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Category: General Interest; Microbial Genetics and Molecular Biology
Inspired by a 2009 colloquium on microbial evolution convened at the Galapagos Islands, Microbes and Evolution celebrates Charles Darwin and his landmark book On the Origin of Species. Through this collection of 40 first-person essays written by microbiologists with a passion for evolutionary biology, you'll come to understand how their thinking and career paths in science were influenced by Darwin's seminal work.
The essays in Microbes and Evolution explore how the evidence of microbial evolution deeply and personally affected each scientist. Prepare to be suprised and delighted with their views on the importance of evolutionary principles in the study of a variety of aspects of life science, from taxonomy, speciation, adaptation, social structure, and symbiosis to antibiotic resistance, genetics, and genomics.
Paperback, 299 pages, illustrations, index.
Charles Darwin spent a few weeks during September and October of 1835 exploring the Galapagos Islands. His observations during that time reverberate deeply in the history of science because the features of the plants and animals that Darwin saw there contributed greatly to the development of his ideas of evolution by natural selection. Of these islands he remarked in The Voyage of the Beagle (1939), “The natural history of this archipelago is very remarkable: it seems to be a little world within itself….” But compared to the myriad microscopic worlds present in every handful of Galapagos soil that Darwin set foot on, the archipelago would not be a “little world within itself” but a vast universe containing countless worlds of unimaginable diversity. For every grain of soil, every drop of water of our planet is rich with microbial life that lies there, waiting to be discovered.
Bacteria had to wait in the wings for many years before they could star in evolution experiments. The new molecular biologists pursued their reductionist methods, while evolutionary biologists, grounded in natural history, did not want to study things they couldn’t even see. It was also difficult to tell bacterial strains and species apart, and many evolutionary biologists were focused on using patterns of similarities and differences to unravel the relationships among organisms. But eventually the field of microbial evolution awakened, and for several reasons. In the 1970s, Carl Woese used differences in DNA sequences to study the evolutionary relationships among bacteria and other microbes, revealing extraordinary diversity beneath their outwardly simple appearances. At the same time, other evolution experiments were pursued with Escherichia coli. Avidians are computer programs that copy their own genomes, and they live in a virtual world that exists inside a computer. But their replication is imperfect, so Avidians sometimes mutate. While most mutations are deleterious, some provide an advantage that allows a mutant to obtain resources and replicate faster than its competitors in that virtual world.
A review of Aristotelian reality, represented by the diversity of bacterial cells with small and reduced genomes which evolved naturally, can help delineate the Platonic idea of a hypothetical minimal cell. The study of minimal cells can benefit enormously from the study of present-day organisms with small genomes by showing how relatively simple biological systems have evolved and currently operate. Thus, cells and reduced genomes of endosymbionts, parasites, and free-living organisms are examples of naturally evolved minimal gene sets. The diversity of lineages, nutritional strategies, and ecological niches occupied by these free-living organisms with small genomes is noteworthy. The smallest photosynthetic cells, represented by Prochlorococcus marinus, have slightly larger genomes (1,660 kb and 1,765 genes). Genomes with fewer genes than the smallest free-living prokaryote belong to parasitic or endosymbiotic organisms and are found in 15 different orders among currently sequenced genomes. The reduction of the flagellar apparatus in Buchnera is a wonderful lesson in evolutionary tinkering that shows its convoluted history in two main respects. First, certain components of the retained flagellar genes serve not for bacterial mobility but, rather, to export proteins that could eventually become involved in infecting new surrounding host cells, ovaries, or embryos, thereby enabling Buchnera to be vertically transmitted to its host’s offspring. Second, and probably more importantly, Buchnera has recovered functions that were present in the ancestors of current free-living relatives, which possess a complete flagellum. If this is the case, the flagellum would be an example of reducible complexity.
Charles Darwin’s research on the spatial distribution of macroorganisms formed an integral part of his arguments for natural selection and played a foundational role in the burgeoning field of biogeography. Darwin recognized three biogeographic patterns that he described in terms of “great facts” in On the Origin of Species. In summary, these are: (i) environmental conditions alone cannot account for the dissimilarity of flora and fauna among geographically distinct regions; (ii) barriers to dispersal significantly contribute to these differences; and (iii) although the spatial variability in community composition within regions is substantial, these communities remain evolutionarily related. The prevailing view of Darwin and his contemporaries was that microorganisms (microbes) are dispersed globally and able to proliferate in any habitat with suitable environmental conditions. Microbial diversity shifts across the surface of the Earth as a consequence of the three forces highlighted by Darwin when considering plants and animals: the environment, dispersal, and diversification. The author’s laboratory is striving to overcome limitations of time, resources, and sequencing efficiency, by developing a spatial theory of community assembly that quantifies the evolutionary relatedness among individuals (or genomes or genes) within and among sample locations across the landscape. This new framework combines four crucial ingredients: spatial dispersal, by which individuals disperse seeds or move across a spatial landscape; evolutionary diversification, through which genetic novelty is introduced to a community; individual-based processes, so that the discrete nature of individuals is accounted for; and demographic stochasticity, the random nature of birth, death, and dispersal processes.
Based upon observations with powerful telescopes, astronomers teach us that the Milky Way has more than 1012 stars and that 1012 similar-size galaxies account for the more than 1024 stars in the universe—roughly equivalent to the number of grains of sand on Earth. The number of microbes on Earth eclipses the number of stars in the universe by many orders of magnitude. And the collective biomass of single-cell organisms on Earth outweighs all of the plants and animals combined. Given the massive number of microbes with seemingly unlimited metabolic diversity, the accumulation of mutations during the past 3.5 billion years could have led to enormous numbers of distinct microbial populations that exhibit high levels of genetic diversity and phenotypic variation. Closely related taxa have nearly identical rRNA sequences, while microbes that diverged from each other hundreds of millions of years ago exhibit greater levels of nucleotide variation. It became possible to infer objective dichotomous evolutionary branching patterns that describe taxonomic relationships for cultured microbes. The expense of sequencing full-length rRNA genes has constrained most molecular inventories of microbial populations. The promise of discovering new phylotypes among the lower-abundance taxa fostered experimental designs where low-resolution procedures—e.g., restriction fragment length polymorphisms—identify putatively distinct clones for DNA sequencing. The combination of rapid gene isolation technology afforded by polymerase chain reaction (PCR) and automated DNA sequencing capabilities soon opened another window on microbial diversity.
