Monday, May 15, 2006

Evolving Evolution

Evolving Evolution

By Edward Ziff, Israel Rosenfield


Despite much recent controversy about the theory of evolution, major changes in our understanding of evolution over the past twenty years have gone virtually unnoticed.[1] At the heart of Darwin's theory of evolution is an explanation of how plants and animals evolved from earlier forms of life that have long since disappeared; but his theory says nothing about the factors that determine the shape, color, and size of a particular fish, whale, or butterfly. Darwin and his contemporaries realized that understanding the evolution of animal forms and understanding how a fertilized egg develops into a whale, cow, or human being must be deeply connected; but they didn't know how to make the connection.

Surprising discoveries in the 1980s have begun to tell us how an embryo develops into a mature animal, and these discoveries have radically altered our views of evolution and of the relation of human beings to all other animals. The new field of study in which these breakthroughs have been made is called Evo Devo, short for evolution and development, "development" referring to both how an embryo grows and how the newborn infant matures into an adult.

Sean Carroll, author of one of the books under review and a coauthor of another, has made important contributions to the understanding of evolution and development. From DNA to Diversity, written with two other scientists, is the second edition of a book that has become a classic for students of evolution. The title of Carroll's other book, Endless Forms Most Beautiful, comes from the famous final sentence of The Origin of Species: "There is a simple grandeur in this view of life... that from so simple an origin, through the process of gradual selection of infinitesimal changes, endless forms most beautiful and most wonderful have been evolved."

In 1830, nearly thirty years before Darwin published his book, two French naturalists—Georges Cuvier and Étienne Geoffroy St. Hilaire—debated the significance of the anatomical similarities between distantly related animals, such as the flippers of whales and the wings of bats. Cuvier held that form was dictated by function: the bat's wing, needed for flying, had a separate origin from the whale's flipper, needed for swimming.

Geoffroy St. Hilaire opposed this view, arguing that the underlying skeletal similarities pointed to the existence of a common archetype for both flippers and wings. While neither man claimed that animal forms could change over generations, St. Hilaire's archetypal form foreshadowed some recent discoveries about development and evolution. No doubt this debate was in the mind of Charles Darwin as he formulated his theories in an attempt to account for the origins of animal forms.

The contemporary Darwinian theory of evolution is based on three ideas: natural selection, heredity, and variation. Small random changes—variations—occur in organisms through mutations of genes, and when these changes give an organism a greater chance of survival, they persist from one generation to the next through natural selection. That is, organisms with traits that make them better adapted to the environment they inhabit will have better reproductive success than other members of the same species that do not possess the advantageous traits. In each successive generation, then, an ever-larger proportion of the species in question will possess the mutation that produces the advantageous traits. "Natural selection," Darwin wrote, "acts solely by accumulating successive, favorable variations." Evolution in the Darwinian view was gradual: "it can act only by short and slow steps." And since, in this view, all changes are random, there are no predetermined directions in which organisms evolve. All living organisms, Darwin claimed, are descended from one or a few common ancestors.

Neither Darwin nor any of his contemporaries knew about the workings of heredity—how we inherit the eye color of our father or the hair color of our mother. The work of the Czech monk Gregor Mendel, first published in 1865, had gone unnoticed in Darwin's day and was only rediscovered around 1900. Mendel had shown that specific traits, such as the color of a pea, or the smoothness or roughness of its skin, could be inherited independently of one another. The new science of "genetics," the idea that units called "genes" within each cell transmit specific traits, such as hair color, from one generation to the next, began in the first decade of the twentieth century. Studies of inherited traits in fruit flies in the following decades established convincing evidence for genes, but they remained invisible. Scientists still didn't know how the gene made it possible for information to pass from one generation to the next, and how mutations in genes could, over many generations, lead to a new species that had a form different from its distant progenitor.

By the 1940s, though the structure of the gene was still unknown, scientists had introduced the idea of the gene into Darwinian theory. They now explained evolution as the consequence of small random changes in genes. This recasting of Darwinian theory was called the Modern Synthesis, following the 1942 publication of Julian Huxley's book Evolution: The Modern Synthesis. The neo-Darwinian theory incorporated the Mendelian idea of genetics, explaining the mechanism of inheritance that was unknown to Darwin. The theory, however, did not account for how particular organisms develop from embryos in the womb to adult forms; that process, known as embryology, was not discussed.

