We are pleased to report that the recipient of the first annual National Association of Biology Teachers (NABT) Evolution Education Award is NCSE member Steve Randak, author of "The Children's Crusade for Creationism" (RNCSE 2001 Jan-Apr; 21 [1-2]: 27-8) and a voice for teaching evolution featured in the PBS series Evolution. Applicants were screened by a panel of judges looking for innovative and effective teaching, professional sharing, and community education efforts to promote accurate understanding of biological evolution.The award is generously sponsored by The Foundation for the Future of Bellevue, Washington, and includes a $1000 cash prize, up to $1000 for travel expenses to the NABT national convention, and a complimentary membership to NABT.

Randak has been teaching since 1967. In those years, he has distinguished himself in all the aspects used as criteria for the award. He has designed a highly successful curriculum, beginning with 4 weeks on the nature of science and deeply infused with evolution. He has created and adapted numerous classroom lessons and activities that effectively teach those topics. Some of those lessons became a part of the ENSI (Evolution and the Nature of Science Institutes) project, and are included in the ENSI web site. He actively participated in the second year of ENSI summer workshops, then became an active Lead Teacher, teaching the program in 7 Satellite ENSIs (SENSIs), reaching perhaps 150-200 teachers directly. He continues to create new lessons; his most popular recent contribution is "Footsteps in Time: Analyzing the Laetoli Trackways".

In addition, he has presented popular evolution workshops at many NABT and NSTA (National Science Teachers Association) conventions over the past 20 years. He has published articles in various journals relating to evolution teaching. One of his most notable innovations was his "historic role-playing": preparing, dressing, and presenting himself to his classes as prominent scientists from the past, including the role of Charles Darwin. He shared his passion and his techniques in an article for The American Biology Teacher. These efforts have garnered international interest.

In spite of his efforts (or perhaps because of his effectiveness), he and his colleagues were confronted with a mass student and community effort to include creationism in the district biology courses. A report on this confrontation, and how well it was handled, was included in the landmark WGBH/PBS series Evolution.

Congratulations to Steve from all of us at NCSE.

Introduction

The advent of high-throughput automated sequencing has given the discipline of genetics the complete genomic sequence of several model organisms, including humans (Lander and others 2001; Venter and others 2001), rice (Goff and others 2002; Yu and others 2002), weeds (Lin and others 1999; Mayer and others 1999; Adam 2000; Salanoubat and others 2000; Tabata and others 2000; Theologis and others 2000), worms (Bargmann 1998; Blaxter 1998; Clarke and Berg 1998; Ruvkun and Hobert 1998), fruit flies (Adams and others 2000; Myers and others 2000), and yeasts (Goffeau and others 1996; Wood and others 2002). This explosion of sequence data has given birth to the new subdiscipline called genomics, which examines organisms from a whole-genome perspective. If our genes are trees and our genomes a forest, then genomics allows geneticists to examine the whole forest at one time instead of spending our time focusing on one or a few trees (Gibson and Muse 2002).

By far the group that hosts the widest range and largest number of organisms whose genomes have been completely sequenced are the prokaryotes, that group we colloquially know as the bacteria. Genomes from both free-living and pathogenic bacteria have been completely sequenced, as have genomes from many eubacteria and several members of the Archaea (Fraser 2002). Because of their small, compact genomes and the relative ease of growing large numbers of them, bacterial organisms make prime candidates for genomic sequencing.

Genomics has revolutionized the way questions are addressed and has provided valuable insight into how genomes evolve (Arber 2002; Doolittle 2002; Knight 2002). Nevertheless, creationists, such as Bryan College's Todd C Wood, are using genomic data to support their contention that living things were independently created only a few thousand years ago. These "recent creationists" claim that completed genomic sequence data from bacteria called mycoplasmas refute evolutionary theory (Wood 2001); this article is an evaluation of Wood's efforts. As we shall see, in order to fit the genomic data into his recent creationist paradigm, Wood has to ignore previous work on mycoplasmal phylogeny and misrepresent contemporary evolutionary thinking with respect to parasitism.