The complex networks of life are driven by the action of microbes, simultaneously synthesizing and consuming, moving metabolites and energy with relentless, tireless efficiency. Communities of microbes are deeply interdependent, and every bacterial species depends on one or more other species for survival. The consequences of this interdependence are profound, making cooperation and collaboration at least as important as competition in the shaping of bacterial communities. The ability to synthesize a toxic protein raises some vexing challenges not only for the target cells but for the producers themselves. How, after all, can a producer strain keep from becoming the victim of its own lethal weapon? It is because that the producing cell also synthesizes an immunity protein that binds tightly to the killing domain of the bacteriocin, rendering it temporarily inactive. This safety catch will remain on until the bacteriocin is safely inside its intended target cell. The delicate balance between producer cells and target cells plays out in a surprising minuet that has been likened to the childhood game of rock-paper-scissors. A bacteriocin-producing strain emerges and acts as "paper" in our game, defeating the sensitive strain as "paper" covers "rock." Eventually, no sensitive cells survive, and only bacteriocin producers rule. But the emergence of a resistant strain from within the producer population plays the role of “scissors.” Little by little, the population shifts from bacteriocin producers to resistant cells: scissors beats paper. Yet in the absence of producers, the cost of resistance is high and the benefits nonexistent.
The antibiotic era, stemming from the first clinical use of penicillin in the 1940s, along with vaccination and sanitation, provided a sense of confidence in medicine that infectious diseases had been conquered. As the U.S. Surgeon General declared in 1967, it was time to "close the book on infectious disease." Bacteria are able to grow quickly to remarkably large population sizes and have an uncanny ability to exchange genes across different species. The evolution of antibiotic resistance is an example of what is often referred to as the “Red Queen effect.” Antibiotics can control many infections, but there are ominous reports of some pathogens now being resistant to all known antibiotics. Some countries are enacting much stricter controls on antibiotic use, and scientists are hoping to develop novel antibiotics that, because of their very nature, do not lead to the rapid evolution of resistance.
This chapter focuses on the genetic and evolutionary aspects of antibiotic resistance, and how an unintended global experiment in selection has taught us about genetic variation and evolution in the bacteria. An antibiotic may fail to reach its intended target, for example, because it cannot cross the cell wall and get inside the bacterium. Genetic alterations can cause previously susceptible bacteria to become antibiotic resistant. This is a major reason why many antibiotics are ineffective against gram-negative bacteria, and why pharmaceutical companies have devoted great research efforts to developing variants of successful antibiotics with different activity spectra. The genetic pathways by which bacteria can evolve antibiotic resistance can be broadly divided into two classes: (i) those where genetic alterations reduce the effective interaction between the antibiotic and its target in the bacterial cell and (ii) those where genetic alterations reduce the chemical effectiveness of the antibiotic molecule itself. An important aspect to consider in the evolution of antibiotic resistance is the source of the genetic alteration responsible for the resistance. The global significance of horizontal gene transfer in providing the raw material for bacterial evolution in general, and antibiotic resistance specifically, is one of the major lessons we are still learning from our use of antibiotics. One way to evolve antibiotic resistance is by mutating the gene coding for the target of the antibiotic. A resistance phenotype can also be generated by any mechanism that inactivates the antibiotic.
For bacteria, survival means weathering periods when no food is available—which is the majority of the time—and reproducing when conditions permit. Rapidly growing bacteria typically form large colonies within a day or two, while weeks are required before some of the small colonies formed by slow-growing bacteria are visible. Research from the author’s laboratory group supports a model for trade-offs in the central flow of information in cells the translation of RNA into protein by ribosomes. This is where cells spend the majority of their energy, linking amino acids together to form a functional protein. And so if there is selection for efficient energy utilization, it makes sense for selection to act on the ribosome. The author found basic difference in the rate at which ribosomes synthesize protein. The rapidly growing bacteria synthesize proteins much faster, but they appear to do so less efficiently. This offers the prospect of a fundamental mechanism that could help explain the distribution of microbes in natural and managed ecosystems. Although it was not immediately obvious how Charles Darwin’s ideas would apply to the microbial world, we are beginning to understand some basic differences in microbes and how the environment may select for survival of the fittest—even in the world of single-celled organisms.
Phage represents the ultimate mash-up of selfish genes producing hopeful monsters—that is, groups of genes that promote their own propagation but which can often result in dramatic changes for the host that acquires them. The author and his group accumulated enough metagenomic data to determine the scale at which the global virome was contributing to the metabolic potential of their hosts. Compared to the microbes, the phage were enriched in genes with functions such as nucleic acid metabolism. More striking was the fact that the viromes also carry many genes associated with other unexpected aspects of metabolism (vitamin, cofactor, cell wall, and capsule synthesis), as well as genes for virulence factors, stress response genes, and chemotaxis genes. The phage-driven evolution of microbial hosts extends beyond the phage themselves. It was shown that many of the changes in microbial metagenomes were actually responses to predation by phage and protists. A most exciting recent development has been the discovery that host cells have rapidly evolving sequences, known as clustered, regularly interspaced, short palindromic repeats (CRISPRs) that serve as a bacterial immune system to prevent phage infections in bacteria. The phage-microbial evolution is much more rapid and dynamic than Charles Darwin could have imagined. Phage transport genes all over the world and change the evolutionary trajectory of the microbes they infect by introducing genes that completely change the phenotypes of their hosts.
Charles Darwin wonderfully surmised that natural selection could account for Earth’s biodiversity, giving rise to what he described in his book as "endless forms most beautiful and most wonderful." Commemorating the 150th anniversary of his book publication, in 2009 the Yale Center for British Art held the exhibit "Endless Forms: Charles Darwin, Natural Science and the Visual Arts," describing the profound and lasting influence that Darwin’s scientific contributions have had on artistic views of the natural world. With Malthus as his muse, young Darwin was inspired to ponder how the natural world was composed of finite resources, which caused a struggle for existence among variants within a population. One apparent theme in the evolution of life is that natural selection often pushes organisms to take on parasitic lifestyles as their creative solution. Organisms may be pushed to lay down their arms and declare detente, by evolving to become mutualists that cooperatively support each other in the struggle for existence. Other amazing mutualisms involving microbes and multi-cellular organisms are awaiting discovery, which will similarly rewrite our understanding of the mutualisms documented by Darwin and other naturalists of his time. Microbiologists tend to focus overwhelmingly on the "bad" bacteria that do us harm and on the ability of microbes to produce antimicrobials that inhibit each other’s growth (again, here microbiologists are strongly interested because they can co-opt these natural products to thwart disease pathogens).