The neo-Darwinian view was reinforced in 1953, when the double helix was discovered, showing how genes composed of the nucleic acid DNA transmitted hereditary characteristics. A molecule of DNA is made up of two long strands of chemical building blocks called nucleotides, each containing one of four bases: adenine, thymine, guanine, or cytosine, which are abbreviated A, T, G, and C. The order of the bases in each strand of DNA determines the information in the DNA molecule, information we can think of as providing an overall plan for producing enzymes and other proteins.

A gene was now understood to be a specific sequence of DNA bases. Genes vary considerably in size, most of them containing between 10,000 and 20,000 nucleotides, though they can be much longer or shorter. Each of our cells carries all our genes, although most genes remain inactive at any given moment. When a particular gene is activated it is first copied into RNA, a nucleic acid that carries instructions from DNA for assembling proteins. The RNA's instructions are then decoded in a process called "translation," and proteins, including the enzymes essential for cells to function, are produced. Proteins in turn form some 50 percent of all living cells.

How are particular genes activated? There are, according to recent research, as many as a hundred trillion cells in the human body, and each cell contains thousands of different types of molecules that vary considerably in size; many molecules move about freely inside the cell. All the cells in a given individual have the same DNA—it is contained in the largest molecules in each cell—and hence an identical set of genes. Which specific genes are activated in a particular cell depends, in part, on the cell's location in the embryo or the adult body. Moreover, the activation of one combination of genes will give rise to a liver cell, while the activation of another will produce a brain cell.

The structure of the double helix made it apparent how changes, or mutations, in the base sequence of a gene could lead to variations in the characteristics of an organism; such mutations could, if advantageous, accumulate over time. The process appeared to confirm Darwin's view that evolution is gradual. As he wrote in The Origin of Species, nature "can act only by short and slow steps. Hence, the saying Natura non facit saltum," nature doesn't make sudden jumps. The standard view, then, was that variation and selection could account for how the simple organisms of early life evolved into the complex forms of the contemporary biological world. After Mendel's discoveries had been absorbed at the beginning of the twentieth century, it was assumed that as changes accumulated between one species and another, there would be less and less similarity in the kind and number of their genes. More advanced species would have many more genes than lower forms of life; and worms, for example, would have few, if any, genes similar to those of fish, mice, or human beings.

Yet it seemed astonishing that random mutations, even over enormous periods of time, could give rise to the remarkable complexity of an organ such as the human eye. "To suppose," Darwin wrote in The Origin of Species,

that the eye with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest degree....

Nonetheless, he continued:

Reason tells me, that if numerous gradations from a simple and imperfect eye to one complex and perfect can be shown to exist, each grade being useful to its possessor, as is certainly the case; if further, the eye ever varies and the variations be inherited, as is likewise certainly the case; and if such variations should be useful to any animal under changing conditions of life, then the difficulty of believing that a perfect and complex eye could be formed by natural selection, though insuperable by our imagination, should not be considered as subversive of the theory.

The neo-Darwinian belief in small mutational changes in DNA molecules over hundreds of millions of years made the preservation of individual genes over long periods of time highly unlikely. It was thought that the diversity of living forms was the consequence of each animal having evolved its own unique set of genes over millions of years as well. Surely human beings, for example, would not have the same genes as worms.

Those assumptions were dramatically overturned when the rough draft of the human genome—the entire set of human genes—was announced in 2001. As it turned out, human beings have far fewer genes than expected— about 25,000 rather than the 60,000 or more that had been predicted. This was about the same number as mice have, and even the tiny worms called nematodes have about 14,000 genes. The number of genes in a given species, therefore, is not a measure of its complexity. Why had biologists so overestimated the number of genes in the human genome? Why is it unnecessary for complex animals such as mammals to have ten times as many genes as worms?

The answers to these questions were already hinted at more than four decades ago. At the time it was known that the bacteria E. coli, which normally live off the sugar glucose, are also capable of producing enzymes that digest other sugars, such as lactose. But biologists noticed that the bacteria only produce the enzyme when lactose is present in their immediate environment. Scientists could not explain how the E. coli somehow "knew" when the lactose-digesting enzyme would be needed.