Mycoplasmas — Mighty but Miniscule

Mycoplasmas are very small, prokaryotic organisms that lack a cell wall. Their small size and flexibility allows them to pass through bacteriological filters — a feature that makes them frequent nuisances in cell cultures. Mycoplasmas also have very small genomes that are one-fourth or less the size of most bacterial genomes — a feature that make them particularly good candidates for genomic studies (Woese and others 1985). Mycoplasmal DNA has higher proportions of the nucleotides adenine and thymine (they are "A-T rich"), and mycoplasmas show unusual nutritional requirements (Weisburg and others 1989). Mycoplasma and mycoplasma-like organisms (MLOs) collectively compose a class of microorganisms called Mollicutes. Mollicutes contains a variety of organisms that show strong symbiotic associations with other living organisms. Some are associated with insects and plants (Entomoplasmas, Mesoplasm, and Spiroplasma), others are oxygen-sensitive and found in the rumens of bovine and ovine mammals (Anaeroplasma and Asteroleplasma), and some associate with plants, insects, and warm-blooded animals, but do not require sterols for growth (Acholesplasma; Tully and others 1993). The largest subgroup within the mollicutes is the mycoplasmas, which consists of organisms from the genera Mycoplasma and Ureaplasma that must associate with humans and other warm-blooded animals to survive; in some cases, they cause human and animal diseases (Razin and others 1998). Not surprisingly, completed genomes of several mycoplasmas are available (Fraser and others 1995; Himmelreich and others 1996; Glass and others 2000; Chambaud and others 2001). The genome of Mycoplasma genitalium (see cover) is the smallest known at 568 070 base pairs (Fraser and others 1995). Many plant MLOs have not been cultured to date, which has delayed their characterization (Lim and Sears 1989).

Mycoplasmas According to Wood

Wood begins his article by asserting that all disease, pain, and suffering are the result of the sin of Adam and Eve (Wood 2001). He states, "Creationists generally explain the Curse-related imperfections as degenerations of originally beneficial structures." This is a common recent creationist belief, but this statement essentially endorses the evolutionary concept of exaptation, in which characters that serve particular purposes initially are later co-opted for new functions (Futuyma 1998). In the case of pathogenic bacteria, these microorganisms possess virulence factors, which help them to cause disease by adhering to or damaging host tissues or evading the host immune system (Hacker and others 1997; Hacker and Kaper 2000; Henderson and others 1996; Kathariou 2002; Law and Chart 1998; Potempa and others 2000). However, according to Wood, these virulence factors arose from features that were not originally used for that purpose. Consequently, Wood would argue, for example, that exotoxin A from the soil bacterium and opportunistic pathogen Pseudomonas aeruginosa, which inactivates eukaryotic elongation factor-2 and causes cessation of protein synthesis and cell death in vertebrate cells (Beattie and Merrill 1996; Beattie and others 1996; Yates and Merrill 2001), somehow originally had a benign function that degenerated to an inimical function after the Fall.

In summarizing a review article by Christopher Wren (Wren 2000), Wood writes that Wren "discusses three possible origins for bacterial pathogenicity" — lateral gene transfer, antigenic variation, and genomic decay. According to Wood, "Of these three themes, genomic decay is most consistent with the creationist idea of a degenerating creation." The Wren review shows that lateral gene transfer, antigenic variation, and genomic decay are trends observed in the genomic sequence data from pathogens. All three events are well documented in the literature and the completion of genomic sequences from pathogenic bacteria has extended our understanding of them. In other words, these events are not guesses about what makes microorganisms pathogenic, but are events for which we have solid genomic evidence.

Wood mentions these trends in the genomes of pathogenic bacteria because he thinks that the mycoplasmas demonstrate the best-documented case of pathogen-associated genome decay, even though members of the genus Rickettsia show pseudogenes and split genes, which are both signs of continuing genomic decay (Andersson and others 1998; Andersson and Andersson 1999a, 1999b; Ogata and others 2001). However, Wood also seems to accept that lateral gene transfer and antigenic variation are contributors to microbial pathogenesis. How appropriate is it to build a model of acquisition of pathogenesis that selects only one of these mechanisms while ignoring the other two?

Wood regards the mycoplasmas as a bacterial group that shows phylogenetic discontinuity from other bacteria because mycoplasmas lack a cell wall and use an atypical genetic code. Such a statement shows enormous disregard for earlier ribosomal RNA studies of mycoplasmas that clearly links them not only with some of the gram-positive eubacteria with genomes that contain low percentages of guanine and cytosine — which includes the Bacillus/Lactobacillus group (Lim and Sears 1989; Hori and others 1981; Maniloff 1983; Walker 1983; Rogers and others 1985) — but also specifically with a small subgroup of Clostridia represented by Clostridium innocuum and Clostridium ramosum (Woese and others 1985; Rogers and others 1985; Woese and others 1980).

Is the lack of a cell wall an adequate reason to consider the mycoplasmas phylogenetically discontinuous from the other eubacteria? The answer to this has to be no. Other bacteria lack cell walls. For example, the archaebacterium Thermoplasma acidophilum lacks a cell wall, but is completely unrelated to the mycoplasmas (Walker 1983; Woese and others 1980; Woese and Olsen 1986; Sanz and Amils 1988; Gaasterland 1999). Thus the lack of a cell wall by itself is not uniquely derived.