Everything that a cell does within a biofilm can have immediate consequences for its neighbors. This includes the most fundamental action of any microorganisms (microbes): cell division. It is argued strongly-and controversially-that we need to find ways to regulate human population growth in order to avert environmental tragedy, an argument that may be more likely to be heeded now than it was originally. Many pathogens for example bacteria, rely on both quorum sensing and secreted products to inflict harm upon us. This includes the secretion of enzymes that kill host tissue by Salmonella enterica (typhoid fever) and Pseudomonas aeruginosa; toxin production by Bacillus anthracis (anthrax) and Vibrio cholerae; and the widespread production of compounds that break down antibiotics, such as the β-lactamases that destroy penicillin. The chapter focuses on microbial societies and the potential for their own microtragedies. Traditional antibiotics act by killing or stopping cell division, and resistant that can grow in the presence of the antibiotic rapidly replace the original susceptible strains. Resistant mutants that re-evolve secretion can promote the growth of susceptible cells around them. And, more than this, the susceptible cells do not pay the cost of secretion, which can put the resistant strain at a competitive disadvantage. At least in principle, this can slow the rise of antibiotic resistance. By recognizing that microbes rely on both sociality and altruism to cause infection, a novel strategy for treatment is revealed.
Opponents of evolution cannot deny the obvious successes of human-driven selection of domesticated animals and generally admit the processes of microevolution in nature. The chapter shows that minor genetic changes can lead to a dramatic shift from the original natural environment (habitat) of the species to completely new ones. In turn, these shifts in habitats could lead to physical separation of the organisms from the same species and their eventual macroevolution into different species. Baas-Becking hypothesis is related to the important similarity between humans and bacteria; humans adapt to different environments not by changing genetically but by inventing various tools that allow us to successfully survive and increase in numbers in new environments. To discuss the basis and significance of natural mutations within bacterial species, it is actually useful to make parallels not with domesticated animals but with ourselves, humans. As much as adaptive mutations seem to be important for microevolution, very few such natural changes are found within species of higher organisms. Studying microevolution of bacterial species can bring light to the elusive processes of microevolution in higher species. An understanding of the microevolution mechanisms and dynamics will bring us closer to grasping how new species and complex physiological systems have gradually evolved.
The pseudogenes must be extremely rare in bacteria compared to plants and animals because bacteria grow rapidly and have small genomes. Work was carried to develop some clever genetic tricks for identifying such "host specificity" genes in Typhi. After years of hard work, it seems that the reason for restriction of Typhi to humans was not because of the acquisition of new genes but because Typhi had mutations in many different genes scattered around the chromosome. In the mid-1990s it became possible to determine the entire sequence of bacterial genomes. The genome sequences of different types of bacteria provided surprising insights into genes not known earlier. But the most striking insights came from comparisons of the genome sequences of closely related bacteria. In contrast to Salmonella Typhimurium, the human-specific pathogen Salmonella Typhi was one of these organisms with a large number of pseudogenes. In addition, many of the pseudogenes were in parts of the genome that had been identified as containing mutations that restrict host specificity. It had to be known whether the pseudogenes are responsible for restricting Typhi to the human host or whether the accumulation of pseudogenes is simply an accident. The genome sequencing studies clearly indicated that pseudogenes occur in bacteria, and the results showed that pseudogenes can influence the host range of bacterial pathogens.
Many bacterial regulatory circuits are not digital but analogue devices. In other words, their responses are not all-or-none but are proportional to the stimulus to which they respond. Overlap and redundancy contribute to bacterial robustness. Bacterial populations benefit from nondeterministic, random variations in their molecular circuitry-called epigenetic variation because the processes are heritable but not due to mutational changes in the DNA. Extrachromosomal DNA has been traditionally viewed as the main toolbox for bacterial genome plasticity. Plasmids are crucial indeed for bacterial adaptation. Studies with clinical isolates have indicated that hypermutable bacterial lineages may adapt better to harsh environmental conditions. While it seems out of the question that such hypermutable lineages may enter an evolutionary dead end, their existence emphasizes the importance of mutation as an adaptive strategy. Population geneticists have predicted that variation of mutation rates in response to environmental circumstances might have selective value. Under comfortable circumstances, however, elevated mutation rates would be unnecessary and probably detrimental. An example of variation of mutation rates upon environmental influence is observed when E. coli is exposed to fluoroquinolones, a class of antibiotics that target DNA topoisomerases, thus blocking DNA replication. Increased mutation rates may produce additional mutations that can further facilitate survival. SOS induction associated with antibiotic challenge is not the only environmentally controlled mechanism known to modulate mutation rates. Bacteria are equipped with analogue devices that permit efficient adaptation to changing conditions. Bacterial populations often display bistable or multistable states, created either by built-in mechanisms or by random fluctuations.
The family Enterobacteriaceae, whose members are often referred to as the enterics, comprises several bacterial species that are known because of the diseases they cause in humans and/or in animals or plants of economic importance. This chapter presents four possible genetic scenarios to account for the differences that exist between the closely related bacterial species, Salmonella enterica and Escherichia coli. It also illustrates how variation in gene regulatory strategies can result in distinct bacterial behaviors. The comparative studies discussed in this chapter have revealed two distinct aspects that distinguish individual enteric species. First, organisms often vary in the environments in which the polymyxin B resistance proteins are produced, and this is often due to changes in the amino acid sequence of a regulatory protein. Second, two related organisms can synthesize the resistance proteins in response to the same signals but achieve dissimilar resistance levels as a consequence of the particular architecture that individual species utilize to promote expression of the resistance genes. The types of genetic differences that distinguish closely related species can be quite different depending on whether one is considering bacterial versus eukaryotic species.
In Darwinian terms, mutations can be either beneficial, neutral, or deleterious. To date author have seen growth advantage in stationary phase (GASP) mutants consume amino acids and proteins better than their unevolved siblings. The research now focuses on understanding the mechanisms that lead to the generation of this genetic diversity and the myriad ways cells can increase their relative fitness. According to author the GASP phenomenon allows us to do something almost as good: one can set up many, many tape players running in parallel and can create true microcosms, tiny universes, where in the beginning all conditions are identical. Experiments like these allow us to explore the mechanisms that lead to the generation of genetic diversity, the raw material of natural selection, and how evolutionary processes, as envisioned by Darwin, continue to shape the biosphere.
Charles Darwin really could have used bacteria, organisms for which you can really measure mutation rates. Astronomical populations of bacteria can be grown with and without stress and their mutation types can be characterized. In fact bacteria helped Lederberg, Luria, and Delbrück show that new mutations can form without any required "stress." Mutants arise continuously in perfectly happy bacterial populations. With great excitement Darwin showed the data (obtained using bacteria) suggesting that Lederberg, Luria, and Delbrück had missed something-Darwin might have been closer to the mark than people realized. The key to evaluating Cairns claims lies in the details of his selection conditions. Small-effect mutations are extremely common, and they can contribute serially to very fast strain improvement. It seems that the mechanisms for DNA replication and repair have evolved to be most effective at preventing mutation types with large phenotypic effects. All of laboratory bacterial genetics use the same principle strong selection. The trick is to block all parent cell growth (no new mutations) and prevent growth of those annoying frequent small-effect mutations. Darwin’s idea of stress-induced mutation may be wrong, but natural selection can take on breathtaking power when common small-effect mutations are allowed to contribute. These effects are revealed by bacterial populations. Under selection, the high speed of genetic adaptation is easily mistaken for an increase in mutation rate—maybe even Darwin underestimated the power of selection.
