A cell constitutes a unitary whole, a unit of life, and in this volume one of the leading authorities on the cell gives us a vivid picture of what goes on within this minute precinct. The result is a richly detailed, meticulously crafted account of what modern science can tell us about life as well as one scientist's personal attempt to wring understanding from the tide of knowledge.

Reviews
"The work is like a breath of fresh air in a scientific world otherwise obsessed with excessive reductionism."--BioEssays

"Witty and erudite, this scientific book hails as a literary achievement. Comprehensive and up to date, Franklin Harold traces the roots--historical, thermodynamic, and biochemical--of today's biological revolution."--Lynn Margulis, co-author (with Dorion Sagan) of both What is Life? and What is Sex?

"This book helps us understand why the search for answers to the riddle 'What is life?' is a noble quest."--Howard C. Berg, author of Random Walks in Biology

Evolutionary Dynamics:

Exploring the Equations of Life

Martin Nowak is Professor of Biology and of Mathematics at Harvard University. He is Director of the Program for Evolutionary Dynamics.

At a time of unprecedented expansion in the life sciences, evolution is the one theory that transcends all of biology. Any observation of a living system must ultimately be interpreted in the context of its evolution. Evolutionary change is the consequence of mutation and natural selection, which are two concepts that can be described by mathematical equations.Evolutionary Dynamics is concerned with these equations of life. In this book, Martin Nowak draws on the languages of biology and mathematics to outline the mathematical principles according to which life evolves. His work introduces readers to the powerful yet simple laws that govern the evolution of living systems, no matter how complicated they might seem.

Evolution has become a mathematical theory, Nowak suggests, and any idea of an evolutionary process or mechanism should be studied in the context of the mathematical equations of evolutionary dynamics. His book presents a range of analytical tools that can be used to this end: fitness landscapes, mutation matrices, genomic sequence space, random drift, quasispecies, replicators, the Prisoner's Dilemma, games in finite and infinite populations, evolutionary graph theory, games on grids, evolutionary kaleidoscopes, fractals, and spatial chaos. Nowak then shows how evolutionary dynamics applies to critical real-world problems, including the progression of viral diseases such as AIDS, the virulence of infectious agents, the unpredictable mutations that lead to cancer, the evolution of altruism, and even the evolution of human language. His book makes a clear and compelling case for understanding every living system--and everything that arises as a consequence of living systems--in terms of evolutionary dynamics.

Evolution down under (Berkeley Edu/EvoLibrary)

If you've seen images of it on the news or in the paper, you won't soon forget it. Devil facial tumor disease (DFTD) causes bulging cancerous lumps and lesions to erupt around the face and neck — often causing enough deformation to make seeing or eating difficult. While it may be something of a relief to learn that this fatal disease affects only Tasmanian devils, marsupial carnivores of Tasmania, its impact on that population has been staggering. The disease was first observed by a wildlife photographer in 1996 and, since then, has reduced the total devil population by half — and in some areas, by as much as 90%! Tasmanian devils were recently listed as endangered and could become extinct in the wild in the next few decades. This summer, however, scientists reported that devils may be responding to DFTD by breeding earlier — before they are likely to be killed by the disease. This change could help the species survive longer, but is it an evolutionary one?

Where's the evolution?It's not yet clear if devils are actually evolving in response to DFTD. Scientists have observed that, before the disease, most females began breeding at two years of age and that many devil females now begin to reproduce at just one year. What's the explanation for these observations? It could be that DFTD has selected for younger-breeding females. After all, few devils now survive to their normal breeding age. Females with genes for early-breeding would have a significant reproductive advantage over females with genes for standard breeding times, and because of this differential reproduction, the population may have evolved. Alternatively, it could be that the genetic makeup of the population has not changed, but that with reduced competition from older females and with more access to food because of diminished devil populations, younger females are now able to breed. The idea here is that devil populations always had the potential for early breeding but that this was previously suppressed by competition from other devils. This second hypothesis relies on a phenomenon known as phenotypic plasticity — alternate traits an organism might have depending, not on different gene versions, but on the organism's current or past environment.