In 1961, Jacques Monod and François Jacob discovered that E. coli bacteria actually have a mechanism that controls the production of the enzyme for digesting lactose. As unicellular organisms, E. coli bacteria have only several thousand genes, each of which is made up of a specific sequence of DNA. A single one of these genes, present in all E. coli, carries in its DNA the genetic instructions needed to assemble the enzyme that can digest lactose; the DNA is copied into RNA, which is then "translated" to produce the enzyme itself. When there is no lactose present in the bacteria's immediate environment, the gene is switched off: its DNA is not copied into RNA and the enzyme is not produced. The reason for this, the scientists discovered, is that a protein called a repressor molecule attaches itself to the DNA site where the copying into RNA begins, thus blocking off the DNA and preventing the gene from producing the RNA responsible for the synthesis of the enzyme.

On the other hand, when the E. coli bacteria encounter lactose, the lactose binds itself to this repressor molecule, causing the repressor to be detached from the DNA site. This unblocks the DNA, allowing the gene to be copied into RNA, and produce the enzyme that can digest lactose. In other words, the repressor molecule acts as a switch that controls the gene's production of the enzyme. Since only a fraction of the total number of genes present in an organism are expressed, or turned on, at any given time, Monod and Jacob conjectured that other genes must be similarly turned on and off.

Although they had not yet found systematic evidence to support these ideas, the discovery of the repressor molecule allowed the two scientists to form a powerful new hypothesis about how genes function. As Jacob recently wrote, in a brief description of the new hypothesis:

It proposed a model to explain one of the oldest problems in biology: in organisms made up of millions, even billions of cells, every cell possesses a complete set of genes; how, then, is it that all the genes do not function in the same way in all tissues? That the nerve cells do not use the same genes as the muscle cells or the liver cells? In short, [we] presented a new view of the genetic landscape.

The deeper significance of the Monod-Jacob model of gene function, and its implications for the nature of evolution, became apparent with the new field of embryo research that arose almost twenty years later.


In 1894, the English biologist William Bateson challenged Darwin's view that evolution was gradual. He published Materials for the Study of Variation, a catalog of abnormalities he had observed in insects and animals in which one body part was replaced with another. He described, for example, a mutant fly with a leg instead of an antenna on its head, and mutant frogs and humans with extra vertebrae. The abnormalities Bateson discovered resisted explanation for much of the twentieth century. But in the late 1970s, studies by Edward Lewis at the California Institute of Technology, Christiana Nüsslein-Vollhard and Eric Wieschaus in Germany, and others began to reveal that the abnormalities were caused by mutations of a special set of genes in fruit fly embryos that controlled development of the fly's body and the distribution of its attached appendages. Very similar genes, exercising similar controls, were subsequently found in nematodes, flies, fish, mice, and human beings.

What they and others discovered were genes that regulate the development of the embryo and exert control over other genes by mechanisms analogous to that of the repressor molecule studied by Monod and Jacob. Eight of these controlling genes, called Hox genes, are found in virtually all animals —worms, mice, and human beings— and they have existed for more than half a billion years.[2] Fruit flies and worms have only one set of eight Hox genes; fish and mammals (including mice, elephants, and humans) have four sets. Each set of Hox genes in fish and mammals is remarkably similar to the eight Hox genes found in fruit flies and worms. This discovery showed that very similar genes control both embryological and later development in virtually all insects and animals. (See Figure 1.)

To understand what Hox genes do, scientists needed to observe the activity of the genes in the developing embryos of flies and mice. Using new technologies that allowed them to observe under a microscope the locations of the Hox proteins in these embryos, they were able to identify an overall pattern of how Hox genes behave. A newly fertilized fly egg looks like a tiny football: one end, or pole, will eventually become the head region; the other end will become the tail region. These and other divisions of the embryo in later development actually followed the switching on and off of the Hox genes in different parts of the embryo. (See Figure 2.)