There are apparently different mechanisms to achieve conjugation if one judges by the lack of sequence similarity among conjugative plasmids. The process of conjugation can be conveniently divided into three basic steps: initiation (or DNA processing in the donor), DNA transport, and termination (or DNA processing in the recipient). The plasmid R388 is an ideal model to study conjugation because of its simplicity. In an envisaged scenario, plasmids are the cavalry in the army of bacterial evolution, the first to arrive to the battlefield. The rationale behind this idea is that by inhibiting conjugation, a two-pronged weapon is used to combat bacterial disease: on one side the spread of antibiotic resistance is avoided, and on the other, some mechanisms of virulence that directly use type IV secretion systems can be directly attacked. In summary, conjugation is an essential feature in the physiology of plasmids. Conjugation plays an important role in the evolution of bacterial genomes. Human pathogenic bacteria have acquired many of their virulent traits, as well as antibiotic resistance, by conjugation. If one learns how to control conjugation, an additional potent weapon to combat human bacterial disease can be obtained.
Bacteria do not reproduce sexually; they have one set of genes rather than two, and their cells simply divide-they never fuse with each other like eggs and sperm. Short pieces of the DNA that genes are made of sometimes move from one bacterial cell to another, and this can randomly mix their different versions of genes if it happens often enough, just like real sexual reproduction does. For a long time microbiologists assumed that these parasites were a bacterial way of having sex-that is, that the evolutionary forces responsible for our sexual reproduction had indeed acted on bacteria too, producing ways to move DNA between cells. Nutrients and temperature conditions are usually very different from those the bacteria experience in their natural environments, partly because they are more convenient and partly because one really does not know what the natural conditions are. But studying bacteria under such unnatural conditions makes it very easy to misinterpret what they do. Most bacteria use nutritional signals, just as the DNA-equals-food explanation predicts. Just as people who read only the newspaper headlines think every lottery ticket is a big winner, a scientist who reads only the research papers about bacterial genome sequences could easily conclude that every new gene is an improvement. In either case, the discovery that bacteria do not have sex means that a big key to the puzzle of the evolution of sex will come from finding out why bacteria need so much less mixing than plants and animals.
A single picture in Darwin’s book displays a hypothetical tree of organisms. Microbiologists helped to put flesh on this skeleton by formulating the universal tree of life based on genome sequence information. From first principles, it is not clear why sexless bacteria should be so diverse. Sex is commonly interpreted as the motor for genetic diversity in a population. Sexless bacteria are in principle immortal-this link between sex and mortality was already intuitively felt in the book of Genesis. Phage provide a mobile source of new DNA, and bacteria can rapidly screen the viral DNA sequence space for useful genes. This process is much quicker than evolving new pathogenic traits de novo. Without exaggeration one might argue that phages-together with other mobile DNA like plasmids or transposons are the major motor for the generation of genetic diversity in bacteria. However, as infections are typically horizontal events occurring between unrelated individuals—in contrast to sex, which relies on vertical gene transmission, i.e., from parent to progeny—the problem with the complicated structure of the bacterial tree finds an easy explanation. Evolution depends on selection applied to genetically distinct organisms, but whether this diversity is created by sex or bacteriophage infection does not matter. Sex is a special case of a more generally defined driver of biological diversity. In fact, Darwinian evolution was operative long before sex evolved. The discussion about the tree of life is not only about its branching pattern, but also is now about the tree itself.
The author’s methods for direct visualization of individual mutation and recombination events in living Escherichia coli bacteria are based only on the shrewd use of a natural DNA modification (methylation of A in the GATC sequences) and of two fluorescent proteins. A special protein involved in the process of DNA error correction (called mismatch repair) binds exclusively, extensively, and stably to uncorrected DNA copy errors, forming a fluorescent focus in the living cell. In recombination, a fluorescent version of the E. coli SeqA protein, which binds exclusively the hemimethylated DNA (a DNA duplex with only one strand methylated), allows us to monitor the integrity of permanently hemimethylated DNA over an unlimited number of generations. The molecular phylogenies of preexisting mutations from genomes of many sequenced natural isolates of E. coli suggest that the acquisition of a mutation at any locus in the genome is about 100 times more likely to occur by recombination than by de novo mutation. The results of a study conducted by the author, appeared as expected from the E. coli– Salmonella enterica serovar Typhimurium crosses: when both partners had mutator histories, genetic recombination dropped 10-fold in mut+ cells but not in cells with mut defects; when only one partner had mutator history, recombination dropped only 3- to 4-fold; but when neither had a mutator history, there was no effect on recombination.
Sex in bacteria is not linked to reproduction—parents passing genes to offspring (via that cycle of sex and reproduction) is the opposite of what we consider to be sex in bacteria. In bacteria, sex is the inheritance of DNA from any source except the parental cell. Asexual reproduction results in an exponential increase in cell numbers: it takes 10 generations to attain 1,000 cell replications and only 70 generations to produce 1021 cells, equal to the estimated number of stars in the universe. The generation times of bacteria are short, on the order of hours or days for those species considered to be "slow growing." Therefore, relatively little time is needed for cell numbers to reach the point where each nucleotide in a genome has been subjected to at least one mutation. Transformation is the uptake of DNA from the environment. Any advantage tendered by acquired DNA is secondary to the real reason that bacterial sex evolved. If a gene is acquired from a divergent source, both the donor and recipient can have identical copies despite the fact that the organisms themselves are unrelated. Expanding this to the point where every gene has the potential to transfer to any organism from any source, and this might cause some systematists to lose sleep: rampant gene transfer would render useless their efforts to assign microbes to meaningful groups and to reconstruct the evolutionary links between organisms, since the closest relatives may be no longer be the most closely related.
This chapter talks about the life and times of the ocean’s smallest photosynthetic cell. The author says that it is difficult to describe the thrill of studying Prochlorococcus. Like most scientific advances, the unveiling of Prochlorococcus involved new technologies, diverse approaches, teamwork, and luck. It became clear immediately that although they shared the "signature" characteristics of Prochlorococcus, MED4 and SS120 were not the same: MED4 could grow at high light intensities that killed SS120, while SS120 could grow under extremely low-light conditions that could not sustain MED4; i.e., the cells were adapted to the light intensities found where they were captured. For every cell that is produced, there is another that is eaten by small predatory cells that must rely on others for their food. This keeps the Prochlorococcus population in check and begins the flow of energy through the marine food web. Since they reproduce by making identical copies of themselves, we know that at any moment in time there must be lineages of identical Prochlorococcus cells in the oceans. Prochlorococcus can photosynthesize, and thrive through diversity, and their federation can adapt.