Furthermore, the ability of bacteria to lose their cell walls is well documented. Cell-wall deficient bacteria (CWDB), or "L-forms" as they are sometimes called, can appear under a variety of circumstances, and intensive antibiotic treatment can select for the formation of persistent L-forms that are resistant to antibiotics that attack cell wall synthesis (Domingue and Woody 1997).

Since the mycoplasmas tend to associate with insect, plant, or warm-blooded-animal cells, the loss of their cell wall is not that difficult to envision. The immune systems of these host organisms constantly search for foreign substances or antigens, and microorganisms that present fewer antigens are less easily recognized by the immune response. Since the cell walls of bacteria contain many potential antigens (Chatterjee 1997; Haslberger and others 2000; Heumann and others 1998; Ryan and others 2001), long-term association of bacteria with specific hosts could select for the generation of CWDB (Paton 1987; Sladek 1986).

Likewise, the origin of the alternative genetic code of some mycoplasmas is not as mysterious as it might initially appear. In some mycoplasmas, the codon UGA, which acts as a translational termination codon in most organisms, encodes the amino acid tryptophan, but besides this exception the genetic code of these organisms is completely standard. Mycoplasmal genomes contain low proportions of guanine (G) and cytosine (C) content, which means that their genomes show the effects of "AT-biased directional mutation pressure", which means that base substitutions in mycoplasmas consistently favor the replacement of C-G base pairs with adenine-thymine (A-T) base pairs. Consequently, C-G-rich codons like CCN, GGN, GCN, or CGN (where N indicates any base) are rare in the coding regions of mycoplasmal genomes, and mycoplasmal proteins have fewer glycine, proline, alanine or arginine residues (see Table 1, p 25). In conserved proteins, mycoplasmas tend to have lysine residues, encoded by AAA and AAG, instead of the arginine residues, encoded by AGG, CGN, and AGA, found in the proteins of other bacteria (Razin and others 1998). Mitochondrial genomes sometimes use an alternative genetic code, and in this case it seems as though selection for a small genome streamlines the total number of tRNAs the genome encodes and favors the use of alternative codons (Knight and others 1999; Saccone and others 2000; Knight and others 2001). Here again the origin of an alternative genetic code is not mysterious (Osawa and others 1992). Therefore the insistence on discontinuity between the mycoplasmas and other eubacteria is almost certainly unwarranted.

Creationist Classification of Mycoplasmas

Since the discipline of taxonomy attempts to group organisms according to phylogeny, creationist classification schemes often suggest some taxonomic reorganization. Such rearrangements reflect the creationist belief that some organisms were created ex nihilo during the Creation Week and diverged since to produce extant organisms (Sarfati 1999). This emphasis on discontinuity between organisms motivated WJ ReMine to suggest a nomenclature for creationist taxonomy by adapting the term "baramin" coined by Frank Marsh in 1947 to refer to a "created kind". According to the nomenclature formulated by ReMine, a "holobaramin" is a "group containing all and only organisms related by common descent". An "apobaramin" is a "group of holobaramins that are separated from all other organisms by phylogenetic discontinuities". Finally, a "monobaramin" is "a group containing only organisms related by common descent, but not necessarily all of them" and a "polybaramin" is a group of organisms that do not share a common ancestor. ReMine gives the following examples to clarify his nomenclature: mammals are apobaraminic, the placental dogs are holobaraminic, but dogs and wolves are monobaraminic (ReMine 1990). It should be noted that this classification scheme still affirms that biological classification should reflect phylogenetic proximity.

In applying ReMine's nomenclature, Wood proposes that mycoplasmas compose an apobaramin. Since an apobaramin is a group of holobaramins that are separated from other organisms by phylogenetic discontinuities, the mycoplasmas must contain holobaramins. This designation is slightly problematic, since the typical criterion for a holobaramin is the ability to produce fertile offspring; since bacteria lack sexual reproduction, such a standard is unreasonable. Therefore the norm for designating a bacterial group as holobaraminic is somewhat arbitrary. Contemporary bacterial taxonomy often uses the percentage of DNA homology among bacterial genomes to distinguish among bacterial species, and such techniques determine phylogenetic sequences with some accuracy (Martin 2002).

Wood considers Mycoplasma genitalium and Mycoplasma pneumoniae to be members of the "same monobaramin". His reason for this is that the genome of M pneumoniae contains all the genes found in the genome of M genitalium, even in the same gene order. Furthermore, the genetic material unique to M pneumoniae is localized to 6 segments of the genome bordered by repetitive sequences. Since the recombination-inducing protein RecA is encoded by the genome of M pneumoniae, it is entirely conceivable that these M pneumoniae-specific segments were deleted from the genome by RecA-dependent recombination to eventually form a genome that resembles that of M genitalium (Himmelreich and others 1997).