Further research will be needed to determine whether the shift in devil breeding times can be chalked up to evolution or to phenotypic plasticity. But even if phenotypic plasticity is the culprit, the marks of evolution on this story are deep. Perhaps most fascinating is the evolution of DFTD itself. Normally, cancer evolves within one patient. A cell happens to accumulate a series of mutations that allow it to obtain extra resources from the body and multiply more quickly than its neighboring cells. Because daughter cells inherit those same mutations for rampant proliferation, the mutant cell types become more common in the body through the process of natural selection. Over time, mutations that further increase this cell lineage's rate of propagation or that increase its ability to survive challenges we throw at it — like chemotherapy — will be similarly favored. But of course, evolution has no foresight. If not stopped by the body or medical treatments, the evolving cell lineage may kill its "host" and, in the process, itself.

DFTD, however, has evolved an ability that is almost unique among cancers — the power to dodge the death of its host by infecting a new animal: DFTD is transmissible. It has evolved into a contagious cancer. Devil mating behavior involves biting around the head and neck, allowing cells from one individual — especially cells from the crumbly DFTD tumors — to be transferred to the wounds or face of a new individual. There, the cells begin to sap the new body's resources and divert those nutrients toward their own proliferation, continuing their deadly advance through the devil population. This transmission results in a strange irony. The cells in DFTD tumors are more closely related to each other than they are to the other body cells in the animal of which they are a part. Though DFTD is technically a cancer, it behaves more like a parasite.

Human cancers, along with almost all cancers, are not themselves contagious because cells that somehow invade a new body are recognized as "foreign" and attacked by the immune system of the would-be host. Our bodies have a remarkable ability to distinguish self from non-self, based on genetically encoded markers on cell surfaces. Non-self markers tag a trespassing cell for destruction. This is part of the reason that transplanting organs usually requires careful genetic matching. In Tasmanian devils, however, this normal immune response does not kick in and oust foreign DFTD cells. That's because these key cell markers (technically known as major histocompatibility molecules), which normally vary widely between individuals, are remarkably uniform among devils. Tumor cells from distantly related devils bear markers similar to a new host's own markers — and so the tumor cells are able to fly under the radar of the host's immune system.

How did the devils wind up with such invariable immune system markers? What opened the door for this mutant cell lineage to evolve a life of its own, transcending the lifetime of any individual devil? The answer here depends on the other side of the evolutionary equation: the Tasmanian devil's history. Devils used to be broadly distributed across Australia. When sea levels rose 12,000 years ago, a small number of devils on Tasmania were cut off from the mainland population, which soon went extinct. This founding population of modern Tasmanian devils did not have as many different gene versions as the larger population had had, resulting in a serious cutback in genetic variation. This is an example of the founder effect — changes in gene frequencies that usually accompany founding a new population from a small number of individuals. Though the Tasmanian population grew in numbers after it was isolated, it was stuck with a low level of genetic variation and passed this deficiency on to modern devil populations. Because there is little variation in the genes that form the basis of their immune response — and because their aggressive breeding behavior allows cell exchange — devils provided a unique opportunity for the evolution of a contagious cancer.

DFTD cells are so successful at multiplying and spreading that they may shortly bring about their own demise. The Tasmanian devil could soon be on the brink of extinction in the wild — and if all the devils die, so too will the cancer. But extinction is not the only possible end to this story. As we heard in the news this summer, the devils may be evolving in response to the disease. Natural selection favors gene variants that help the devils survive the disease and reproduce. Those favorable gene variants might underlie shifts in life history strategies (as recent research hints at), in behavior, or in how the devils' immune systems fight the cancer. Evolution may yet stumble upon a solution for the devils. In the meantime, biologists are working to develop a vaccine and to curb the cancer by culling or isolating infected devils. But this is a race against time, and it's not yet clear whether the biologists' interventions or the devils' continuing evolution will come fast enough to save them from extinction.

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