This chapter talks about deciphering the language of diplomacy give and take in the study of the squid-vibrio symbiosis. The colonization of epithelia by microbes is the most common and ancient form of animal symbiosis. Throughout the evolutionary history of animals, from early beginnings through the invasion of the land, and into the current biosphere, the most common type of animal-microbe association has been the colonization of the outer surfaces of animal epithelia by populations of one or more microbial species. For the last 20+ years, biologists have been studying the processes by which bacteria colonize animal epithelial surfaces, using the model association between the Hawaiian bobtail squid, Euprymna scolopes, and the marine bioluminescent bacterium Vibrio fischeri. The study of this association evolved as "symbioses" between biologists from two very different fields, microbiology and animal biology. Distinct species have evolved strange new abilities that allow them to inhabit even the most forbidding of environments. Critical to the development of this research over the past 20 years has been the willingness of our students and collaborators to join us in this adventure. These important tools have allowed us to begin deciphering the molecular language of symbiosis between bacteria and animal epithelia.
Worker attine ants carefully tend the fungus and forage for substrates to use as nutrients to support its growth. In exchange, the fungus serves as the primary food source for the colony. Functionally, this is similar to human agriculture, but instead of growing plants, the ants grow fungus. The foraging activity of these ants is so prodigious that they are one of the most dominant herbivores of Neotropical ecosystems. Pseudonocardia are members of the Actinobacteria, a group well known for their ability to produce potent antibiotics. Indeed, the majority of antibiotics used in human medicine are derived from Actinobacteria. So, it is perhaps not surprising that through natural selection fungus-growing ants “discovered” the benefit of obtaining antibiotics from these bacteria. This relationship, however, not one-sided, as Pseudonocardia benefits from its symbiosis with the ants. Studies indicate that over their long evolutionary history, attine ants have been continuously threatened with famine induced by Escovopsis infections of their fungus garden; to help mitigate this threat, the ants have been employing antibiotic-producing bacteria for millions of years. The fungus garden serves as the external digestive system for the ants; the garden converts leaves into energy for the ants. It has long been assumed that nutrient provisioning to the ants from the garden is only mediated through the ants’ fungal mutualist. Through the formation of symbiotic associations with their fungus and bacteria, the ants obtain access to the metabolic capacity of these microbes, including the capacity to degrade plant biomass and produce antibiotics, respectively.
This chapter talks about the symbiosis of microbes and mitochondria. Mutations, including deletions of DNA, happen constantly, so the unused genes have long since disappeared from the genomes of mitochondria that inhabit our cells. In fact, mutations are still raining down on the genomes of our mitochondria, and these continue throughout our lives, contributing to various diseases and disorders. These malfunctions are the main reason we even think about our mitochondria. Another reason the mitochondria can live with so few genes is that many of the ancient genes of the mitochondrial ancestor have changed addresses, moving from the chromosome of the mitochondrion to our own chromosomes but sending their working products back to the mitochondrial homeland to carry out needed work. Some symbiotic bacteria have fewer than 200 genes, and the symbionts we call organelles can have even fewer, as in our own mitochondria with their miserly 15. Buchnera uses its ancestral genes for making the amino acids tryptophan and leucine, which are nutrients that a host needs. But these genes have been copied many times on tiny extra chromosomes (plasmids), an arrangement that allows hyperproduction of the amino acid products. Both symbionts and domesticated breeds can evolve extreme features over short periods on an evolutionary time scale. These extremes are produced mostly by exaggerating some functions, rather than by acquiring anything truly novel. And just like our domesticated animals and plants, symbionts themselves can be large, typically much larger than their free-living wild relatives.
By the early 1990s, it was becoming clear that carriage of H. pylori increased risk for peptic ulcer disease and for gastric cancer, where both are consequences of the Helicobacter pylori induced gastric inflammation, although in separate ways. In recent years, using more sophisticated analytical techniques, there has come greater support for the notion that H. pylori has colonized humans since before the out-of-Africa migrations of about 58,000 years ago, and that as humans migrated to all parts of the world, they brought their H. pylori strains with them. It has been hypothesized that for H. pylori and humans, there are actually a series of equilibria, nested in one another, that create the governing boundaries at each level. Postulated benefits for humans for early-life carriage of H. pylori include resistance to colonization by exogenous pathogens (through manipulation of gastric pH and gastric immunity, as well as direct competition), as well as close regulation of metabolism, through gastric leptin (5 to 10% of body total) and ghrelin (60 to 80% of body total). In summary, H. pylori has evolved over a long period of time as a highly interactive member of the human gastrointestinal microbiota. There is extensive evidence that H. pylori coevolved with its human hosts, enabling its nearly universal gastric persistence. The interaction had little or no cost (and possible some benefit) to its early-in-life hosts, but also conferred certain late-in-life disease costs, including gastric cancer.
In this chapter, the author talks about her search of the evolution and sequencing of proteins. She has spent years searching for meaning in one of the virtual rooms of the Library of Mendel, the Maynard-Smith Collection, which houses the set of all possible protein sequences. Meaningful proteins-proteins that do something-are extremely rare, because there are far more ways to be meaningless. Each sequence is surrounded by its one-mutation neighbors, that is, by all the proteins that differ from it by a change in a single amino acid letter. Maynard-Smith set up his library with as many dimensions as there are ways to make a mutation. The author and her students have spent the better part of 20 years taking sometimes straight and sometimes slightly crooked paths in Maynard-Smith’s library of proteins. Most of the possible mutations do not have a big effect, as far as the author can tell with her limited eyes. And, of course, some of the mutations can greatly damage or even destroy a protein (and remove it from the gene pool). We have to discover interesting new proteins by making them and seeing what they do. The author has found that a walk in Maynard-Smith’s collection is a wonderful way to discover these new proteins.