While it is certainly reasonable to suggest that M genitalium and M pneumoniae are directly related by common descent, why should we exclude other mycoplasmas, since 16S rRNA analyses link other mycoplasmas, like M muris, with M pneumoniae (Weisburg and others 1989)? Also, these same studies definitively link the mycoplasmas to the gram-positive bacteria with low percentages of G-C base pairs, even though the mycoplasmas do show some diversity as a group (Woese and others 1985). These data suggest that the mycoplasmas are related to low G-C gram-positive bacteria and form a coherent, though diverse, phylogenetic unit. Such a close affinity with another bacterial group and the somewhat downsized nature of mycoplasmas is hardly coincidental. Certainly the best inference to draw from these data is that the mycoplasmas evolved from a common ancestor (Weisburg and others 1989; Maniloff 1983; Woese and others 1980). This makes their designation as "apobaraminic" highly questionable.

In discussing the sequenced Mycoplasma genomes, Wood uses outdated information. At its initial publication, workers thought that the genome of M genitalium contained 468 genes (Fraser and others 1995) and this is the number used by Wood. Since that time, however, further work and annotation have definitively shown that this was an underestimate. A global mutagenesis study published in 1999 has shown that the genome of M genitalium contains 480 protein-coding sequences and 517 total genes (Hutchison and others 1999). In addition, the genome of M pneumoniae does not encode the 677 genes that Wood quotes from the original reference (Himmelreich and others 1996). Instead, further annotation has shown that the genome of M pneumoniae encodes 688 proteins and 42 RNAs, for a grand total of 730 genes (Dandekar and others 2000). All of these studies were published before Wood's paper, but none is cited or discussed by him.

Mycoplasmas - Made to be Small or Got Small After Getting Made?

Because of their greatly reduced genomes, mycoplasmas lack a variety of biosynthetic genes, and Wood thinks that this is an important feature of their genomes. This leads to a potentially interesting question:

But how do we know whether the created ancestors of M genitalium or M pneumoniae had the ability to synthesize amino acids? Could the lack of amino acid synthesis genes be a design feature of this baramin? (Wood 2001: iii)

First of all, a lack of biosynthetic capacity is a common feature in many pathogenic bacteria, and genomic reduction is a hallmark of strict parasites (Andersson and others 1998; Ogata and others 2001; Fraser and others 1997; Fraser and others 1998; Kalman and others 1999; Stephens and others 1998; Read and others 2000). Therefore there is nothing unusual about the lack of biosynthetic machinery in the mycoplasmas.

Second, Wood never really answers the questions he posed above, even though he makes it clear that he thinks that M genitalium arose from M pneumoniae or an M pneumoniae-like organism. Therefore, we will answer them. According to contemporary evolutionary thinking, since bacteria arose before warm-blooded animals, all microorganisms that live on or inside animals had to evolve from free-living bacteria that eventually formed symbiotic relationships with warm-blooded animals. All organisms must have some kind of biosynthetic capacity in order to survive unless they are parasites and acquire all their nutrients from the host. Thus it makes sense to postulate that the ancestors of contemporary mycoplasmas almost certainly had some kind of biosynthetic capacity.

From the creationist perspective, if mycoplasmas were originally created to inhabit the bodies of animals, then they might have already had reduced biosynthetic capacities, in the same way that organisms living in milk are unable to synthesize amino acids found in milk. Alternatively, mycoplasmas could have been created as free-living organisms that eventually became animal commensals and parasites.

Which of these hypotheses fits the evidence? According to Wood, the decay of the genomes of mycoplasmas fits the Creation/Fall model, since the Fall is the event that begins the cycle of degradation. However, genomic reduction as an adaptation to a parasitic lifestyle also fits the theory of evolution, and many obligate intracellular parasites show extensive genome reduction (Andersson and others 1998; Ogata and others 2001; Kalman and others 1999; Stephens and others 1998; Read and others 2000). Furthermore, the kinship the mycoplasma share with the Clostridium group is not a surprise for the evolutionary model, but it does pose some problems for the Creation/Fall model.

Another piece of data that fits the theory of evolution is that mycoplasmal genomes show signs of gene duplication as well as genomic degradation. The genome M pneumoniae shows duplication of the lipoprotein genes (Himmelreich and others 1997) and in the genome of Ureoplasma urealyticum there are 6 closely related iron transporter genes that apparently arose by means of gene duplication (Glass and others 2000). In addition, Mycoplasma pulmonis is capable of phase variation whereby it alters its outer membrane protein composition to escape detection by the immune system. The genome of M pulmonis contains several variable surface antigen or vsa genes, and the number of vsa genes varies between strains, thus demonstrating the occurrence of gene duplications within one species of Mycoplasma (Chambaud and others 2001).