The mechanism that causes the Hox genes to behave in this way is initiated by the release of proteins from the cells of the mother's body across the newly fertilized embryo. These proteins control the activities of the Hox genes and are released in varying concentrations, causing Hox genes to produce Hox proteins in specific places. As the embryo grows, the production of Hox proteins divides the embryo into a series of segments, or distinct regions, from which subsequent development occurs. Other genes are then activated within each segment, a finer division of the embryo is established, and wings, antennae, and other body parts are formed. In general, scientists reasoned, Hox genes establish the basic division of the embryo into distinct compartments, and each compartment, in turn, establishes the regions of the embryo where development of specific body parts and functions takes place. Still, the details of the mechanisms that a cell uses to establish its position in the embryo remain incomplete.

In fact, Nüsslein-Vollhard and Wieschaus found that within the fly's embryo there was an overall pattern in which genes were turned on or off; and they saw in this pattern the overall body plan for the full-grown fly. In other words, the activity of the Hox genes, including the formation of compartments within the embryo and the control of other genes that guide development, provided a system of organization that dictated the final adult form of the fly.

The presence of a body plan in the genome, whether of a fly, a whale, or a human, was unexpected by embryologists. Previously, most of them did not think that development of embryos was controlled by genes; they had assumed that the different parts of developing embryos were determined by physical interaction between neighboring cells and that there was no overall division of the embryo according to a genetic plan. Experiments had shown, for example, that removing developing wing tissue from one part of an embryo and implanting it elsewhere still gave rise to a wing, although an abnormal one. Scientists attributed the abnormality to the effects of the neighboring cells in the embryo. This was wrong. In fact it was caused by the disruption of the body plan.

This new understanding of Hox genes was aided by the discovery that the proteins produced by these genes function in a way that is analogous to Monod and Jacob's repressor molecule. Specifically, although they have different properties, all Hox proteins contain a molecular structure that makes them attach to DNA sites that control genes. This meant that Hox proteins, like the repressor molecule, act as switches that turn neighboring genes on and off.[3]

Hox genes, as Carroll explains, are in fact one of many kinds of genes that direct embryo development by a mechanism of switches. One example that is not a Hox gene is the gene that controls the development of the eye in fruit flies. If this gene (called Pax 6) is damaged when it mutates, the fly fails to develop eyes. We now know from the experiments described in Carroll's book that the Pax 6 gene is also found in butterflies, mice, and humans. Indeed, Pax 6 genes are interchangeable. The Pax 6 gene from a fly will turn on genes that make eyes in mice, and the Pax 6 gene from a mouse will turn on genes that make eyes in flies.

It had long been assumed that eyes had evolved independently in different species. The structures of mammalian eyes and insect eyes are very different and it would seem most unlikely that they had followed a similar evolutionary path. Mammalian eyes, for example, have a single lens that focuses an image on the retina. Insects have eyes with many tube-like structures, each tube having its own lens and retina. Yet the discovery of the Pax 6 gene gives us reason to believe that the evolution of the eye in all the animals followed related, and to some extent common, paths, though we cannot completely exclude the possibility that each kind of eye evolved following completely independent pathways. In addition to the Pax 6 gene, genes have been found that control the genes responsible for the development of the different kinds of "hearts"—or mechanisms that pump blood—whether in fruit flies or humans, again suggesting similar evolutionary pathways. Indeed the development of legs, wings, arms, fins, and other fish and marine animal appendages are all under the control of virtually identical genes and, as with the Pax genes, in many cases are interchangeable.

These findings strongly support the Darwinian view that animals descend from one or a few ancestors. However, contrary to the previously accepted neo-Darwinian view, the same findings showed that different animal forms are not primarily a function of distinct gene pools that have evolved over millions of years. How then do similar collections of genes create the enormous diversity of living forms? In Sean Carroll's view, what creates diversity is the patterns in which genes are turned "on" and "off." The different appendages found in centipedes, fruit flies, lobsters, and brine shrimp are created by varying combinations of Hox gene activity in the developing insect or crustacean embryo.

"Switches," Carroll emphasizes, "enable the same...genes to be used differently in different animals" [his italics]. In other words, a Hox gene produces a protein that binds to the DNA's sites where genes copy into RNA and can thus turn genes "on" or "off."