As Charles Darwin has taught us, evolution happens through natural selection. Small things, which in any given instance might not appear significant, can grow to have great importance when the environment changes. Bacteria could be used to clean up the messes humans made of their environment if the conditions were right for them to grow. Microorganisms are amazing. They invented the metabolic machinery that sustains all life today. Indeed, the cellular compartments where energy is made in the human body and plants are nothing more than the remnants of ancient bacteria that were engulfed by and entered into symbioses with other cells long ago. But the vast majority of bacteria play important roles in sustaining both human health and the health of our planet. Conventionally, when structurally complex organic molecules are identified from any given sample, they are interpreted as biomarkers of cyanobacteria—the microorganisms that invented oxygenic photosynthesis, the conversion of water to oxygen in sunlight—and hence, they are assumed to be biomarkers of oxygenic photosynthesis itself. The remaining challenge will be to identify new biomarkers to help constrain the timing of major metabolic breakthroughs, such as oxygenic photosynthesis, and shed light on how these breakthroughs came to be. In anticipation of the continued appearance of new clues, the development of increasingly powerful technologies, and the aid of talented colleagues, the author has no doubt that the pursuit of the molecular equivalents of billion-year-old Rosetta Stones will provide enough excitement to last my lifetime.
The conventional fossil record is built of hard parts—bones, shells, and decay-resistant organic tissues buried in the sediments that accumulate on floodplains, in lakes, and on the seafloor. In the 1950s, geologists first began the routine application of radioactive decay to problems of geologic age. The geologic record of microbial life is preserved in four distinct ways. First, bacteria and protists leave what we can consider an extension of the conventional fossil record: cell walls and extracellular envelopes preserved directly in sedimentary rocks. Second, microorganisms also leave molecular fossils that complement the record of morphology. Sediments transported across the seafloor interact physically with microbial mat communities, providing a third and distinctly different biological signature in sedimentary rocks. Finally, microbial populations can actually influence the composition of seawater, providing a distinct chemical signature in minerals precipitated from ancient oceans. One can hazard only broad guesses about the biological properties of early microorganisms, but one can make one key statement with confidence: early cells lived without oxygen. The plants and animals so conspicuous in our own world are evolutionary latecomers, intercalated into ecosystems that were already 3 billion years old when sponges first gained a foothold on the seafloor. The author suspects that the correct explanation will not point to physical or biological processes acting alone but, rather, will emphasize the interactions between Earth and life.
It is a known fact that bacteria (and archaea) are genetically, phylogenetically, and physiologically very diverse. Microbial microevolution has been and is still being analyzed in very elegant laboratory experiments in which microbes are allowed to mutate, adapt, and evolve in test tubes under very stringent and therefore reproducible and adjustable conditions. The "Evolution Canyon" (EC) system in Israel turned out to be a suitable sampling place for such microevolutionary studies. For more than 20 years, adaptation and speciation of macroorganisms have been explored in EC, with Drosophila flies and wild barley being two of the most prominent model organisms. Compared to proteins and genomes, the cell membrane is hardly in the focus of mainstream research. The potential research topics appear to be endless. The author focuses on addressing some of these issues, and expects that comparative genome sequence comparisons will soon aid one in understanding how these evolutionary changes are implemented on the molecular level of genes and their expression. It is perhaps too naïve to expect that the observed traits indeed evolved precisely in those sites from where the Bacillus simplex bacteria have been isolated, taking into account that there are probably thousands of such east-west-directed canyons on the globe and that sporulating bacteria like bacilli easily migrate with the wind from continent to continent. But most probably, such sharp microclimatic contrasts in immediate proximity reinforce within-species evolutionary splits, and therefore EC represents a beautiful site to study microevolution in natural habitats.
Microbes started to be identified and associated with certain diseases, but it then took several decades before scientists started to glean answers about the identity of pathogenic microorganisms in comparison to their nonpathogenic counterparts, the nature of virulence traits, and the host response-quickly termed immunity. Genetics—more precisely, molecular genetics—was key to this understanding. The saga started with a bacterial pathogen. Recent genomic data on the causative microorganisms have illuminated some key aspects of their pathogenesis, particularly the correlation between genome reduction and obligate intracellular parasitism in Mycobacterium leprae. Regarding gene destruction, Shigella is characterized by a large number of pseudogenes, in comparison to Escherichia coli K-12, caused either by frameshift point mutations, deletions, or integration of insertion sequences which are present in very large numbers in the Shigella genome, compared to E. coli K-12. Moreover, further analysis indicated that when different Shigella and EIEC strains were compared, different types of deletions were accordingly observed. Elaborate enzymatic activities such as deubiquitinases and phos-pho-threonine lyases, an original family of E3 ligases, have been identified in both animal and plant pathogens. However, it remains a mystery in which original species (eubacteria, archaea, or primitive eukarya like protozoans) the core of genes that led to the diversification of the current pool of type III secretion system of Shigella(TTSS) effectors originally appeared. In the words of François Jacob, TTSS is a natural selection that gives direction to changes, orients chance, and slowly, progressively produces more complex structures, new organs, and new species.
Adaptive radiations are in fact commonplace; indeed, the vast majority of life’s diversity appears to have arisen through successive adaptive radiations, the most famous perhaps being the radiation that took place approximately 530 million years ago during the Cambrian period (the Cambrian radiation) and from which arose the major groups of complex animals. The author’s own interest in the emergence of diversity began with the common plant- and soil-colonizing bacterium Pseudomonas fluorescens and its propagation in unshaken test tubes (microcosms). Necessary to bring the study of evolution into line with advances in genetics and molecular biology is knowledge of the mutational origins of new phenotypes, and, critically, understanding of the connection between genotype and phenotype in sufficient detail so as to explain precisely why natural selection favors one type over another. Recent discovery of repeated molecular evolution—not just in laboratory populations of microbes but also in natural populations of insects and plants—has brought renewed interest to this possibility, but mechanistic insight of the hard-proof variety has been lacking. Indeed, the author’s recent work on the genetics of wrinkly spreader diversity provides evidence that genetic architecture does indeed contribute to the repeatability of evolution by biasing the molecular variation presented to selection. Among the most exciting of contemporary issues is genetic architecture—the genotype-to-phenotype map—and its influence on the evolution of populations. With the emergence of improved understanding of this map-its definition, its formulation, and the constraints it imposes-rules by which the outcome of phenotypic evolution might be predicted may just arise.
The fungus Amanita muscaria has a mushroom that looks startlingly familiar whether it is collected from France, Russia, Alaska, California, or New Zealand; the mushroom is bright red and has white spots. This is the species most often targeted by the fairies and bunnies drawn for children’s books. The assumption that fungal spores are passively dispersed by air and water is at odds with obvious biomechanical adaptations to reach or create wind. In nature, fungal dispersal may normally involve active dispersal, as well as wind and water, but now humans also carry species among continents. Humans move species by accident and also to support agriculture, forestry, and horticulture. The fungi function as extensions of a root system and facilitate access to scarce soil resources. For this reason, tins of soil with fungal spores were shipped from Europe and across southern Africa. Microbes are rarely the targets of conservation, but data for plants and animals suggest that introduced species cause harm to local biodiversity. Extinctions are associated with introduced species that spread and fill a habitat. Fungi may go unnamed and ignored, but it seems quite likely that climate change, habitat loss, and also introduced species will cause both a massive rearrangement of current fungal biodiversity and extinctions.