Because mycoplasmas show reduced genomes, any gene duplications are probably indications of adaptations to a parasitic or commensal lifestyle. Other examples of obligate intracellular parasites with genomes that host both examples of gene decay and adaptive duplications are the Rickettsia (Ogata and others 2001). Gene duplications are examples of organisms' increasing the "information content" of their genomes, and they conflict with the creationist dictum that "mutations never add information but only reduce it" (Grigg 2000). Thus the evidence suggests that the mycoplasma not only downsized their genomes, but also reinforced other genes to make themselves better pathogens. This favors the evolutionary explanation for the origin of mycoplasmas, since the gene decay found in mycoplasmas does not occur alone, but in combination with gene duplications.

Parasites — Creation or Evolution?

Finally, Wood wishes to construct a framework for how mycoplasmas became human parasites after the Fall. To do so, he compares his ideas with mainstream thoughts on the evolution of parasitism. Wood writes: In the evolutionary model, pathogenicity and parasitism is thought to progress from very virulent (aggressive) forms to harmless or even mutually beneficial relationships. Advocates claim that natural selection will favor hosts that are resistant to the parasite and parasites that are not rapid killers of their own host environments. Thus as time progresses, the parasites evolve to less virulent forms and the hosts become tolerant of the more benign forms of the parasites (Wood 2001: iii).

Instead, Wood argues, God created the mycoplasmas as mutualists or commensals that became parasites after the Fall. The adaptation to parasitism included degradation of the mycoplasmal genome. Thus, the evolutionary scenario is challenged by the Creation/Fall model, which predicts just the opposite.

Unfortunately, the evolutionary story Wood tells is oversimplified. His reference for the concept of natural selection's decreasing virulence is a 13-year-old textbook (Pianka 1988). In the 1988 edition, Pianka qualifies this general expectation, writing: "In other situations, such as when a parasite finds itself engaged in a race against its host's immune response, selection may actually favor increased virulence" (Pianka 1988: 296). One must ask why Wood did not consult a more recent edition of Pianka, in which he would have found this revised discussion of the action of natural selection on virulence in parasitic organisms:

To the extent that natural selection favors evolution of reduced parasite virulence (see also subsequent discussion), parasite interactions may evolve gradually toward commensalisms and ultimately even become mutualistic interactions. Of course, selection could also proceed in the opposite direction (reverse arrows). Such changes may also occur during ecological time, as during the ontogeny of parasites (Pianka 1999: 323-5).

Pianka then gives examples of natural selection's decreasing virulence in the case of the myxoma and influenza viruses and increasing virulence in malarial parasites (Pianka 1999). Therefore the result of natural selection on the virulence of parasites is not a simple equation that applies to every case. Pianka closes this discussion with the statement "natural selection should favor levels of virulence for parasites with different types of transmission between hosts" (Pianka 1999). Thus Wood has contrasted his own recent creationist view with an inaccurate rendition of contemporary evolutionary thinking regarding parasitism, which amounts to the construction of a straw man.

Conclusion

In conclusion, Wood's article does little to establish any evidence from sequenced bacterial genomes for recent creationism. His paper ignores the published data on mycoplasmal phylogenetics, creates a straw man of modern evolutionary thinking, and applies a taxonomic system that has no demonstrated efficacy in classifying extant microorganisms. Further sequence data from other model organisms is forthcoming and it is likely that such data will only make the creationist case that much more difficult to accept.

According to the book jacket, this book consists of "a detailed history of one of the most important and dramatic episodes in modern science, recounted from the novel vantage point of the dawn of the information age and its impact on representations of nature heredity and society. Drawing on archives, published sources and interviews, the author situates work on the genetic code (1953-70) within the history of life science, the rise of communication technosciences (cybernetics, information theory and computers), the intersection of molecular biology with cryptanalysis and linguistics, and the social history of postwar Europe and the United States." This is an accurate, but incomplete, description of the book. In addition, and perhaps more importantly, the book is a discourse on why the author believes that the genetic code is not really a code in the true sense of the word, and why DNA contains chemical and biological specificity but not information per se. In the first chapter, she writes:

My thesis is that molecular biologists used "information" as a metaphor for biological specificity. However, "information" is a metaphor of a metaphor and thus a signifier without a referent, a catachresis. As such, it became a rich repository for the scientific imaginaries of the genetic code as an information system and a Book of Life. The information discourse and the scriptural representations of life were inextricably linked. Metaphors, as I will examine, are ubiquitous in science, but not all metaphors are created equal. Some, like the information and code metaphors, are exceptionally potent due to the richness of their symbolisms, their synchronic and diachronic linkages and their scientific and cultural valences (p 2).