This has an important consequence for evolution: mutations in Hox genes will affect the ways in which they act within the embryo, thereby altering the proteins' functions as switches. When the proteins' functions are changed, in turn, this causes them to control genes that are needed for development of a specific physical trait in new ways. In this view, evolution is largely the consequence of random mutations in genetic switches. Genes remain intact, but under new patterns of control. Their function is altered. Complexity and variety are created, at least in part, by combining the activities of old genes in new ways. Carroll's view—what we might call the switches hypothesis—emphasizes the importance of changes in patterns of turning genes on and off rather than changes in the genes themselves. However, even the most ardent supporter of the switches hypothesis would admit that not only Hox genes but other genes change as well. But the contribution of these changes to evolution is far less than we had previously believed.

In fact, vertebrates—reptiles, birds, chickens, mice, pythons, and humans— do have more genes than insects, though far fewer than had been expected before the human genome was revealed. The increase in the number of genes in these animals is partly responsible for their complexity and diversity. But as Carroll notes, "frogs and snakes, dinosaurs and ostriches, giraffes and whales, have evolved around a similar set of four Hox gene clusters. So again, the mere number of Hox genes does not tell us how these forms evolved." The diversity of these animals comes from changes in the ways genes are turned on and off.

For example, though the giraffe has a long neck, it has seven cervical vertebrae, the same number as humans, whales, and all other mammals. Hox genes control this number, but they may also control cell proliferation and consequently the size of the vertebrae. The giraffe's larger vertebrae may have developed because of mutations in the Hox genes controlling the size of vertebrae. Giraffes with large vertebrae and longer necks could feed off tall trees and were consequently selected over other giraffes. Changes in gene regulation, not new genes, gave rise to the long-necked giraffe.

Evolution, then, depends on new patterns of gene regulation rather than the creation of new genes. Indeed, it is not meaningful to talk about the function of a single gene in isolation. Genes only function in the context of the organism. There is no single gene for an eye, a limb, or language, much less such tendencies as homosexuality. Genes function in relation to other genes and intercellular signals, much as words vary in meaning and function depending on the way they are used in sentences and the contexts in which they are spoken. It is the combinations of gene activity, which may be different in different species, that create the form of the organism. "We can begin to think of individual groups—insects, spiders, and centipedes, or birds, mammals, and reptiles, as well as their long extinct fossil relatives—not so much in terms of their uniqueness, but as variations on a common theme," Carroll writes. And surprising, too, is the evidence that all animals, from worms to humans, probably descend from one or a few primitive bacteria. Darwin would have been pleased to discover molecular evidence for his "common descent."


A powerful new theory adds considerable weight to this view, putting Carroll's work in a larger perspective. In The Plausibility of Life, Marc W. Kirschner and John C. Gerhart take a broader view than Carroll's on the questions of development and evolutionary biology. They agree that Hox genes make an important contribution to the mechanisms of evolution, but they argue that there are a number of other fundamental properties of organisms that give direction to evolution. The weakness of Darwinian theory—and one that has been seized upon by secular critics of evolutionary theory—is its failure to explain how the gene determines the observable traits of the organism. From an evolutionary point of view, how can complex organs such as eyes, arms, or wings evolve over long periods of time? What about the intermediary forms?

The Darwinian view was that early evolutionary forms of arms, legs, or wings might have initially served other purposes (insect legs, for example, might have evolved from gills their ancestors used for respiration). Such transformations of purpose are certainly important in evolution, Kirschner and Gerhart argue, but there must be other mechanisms at work as well. Concerning the human eye, for example: How is it possible for the different parts of an eye to evolve simultaneously—the lens, the iris, the retina, along with the blood vessels necessary for supplying the eye with oxygen and nutrition as well as the nerves that must receive signals from the retina and send signals to the muscles of the eye? Could these precise nerve and vascular networks be created by gradual random changes in genes over long periods of time, as Darwin claimed? Similarly, how can random mutations and natural selection create not only the necessary muscles and bone that make up the arm, for example, but organize the blood supply and nerves so that, after hundreds of thousands of years, an animal evolves with functioning arms, legs, and eyes? The Darwinian view that developing organs can serve different purposes at different times seems incomplete at best.

Darwin thought that at any given time variations in the forms of organisms were purely random. This is true of the neo-Darwinian view as well. However, recent research has shown that even though mutations are random, the effects of a mutation will be restricted, and may alter only one part or trait of an organism. A good example of the restricted effects of mutation is provided, as Kirschner and Gerhart point out, by the body plans created by Hox genes. Because they are contained within the different compartments of the embryo established by the body plan, individual parts of an animal can evolve independently of each other. For example, the lizard has limbs, the python has vestigial limbs, and the advanced snake has no limbs at all. These variations in limb structure have evolved without major changes in other parts of the body plan.