Charles Darwin and other naturalists of his time traversed the globe to survey the diversity of plants, animals, and insects and their distributions around the world. They combined these surveys with their contemporary understanding about the history of Earth to develop an evolutionary model for the origins of species through natural selection. One hundred fifty years later, microbial naturalists are uncovering a whole new world of diversity that will lead to a sea change in our understanding of evolution. Initial surveys of microbial diversity suggested that microbes did not fit this conventional model of evolution. Microbial naturalists were unable to identify mechanisms that would disconnect microbial populations from one another. Our initial analyses suggest that primary differences come not from natural selection by abiotic environmental variables between locations, but from interactions between microbes in each location, specifically between Sulfolobus and its viruses and other microbial parasites. The study of microbial evolution lags behind that of macroorganisms, and it seems that there are relatively few microbiologists choosing microbial naturalism. It is clear that the new generation of microbial naturalists who set out to explore the distribution of natural diversity now wields not only the strong lens of genomics but also the power of molecular biology and genetics, which will enable them to discover the fundamental laws of evolution that apply to all of life on Earth.
Bacteria, like all creatures, use every available tool to increase their odds of surviving, including adopting specific shapes. Long or very tiny bacteria resist being eaten by protozoa, very long ones are not easily washed from the soil, thin cells accumulate nutrients more readily from watery environments, rod-shaped bacteria move more certainly towards food sources, spherical ones may produce more progeny per gram of resource, spiral ones race more quickly through viscous fluids, flat ones expose more surface area to light, cells just the right size float at just the right depth in lakes and oceans, and triangular cells fit together like so many slices of pie. In fact, spherical cells appear to be dead ends, because once a family line becomes coccoid, no later generation returns to being a rod. So it looks like spherical cells are degenerate forms, not primordial ones. Instead, individual cells are gloriously weird and highly aberrant, so that a single culture represents almost every known bacterial shape. So far the morphologies are random, and a mutant that has not been isolated grows with just one particular new shape. But the fact that mutants explore the “shape universe” implies that a bacterium can adopt any shape. All that is needed is a mechanism to capture a specific shape and fix it in place. As the community of researchers identifies and investigates these mechanisms, we will, once again, be following in Charles Darwin’s footsteps as we complete our understanding of how and why these came to exist.
In this chapter on postphylogenetics, the author narrates how his lab detoured into the physiology and molecular biology of halobacteria (properly haloarchaea). Resistance to antibiotics, on the rise in hospitals around the world, was shown by Japanese microbiologists to be due to the transfer between them of small circular DNAs, called plasmids, bearing genes for such resistance. There is continuing debate about the significance of gene exchange, which is called either lateral gene transfer (LGT) or horizontal gene transfer-terms of identical meaning, but like personal computers and Macs, each with its own vigorous defenders. Phylotyping had been until now pursued as if its primary goal were the enumeration and identification of microbial species, as their distributions and abundance are influenced by biotic and abiotic forces.
Many bacteria have a propeller device called a flagellum on their surface that allows them to swim from one place to another. Bacterial flagella are complicated structures that have been touted by creationists as an example of “irreducible complexity” in an effort to refute evolution by natural selection. Flagella of Escherichia coli and Salmonella consist of thin helical propellers turned by rotary motors in the cell membrane, thereby allowing the bacteria to move from one place to another in an aqueous environment. This motility provides an enormous survival advantage by allowing bacteria to move toward nutrients or away from harmful substances. The flagellar motor obtains energy from the membrane ion gradient, harnessing the flow of ions from outside to inside the cell to drive rotation of the propeller filament. The rigid flagellar filament is built from several thousand subunits of the protein flagellin (encoded by the fliC gene). In the time since the flagellum was nominated as an example of irreducible complexity, some important evolutionary relationships have come to light which show that the flagellum is not irreducibly complex and which provide the outlines of a credible pathway for flagellar evolution. The Exb proteins function in the active transport of vitamin B12 and other essential molecules across the outer membrane, while the Tol proteins function in maintenance of the outer membrane. Thus, rather than debunking Darwin, the bacterial flagellum actually provides further evidence for the evolution of complex structures via natural selection.
Nature walks aside, studying the natural history of microorganisms is uniquely challenging for a host of reasons, one of which is that there are many different microbial species—or at least groupings that look and act like species. The author saw metagenomic data in the form of genes taken from seawater to identify marine bacteria and was fascinated to discover that although similar genes clustered to form groups, no two were identical. Bacterial and archaeal cells do not pair, recombine gametes, and undergo meiosis. Among others, two observations are critical to understanding the arguments about microbial speciation. The first is the importance of the vast size of microbial populations in nature, and the second is the subtler concept of neutral variation and sequence space. Microbes are the frontier beneath our feet, yet it has taken a long time for Charles Darwin’s ideas to approach their full potential for interpreting microbial diversity. The natural selection is probably very efficient at improving microorganisms to make them nearly ideal machines for reproducing in natural environments, but at the same time the age and size of these populations, the constantly changing environments they must adapt to, and their varied repertoires of DNA acquisition mechanisms make them extraordinarily diverse.
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The Quarterly Review of Biology
We owe everything and nothing to Charles Darwin and Alfred Russel Wallace.
The 150th anniversary in 2009 of the publication of On the Origin of Species motivated Roberto Kolter and Stanley Maloy to ask their colleagues in microbiology to write for the general public about the connection between work and Darwin and Wallace’s discovery of natural selection. The goal was to teach the public about the reality of evolution and its essential role in explanations of the world around us. The resulting 39 essays cover a wide variety of topics, taxa, and perspectives on the world that Darwin “never saw”; these essays make clear the insights arising from Darwin and Wallace’s seminal discovery. For example, the evolution of antibiotic resistance can only be explained via natural selection (see essays by Kolter and Hughes).
Yet, at the same time, microbiology owes Darwin and Wallace nothing. I exaggerate to make two points. It is startling to read this volume and find only the briefest of mentions of two of the four greats whose work established microbiology as a science—Robert Koch and Louis Pasteur—and no mention of the other two—Martinus Beijerinck and Sergei Winogradsky. Their contributions underscore that microbiology owes Darwin and Wallace, in fact, not nothing, but little in a historical sense. Great science done by others made microbiology and this science is as inspiring and beautiful as the science Darwin and Wallace did. Ignoring this history hinders public understanding of science and its history. In addition, as we go forward, we do not owe Darwin and Wallace in a way that necessitates assigning natural selection an exclusive explanatory role. However, other influences on evolution such as genetic drift, genetic constraints, and phylogenetic inertia are little mentioned in this volume and/or incorrectly described, and accordingly, readers gain only a partial understanding of the progress made in evolutionary biology since Darwin and Wallace. Ultimately, this absence hinders public understanding of evolution. After all, what could be less appealing than a field that has not advanced conceptually in 150 years? Of course, as biologists we know better; we know how dynamic and modern the science of evolution is, even as it still rests upon the insights of Darwin and Wallace. The trick is to accessibly transmit this understanding to the public.