After reading the book jacket, the preface and the first chapter, one is left with the question "Who is the target audience for this book?" As best I can tell, it is aimed at professional science historians. The writing is too difficult and unfriendly to be aimed at the amateur science history enthusiast. Furthermore, the author assumes that the reader already is familiar with the history and the individuals involved. A simple, limited biography on each of the key individuals at the end of the text would have gone a long way to help the reader. It is likely that a neophyte enthusiast who managed to maintain interest while wading through the difficult text would quickly be confused and frustrated by the constant infusion of new names, all without adequate introduction.

Yet I cannot imagine that the professional science historians would be much interested in this book either. The author's approach seems to be more fragmented than unified in her attempt to link molecular biology, linguistics, information theory, and yes, her own personal philosophy into this historical account of the unraveling of the genetic code. Had Kay restricted herself to describing the history of the unraveling of the genetic code, the text would have been much more accessible. This is all the more disappointing because the source material is rich and varied, consisting of quotes, letters, interviews, photographs, and drawings. It is unfortunate that Kay places such a large burden on her reader, expecting that the reader can pull together the salient details and form a coherent picture of this compelling and world-changing story with little help from the author.

While the writing style and her decision to focus on so many disciplines make the book a difficult read, it is actually her apparent philosophy on the nature of information and its relationship with DNA that I have the most problem with. Interwoven with Kay's description of the insights, experimentations, and technology that resulted in the discovery of the genetic code is her description of the researchers' struggle to reconcile their viewpoints on linguistics and information technology with their laboratory observations. On one end of the spectrum is the view that the "genetic code" is nothing of the kind; rather, it is a metaphor for biological specificity. At the other end of the spectrum is the view that the "genetic code" is actually the language for life, complete with all of its spiritual and scriptural qualities.

Kay, judging from her thesis statement in chapter 1 as well as her discussion in the conclusion, is a supporter of the first view. In a sense, her view, or others' for that matter, should not really matter. Whether one believes that the genetic code is a representation of the "Word of God" or that it is merely a representation for the biological specificity necessary for life, this belief does not change what it is. In the process of learning about or trying to understand something, we naturally liken things to one another. We relate the unfamiliar to the familiar and then document the differences. "'This' is like 'that' except for the following differences."

Thus, in trying to understand how a section of DNA relates to a specific protein, some researchers found similarities to a code, while others found similarities to a language, and others found similarities to neither. What I have to take issue with is Kay's assertion that DNA does not really contain information; rather, it represents biological specificity. In her conclusion, she argues for this by pointing out that despite our knowledge and understanding of the genetic code, science has been largely unsuccessful in understanding what we have read: being able to distinguish coding and non-coding sequences, being able to sort out the plethora of polygenic disorders, and finding any true promise in the field of gene therapy. This philosophy smells too much to me like that of the creationist: "Life (or some feature of it) is too complex to have evolved on its own. Therefore God (or some other designer) must have designed it." Kay seems to be arguing that because today we do not have all the answers, because we are not "fully literate in the language of DNA" (to use a different metaphor), that DNA does truly contain information.

In my opinion, DNA does contain information, information that directs a cell in how it should operate and behave. Today, when given an mRNA sequence, computer programs without the aid of human intervention can read that sequence and give the amino acid sequence of the resulting protein. Additional progress has been made in identifying signals for intron-exon junctions, transcriptional start and stop sites, and other regulatory signals. Today, our understanding of these sequences, this DNA information, is incomplete. Our understanding is even more limited when we consider the global landscape of the genome. How does a cell know which regions of the genome to leave active, while silencing others? How is development regulated? We understand that there is a dizzingly complex series of feedback loops, where DNA, RNA, protein, carbohydrates, fats, and a variety of small organic molecules all interact for the survival or death of the cell, tissue, organ, and organism. The information for these interactions, the instruction set, is all contained in the DNA. Our knowledge and understanding of this information is currently imperfect and incomplete. The complexity that results from the interactions between the cellular (and extracellular) components makes it difficult to tease out the necessary signals and information. This results in a "chicken or egg" sort of paradox. Again, regardless of what one's view is, it does not change the way things actually are. To deny that DNA contains information, based on our current inability to use it to describe life, is simply shortsighted.

In the end, I cannot recommend this book. Although I am impressed with the thoroughness and completeness of her research, I find that the process of bringing these ideas together has resulted in text that is unnecessarily dense and that ultimately falls far short of the promise inherent in this naturally compelling story.