This independence means that mutations can occur within a single region of an embryo that may or may not be beneficial; in any case, fewer of the mutations will be lethal for the developing organism. In other words, while evolution is constrained by the body plan created by the Hox genes, this constraint gives nature a much greater freedom to experiment with variant forms through random mutations. If there were no body plans with separate parts, most variations would be lethal to the entire organism and evolution would be much, much slower. Suppose we wanted to design new windows for airplanes that would improve the visibility for passengers, resist cabin pressure, and better insulate passengers from the cold. We would test the new window designs without changing their positions on the body of the plane. If we had to redesign the entire plane every time we changed the window design, we would be much slower in developing new and more efficient planes. Similarly, Hox genes can, through mutations, shift the pattern of organization within a part of the embryo, allowing evolution to experiment with new forms, such as wings and longer necks, without affecting other parts of the embryo.

Kirschner and Gerhart thus place the activity of Hox genes inside the embryo in a broader perspective. They agree that Hox genes are important in organizing the embryo into discrete parts, a process they call the invisible anatomy (it is only visible with the aid of recent technology). But they argue that the function of Hox genes is only one of a number of "core processes" that act as constraints on evolution. The storage of genetic information in DNA and the mechanisms for translating that information in the synthesis of proteins are examples of core processes. Other kinds of core processes that are used by cells include biochemical mechanisms, such as the digestion of nutrients by enzymes. These mechanisms were established at an early stage in evolution and are still used in human cells, worms, and bacteria. Because of these core processes, natural selection is presented with a variety of forms that are more likely to succeed than if there were no constraints on variation at all. Should a new advantageous process arise by mutation, it can be incorporated into the functional repertory of the organism, and it is then inherited over generations.

Another kind of core process that can, by constraining development, create forms that are more likely to succeed is what Kirschner and Gerhart call "exploratory behavior," such as the method used by ants when foraging for food. Ants leave their nest and take random paths. As they move about they secrete a chemical substance called a pheromone that leaves a scent along the path they are following. If an ant fails to find food it will eventually return to the nest, using the pheromones it has deposited to guide it back to the nest. However, an ant that finds food will deposit more pheromones as it returns to the nest. This will reinforce the scent of the trail that led to food and other ants will now follow the reinforced trail.

Nonetheless, not all the ants will follow the successful trail. Some ants will set out on random paths in search of other sources of food and if successful they, too, will establish paths for subsequent ants. Eventually, the ants will have established a detailed map of paths to food sources. An observer might think that the ants are using a map supplied by an intelligent designer of food distribution. However, what appears to be a carefully laid out mapping of pathways to food supplies is really just a consequence of a series of random searches.

Other exploratory processes are important for the development of the vascular and nervous systems in a growing embryo. While the details of the individual processes vary considerably, the guiding principles are similar to those of ant foraging: just as the ants randomly explore the terrain around their nest, capillary vessels sprout off from the larger blood vessels and randomly explore the surrounding tissues for the signals coming from cells deprived of oxygen; they then can bring blood containing oxygen to the cells. And just as contact with food makes the ant reinforce the path that led to the food, the sprouting capillary vessels establish permanent contacts whenever they encounter tissue with oxygen-deprived cells. Similarly, fine nerve endings extend themselves randomly, establishing stable connections between nerves and muscles whenever they receive electrical and chemical signals coming from muscles.

Hence, unlike the eye or hand, whose forms follow from the body plan that is programmed by Hox genes in the developing embryo, the apparently well-designed and integrated nervous and vascular systems that serve such organs do not require predetermined paths and wirings. Darwin's view that small simultaneous changes would give rise to organs as complex as the eye is in principle true, but in need of modification. It is the very constraints created by the Hox genes and the other core processes (e.g., the exploratory behavior of capillaries and nerve endings) that permit complex designs to emerge over a relatively short period of time from a biological point of view (hundreds of thousands of years, or perhaps even less). As Carroll and Kirschner and Gerhart observe, some alteration of genes is still necessary if the changes are to be passed on from one generation to another. But the genetic alterations are considerably simpler and fewer in number than had been formerly imagined.

While Carroll argues—a claim that is at the heart of Evo Devo—that embryological development gives us the deepest clues to the mechanisms of evolution, Kirschner and Gerhart move beyond embryology to show that metabolic and physiological processes are also critical to evolutionary change. Their approach, which they call the theory of "facilitated variation," attempts to show how the regulation of genes inside the embryo, as described by Carroll, is part of a larger set of processes that allow organisms to experiment with evolution in a tightly controlled way. According to this theory, the mutations, or variations, needed to drive evolutionary change can occur with little disruption either to the basic organization of an organism or to the core processes that make its cells function.

We now have a far deeper understanding of evolution than even a decade ago.[4] And although our knowledge is still incomplete, our new understanding, as the books under review admirably show, has opened the way toward a comprehensive account of evolution and has supplied solid answers to the critics of evolutionary theory.


[1] For their critical readings and comments on this article, we would like to thank David
Botstein, Nathaniel Heintz, Luisa Hirschbein, David Ish- Horowicz, and Richard
Lewontin, none of whom should be held accountable for this text, for which we take full responsibility.

[2] No one group found all of the Hox genes. Lewis started his work in the late 1950s, earlier than Nüsslein-Vollhard and
Wieschaus, but much of the work of the two groups was contemporaneous. Both groups realized that development was under genetic control. Although Lewis focused on specific Hox genes, Nüsslein-Vollhard and Wieschaus saw the importance of identifying all of the genes that controlled the body plan, and they identified most of them.

[3] Hox proteins behave in this way because of a particular genetic feature of the Hox genes that produce them. Within their genetic composition, all eight Hox genes possess a nearly identical section of DNA, called a
homeobox. When Hox genes produce Hox proteins, the homeobox region of the Hox genes carries the genetic information to produce a specific part of these proteins called the
homeodomain. Once the protein is assembled, its homeodomain attaches to DNA sites that control genes, allowing it to function as a switch.

It is this particular characteristic that gave the Hox genes their name. In homage to Bateson, the identical sections of DNA were called "homeoboxes," since they were present in genes that, when mutated, resulted in Bateson's monsters, or "homeotic" mutants. The term "Hox gene" is a whimsical combination of "homeotic" and "homeobox."

[4] While classical genetics relies on changes in the order of the bases in the DNA strands, other heritable changes have been discovered—changes in the chemical makeup of the bases that control gene activities, for example—and are increasingly recognized as important in development and evolution. For example, the base cytosine might undergo a chemical modification involving the addition of a single carbon atom.

The New York Review of Books:
Volume 53, Number 8 · May 11, 2006

Copyright © 1963-2006 NYREV, Inc. All rights reserved. Nothing in this publication may be reproduced without the permission of the publisher. Illustrations copyright © David Levine unless otherwise noted; unauthorized use is strictly prohibited. Please contact with any questions about this site. The cover date of the next issue of The New York Review of Books will be June 8, 2006.


At 5/15/2006 08:13:54 AM, Anonymous said...

Nice Site!!

At 9/09/2006 09:10:04 PM, mortimore3x7 said...

“…every single concept advanced by the theory of evolution (and amended thereafter) is imaginary and it is not supported by the scientifically established facts of microbiology, fossils, and mathematical probability concepts. Darwin was wrong.”

“...The theory of evolution may be the worst mistake made in science.” I. L. Cohen, member of the New York Academy of Sciences and officer of the Archaeological Institute of America.

I searched the internet for evidence of transitional fossils of the vision system, or anything that could show us evidence of a slow gradual process of evolving eyes (there must be billions of such fossils or other such supportive evidence). I would like to find out where I might be able to go see one of these fossils.

Strangely, couldn't find a thing, only a goofy Pbs spoof...

which hypothesizes about a light sensitive skin patch that might be able to evolve into eyes.

What is the mechanism that drives the process of the evolution of vision? Beneficial mutations that would add the level of functionality required for a vision system have never been observed. Nor is there evidence that any such mutation has ever occurred that would account for such an increase in the genetic load. I have an imagination too, so I offer this scenario to add to the likelihood that it might have happened (pure speculation)….