Readers who were enchanted with the first volume of Janet Browne's biography of Darwin will be equally pleased with this one. Here again Browne presents Darwin as the central figure in an expanding circle of contexts: the context of family, of upper-middle-class gentry, of Whig politics and religious outlook in a rapidly industrializing nation, of British naval domination and colonial empire around the globe. Darwin himself appears as a wealthy country gentleman settled comfortably in his house at Downe, surrounded by family and servants, in close touch with his scientific friends by letter and by occasional visits, protected from unwanted social engagements and professional responsibilities by chronic poor health, devouring scientific books and journals, observing and experimenting on the potted plants, pigeons, bees, and earthworms in his study, gardens, aviary, and the surrounding countryside, enlisting the aid of his children, servants, plant and animal breeders, and correspondents foreign and domestic in his search for facts, facts, facts — which would support his "subversive" theory of evolution by natural and sexual selection.

When Alfred Russel Wallace sent him an essay setting forth a similar theory and asked his help in getting it published, Darwin was forced into action. Darwin's friends Charles Lyell and Joseph Dalton Hooker arranged to have Wallace's essay and some of Darwin's unpublished writings — including a letter to the American botanist Asa Gray predating Wallace's essay — read before the Linnaean Society and published in its journal. Relieved but shaken, Darwin went to work preparing an "Abstract" of the big species book entitled "Natural Selection" begun in May 1856. In November 1859, Darwin's "Abstract" appeared in print under the title On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life.

Janet Browne's account of Darwin's style of presenting his argument (p 53-7) is a masterpiece of interpretation and analysis linking that style to Darwin's gentlemanly personality, his use of well-known literary genres, his homely illustrations from the practical pursuits of gardeners and plant and animal breeders, his connections with leading men of science, and his implicit evocation of the competitive ethos and secularizing appeal to natural law in an industrializing British nation. "And what a book it was", writes Browne. "Few scientific texts have been so tightly woven, so packed with factual information and studded with richly inventive metaphor."

As to Darwin's mode of reasoning by analogy, Browne is certainly right that Darwin regarded the analogy between artificial and natural selection as "the best and safest clue" in unraveling the secrets of nature. In place of Aristotle's analogy of nature as a well-run household economy, Darwin proposed the metaphor of "natural selection" — evoking both progressive British scientific agriculture and the competitive market economy extolled by Adam Smith. But whether Darwin's metaphor was intended to suggest a godless probabilistic universe governed by "irregular, unpredictable contingencies", by "statistics and chance", as Browne seems to suggest (p 56, 283), seems doubtful. Although Darwin's theory can be seen in retrospect as requiring a revised philosophy of science, Darwin himself seems to have tried to be a good Newtonian scientist. In his big pre-Origin species book, he defined nature as "the laws established by God to govern the universe" — "his most magnificent laws" he had called them in his notebooks. In the Origin these became "the laws impressed on matter by the Creator", the succession of organic forms produced by them "ennobled" in the light of Darwin's theory.

Nor was Darwin's view of nature as "bleak" as Browne depicts it. He believed that natural selection brought about gradual organic "improvement", not simply adaptation. The more evolved forms tended to be "improved" forms. "If I have a second edition", he wrote to Lyell in 1860, "I will reiterate 'Natural Selection' and, as a general consequence, Natural Improvement." And he could sound like an evolutionized William Paley when, as in the closing paragraph of the chapter on "The Struggle for Existence", he reflected that "we may console ourselves with the full belief that the war of nature is not incessant, that no fear is felt, that death is generally prompt, and that the vigorous, the healthy, and the happy survive and multiply."

Having led her readers through the Origin, Browne gives a stirring account of how Darwin from his study, largely by correspondence, orchestrated the campaign to ensure its favorable reception, sending copies to his foreign correspondents and superintending arrangements for translations, combing the reviews, cheering on Huxley, Lyell, Hooker, Gray, and others in their efforts to assist him, and paying for republication in pamphlet form of favorable reviews. "Darwin's opponents", Browne writes, "failed to achieve anything like the same command of the media or penetration of significant institutions. Within a year after publication, it was nearly impossible to break into Darwin's tightly integrated group without some express homage to evolution."

In Part II of Browne's second volume, devoted to the 1860s, we see Darwin alternately at work on the successive revised editions of the Origin, on his beloved sundews, orchids, and Venus fly traps, on two fat volumes on variation under domestication (containing his ill-fated theory of heredity called "pangenesis"), and on the growing anthropological and archaeological literature concerning cultural evolution, until overwork ruined his health and aged him noticeably. Janet Browne weaves the story of these years skillfully, empathizing with Darwin's love of observing and experimenting on plants, noting how all his research was directed toward vindicating his theory of evolution by natural selection, how that theory and Malthusian political economy were part of a common cultural context, how Darwin's Origin was received by philosophers, philologists, literary figures, American transcendentalists and Unitarians, and by scientists such as Alfred Russel Wallace and his erstwhile traveling companion in Brazil Henry Walter Bates, and, finally, how science had become Darwin's lifeline. "Without this, he had 'nothing' to make his life worth living."

As the post-Origin decade drew to a close, Browne explains, Darwin felt compelled to publish his views on human evolution — views he had feared to make known, hoping that Lyell or Wallace would step forward. Determined to defend his theories, Darwin began work on the book which, after considerable negotiation with his publisher, bore the title The Descent of Man and Selection in Relation to Sex.

In her discussion of this, the most revolutionary of Darwin's books, Browne cannot muster the same enthusiasm she displays in her account of the Origin. Darwin, she says, was trying to do too many different things — the natural history and lineage of mankind, the mental faculties of animals and humans, the origin of language, morals, and music, sexual selection in animals and humans, and the human progress from savagery to civilization. Browne reports Darwin's views on these subjects mostly without comment, although she obviously has reservations about some of these views. We learn that Darwin thought that language had emerged gradually from the vocalizations of apes, that religious belief was nothing more than a primitive urge to bestow a cause on otherwise inexplicable natural events, that moral values were relative, that there had been a progressive advance in moral sentiment ("the 'higher' values were, for him, ... the values of his own class and nation"), that "although he rejected the outward trappings of the established Anglican religion, he subscribed wholeheartedly to its underlying values and presumed the onward march of civilization", that men possessed an innate intellectual superiority over women, and that his theory of sexual selection could explain not only the diverging physiques and behavior patterns of males and females but also the origin of human geographical diversity, perhaps even the foundations of human civilization itself.

The theory of sexual selection, Browne declares, lay at the center of his argument concerning human evolution. Why Darwin should have devoted more than half of his book on humans to sexual selection in non-human animals remains unexplained. Browne suggests that Darwin was making an analogy to artificial selection, in which "breeders chose traits for 'use or ornament," imposing their own taste or judgment on organisms".

But Darwin was not done with humans. No sooner was the Descent published than he resumed his studies on the expression of emotion in humans and nonhuman animals — the third and final link in the merging of human and animal evolution which Darwin had envisaged in his 1830s notebooks. Once again, through Browne's fluent prose, we see Darwin ransacking his old notes, studying the expressions of children and domestic pets, firing letters in every direction, contacting directors of lunatic asylums and medical and art photographers for photographs to illustrate his thesis. "The expressions that pass over human faces", writes Browne, "were, to him, a daily, living proof of animal ancestry." And it struck a responsive chord in his readers. The Expression of the Emotions in Man and Animals sold very well.

In Browne's last 3 chapters, we see Darwin returning to his beloved botanical studies and his earthworms, enjoying Punch's ape-man cartoons, managing a stream of visitors with the aid of his family and friends, answering letters inquiring about his religious views without equivocation ("these were the most godless years of his life"), promoting his sons' careers, accepting the honors bestowed upon him with due modesty, promoting the cause of science in every way he could, and, in May l876, beginning work on an autobiography. In Browne's view, Darwin, for all his brilliance in analyzing scientific problems, was not good at self-analysis. "He was", she says, "constructing himself not as a person, living and growing, but as a series of publications, an author." Only on the subject of religion did he drop his self-protective guard. He seemed, says Browne, to accept loss of faith as an inevitable feature of the life of a scientist. "No other experiences, he implied, could match those he encountered in science." Inward conviction of God's existence could not be trusted, nor could he trust his own reason in the matter, knowing that his mental faculties were developed from "a mind as low as that possessed by the lowest animal."

Although Darwin could not know it, at the same time that he was writing his autobiography, Arthur James Balfour was hard at work on a book entitled A Defence of Philosophic Doubt. Being an Essay on the Foundations of Belief. This book, published in 1879, contained a searching critique of the positivistic, agnostic, empiricist philosophy of science and nature advocated by John Stuart Mill, Herbert Spencer, John Tyndall, and others, and proposed instead that both science and theology were attempting to represent in human terms a reality transcending the power of human thought to imagine correctly or grasp fully. In 1895, in his next book Foundations of Belief, Balfour extended his critique to embrace Darwin's evolutionary naturalism, arguing that it deprived the Victorian values cherished by Darwin, Huxley, and Balfour himself of any rational foundation, thereby undercutting the foundations of Western civilization. Huxley, then struggling with his final illness, mustered enough strength to defend agnosticism and predict the eventual triumph of the scientific spirit over Judaeo-Christian obscurantism. The debate over evolutionary naturalism thus begun is still with us. One wonders what Darwin's position would be in the light of twentieth-century developments in science, warfare, and Western culture.

Janet Browne's biography does not raise these questions. But no one has described Darwin in his Victorian context better or more engagingly than she. Her prose is well-nigh perfect, her research exhaustive, her powers of empathy remarkable, her 24 pages of illustrations fascinating and illuminating, her judgments well balanced. Darwin could not have asked for a more sympathetic, discerning, and thorough biographer.