A light sensitive skin patch would have to communicate with a primitive brain:

Skin patch: “You know Mr. Brain, it would be great if I had full color stereoscopic vision, give me a little more DNA, make it happen Scotty.”

Mr. Brain: “You’ve got it Skin patch, I can see how two eyes will help us have better depth perception, plus color differentiation would help me pick the right color of flowers for my girlfriend, it will be a lot of extra work, but I think we can do it.” (catch: there must be a feedback system between the molecular DNA level and the environment including the organism as a whole which directs this slow gradual process.)

Skin patch: “Don’t forget Mr. Brain… that you’ll have to add a multilayered visual cortex (billions of brain cells) to help you differentiate between, colors, contrast, night/day vision, motion… etc”

Mr. Brain: “No problem Skin patch, done. Just give me a couple of hundred million years…”

At 10/10/2006 08:08:23 PM, mortimore3x7 said...

“Given how much is now known, it might be fair to ask, are we finished with the retina, or are there more surprises on the horizon? ... The most recent surprise has been that a previously unknown ganglion cell type appears to function as a giant photoreceptor itself, without needing input from rods or cones. This ganglion's cell membrane contains light-reactive molecules known as melanopsins. Given such unexpected findings, it appears that there may still be much more to learn about how the retina works.”;jsessionid=baa4Z8J0ZiDsH_?fulltext=true, page 5.

Once those amazing (and I mean amazing, seriously) scientists have the retina completely reverse engineered and understood, and other scientists have all the other components of the vision system figured out, will they then be able to describe how it might have evolved?

In my previous post… the scenario of the light sensitive skin patch and brain communicating sounds ridiculous, but even so, it is not half as absurd as the idea of vision evolving.

As the number of identified parts in vision the system increases we begin to understand the critical dependency of different parts in relation to each other. The difficulty of explaining a gradual evolution of the system by slight modification skyrockets, and the likelihood of indirect scenarios plummets. In evolution terms you have to be able to explain how you can build this system gradually when there is no function until you have all of the parts in place.

Natural selection must select for a functional advantage in order to account for these systems of molecular machines, but in most cases natural selection eliminates. There are thousands of such molecular machines, the flagellum is the best example that I can think of, but when you consider the retina (the heart of the vision system) irreducible complexity becomes even more apparent.

Probably the most crucial feature of the flagellum is the ASSEMBLY INSTRUCTIONS, never even addressed by opponents of irreducible complexity. A precise sequence of assembly must build the structure from the inside out. Now try to imagine what the assembly instructions for the complete vision system might look like translated into English.

There is a feedback mechanism between visual cortex and the muscles (ciliary body) that controls the lens which allows the eye to focus on what we want to see. Which came first, the visual cortex, the ciliary body, or the nerves that connect the ciliary body to the visual cortex? Or did they slowly evolve together. Since the lens and pupil need each other to focus, is the lens useless without the pupil? I could ask the same question about the lens and the pupil… which came first?

Should we be impressed that an unintelligent process is able to evolve (by trial and error) a symphony of amazing “cells” (biological machines) that work together so that photons could be transformed into electrical pulses, which are then demodulated into full motion images in the visual cortex which we see somewhere in an intangible mind? Or should we admit… I don’t think evolution can account for the complexity of life.

In addition, these aren’t just photons that are being transformed. The photons come into the eye in a wave. A component of this wave is a frequency. We see a very small spectrum of “light” energy known as the visible range of the spectrum, 400 to 700 nanometers. This works out to 5.4 tera-hertz (5,400,000,000,000hz) on center frequency. I would like to know how an un-intelligent process “chose” this range of the electromagnetic spectrum as the light that we see. A long slow gradual process? I work on electronic equipment that operates in the 10khz to 1 gigahertz range, and the electronic circuitry that enables us to use this frequency is very sophisticated, it was designed. Not an argument for design, just an observation, connecting the dots.

Darwin had no concept of molecular machines. Darwin’s “natural selection” simply fails to account for the existence of these sophisticated living systems of biological machines.

There are many things that evolution can’t explain. Darwin stated: “If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous successive slight modifications my theory would absolutely break down.” There is no question about why Darwinists want to minimize the implications of irreducible complexity.


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