Despite these gaps in regard to the history of microbiology and the content of modern evolutionary biology, many of the essays succeed in accessibly communicating the excitement that microbial research provides (along with the hard work). Notable in this regard are the essays by Lenski on long-term evolution, Green on biogeography, Rohwer on phage, Foster on social evolution of bacteria, Casade´- sus on adaptation, Redfield on sex, Chisholm on photosynthetic marine bacteria, Currie on ants and bacteria, Moran on aphids and bacteria, Sansonetti on pathogenic bacteria, and Whitaker on bacteria and viruses. Unfortunately, some essays depart markedly from the level of accessibility needed by the “general” public and will likely be skipped over. Nonetheless, this volume is one I recommend to anyone interested to learn about how far we have come in regard to evolutionary understanding of the world that Darwin never saw.
Despite these gaps in regard to the history of microbiology and the content of modern evolutionary biology, many of the essays succeed in accessibly communicating the excitement that microbial research provides (along with the hard work). Notable in this regard are the essays by Lenski on long-term evolution, Green on biogeography, Rohwer on phage, Foster on social evolution of bacteria, Casade´- sus on adaptation, Redfield on sex, Chisholm on photosynthetic marine bacteria, Currie on ants and bacteria, Moran on aphids and bacteria, Sansonetti on pathogenic bacteria, and Whitaker on bacteria and viruses. Unfortunately, some essays depart markedly from the level of accessibility needed by the “general” public and will likely be skipped over. Nonetheless, this volume is one I recommend to anyone interested to learn about how far we have come in regard to evolutionary understanding of the world that Darwin never saw.
The Quarterly Review of Biology
Volume 89, Number 4
Reviewer: Steven Hecht Orzack, Fresh Pond Research Institute, Cambridge, Massachusetts
Review Date: December 2014
Maybe it’s the lava fields in the Galapagos, maybe it's the giant tortoises, but something caused a bunch of microbiological luminaries to come out of their shells and write a bit about what they think and feel regarding evolution. A meeting held in those islands in 2009—being Darwin’s 200th birthday—brought together some 40 people instructed to discuss microbes and evolution. Out of this came an extraordinary thin volume, an anthology of lively essays that largely succeeded in laying bare the personal reflections of the participants. And they wrote in plain English. This is quite an unusual book in the history of scientific writing. Although many people have written notable personal accounts of how they relate to their science, rarely has there been such a successful convergent effort.
The book encompasses a large variety of topics related to the subject at hand. Relatively few chapters actually focus on evolution directly, but this probably reflects the relative newness and paucity of laboratory studies in evolutionary microbiology. In some cases, the connection seems to be a bit of a stretch, based perhaps on the Dobzanskyian dictum. By stating that Nothing in biology makes sense except in the light of evolution, Dobzansky forced all biologists to pay at least lip service to connections between their work and the Big E. This is not always an easy thing to do, and in some cases, the efforts in the book can be called intrepid. But even in the seemingly less-related chapters, the nexus is not perfunctory and Darwin’s presence is keenly felt. And the ideas are consistently presented in a readable, ever stimulating fashion. In the end, about half of the participants had something to say about Darwin; the other half, what Darwin would have said about them.
To give you the flavor of what's inside this book, here are a few bons mots, chosen almost at random.
Whether viewed from the bow of the Beagle or through the lens of the microscope, all life is bound by the same evolutionary rules. P. 41
Please don't tell my mother, but for years I’ve wanted to be Charles Darwin. P. 263
...we can expect natural environments to contain a lumpy continuum of microbial genotypes and phenotypes. P. 273
So most of the evolution on this planet is actually being carried out by entities Darwin never imagined and at a scale he never could have considered. P. 69
I found this a most satisfying book, laced with charm and sharp insights. Buy it, treasure it, and keep it for your grandchildren. It will wear well. And, at the price, this is a bargain you may never see again.
Small Things Considered
Reviewer: Elio
Review Date: July 2012
The idea for this book emerged from an American Academy of Microbiology Colloquium in 2007 in the Galapagos, and was intended by the editors to celebrate the 200th anniversary of the publication of Darwin’s Origin of the Species and the Descent of Man. The editors have assembled 40 provocative chapters by some of the leading evolutionary microbiologists who resent their personal perspectives of their work. The microbiological sweep of the book is irresistible, including evolution of diversity, speciation, phylogeny, shape, the origin of mutation, social behavior, adaptation, antibiosis, photosynthesis, ants, geomicrobiology, sex, and roller derby. But there is an underlying theme to the book that unites the topical diversity and reflects Dobzhansky’s aphorism that “Nothing in biology makes sense except in the light of evolution.” It is almost as if the book were really titled If Darwin Were Alive Today, What Would He Be Thinking About?
As I read each of the essays in preparation for this review, my strategy was to describe only a small handful of the essays as exemplars. Alas, after reading the fırst 15, I had selected all of them. So I have instead relied on my own biases and interests to select the exemplars, but I assure you that every one of the 40 essays in this remarkable book merits your attention.
Imagine a system for studying an animal microbe symbiosis where the host doesn’t bite, goes through a developmental cycle that can be duplicated in the lab, whose microbe is a luminescent bacterium, confıned as a pure culture in a defıned space and able to be easily cultivated. And oh, by the way, lives in the warm waters of Hawaii. Ned Ruby and Margaret McFall-Ngai have characterized such a system and de- scribe it in their essay “Deciphering the Language of Diplomacy: Give and Take in the Study of the Squid-Vibrio Symbiosis.”
For those for whom the 16S RNA-based Tree of Life and the phylogenetic approach to understanding the relationships among microbes are dogma, the following quote from Ford Doolitle’s essay “Postphylogenetics” will give pause. “. . . it seems likely that neither the Tree of Life . . . nor the phylotype-based environmental microbiology will survive the 21st century with all its paradigms intact.” But more optimistically “. . . there is beyond a doubt a Tree of Life connecting all organisms (Howard Ochman, “Sexual Diffıculties”).
Forest Rowher (“Phage: An Important Evolutionary Force Darwin Never Knew”) discusses an aspect of evolu- tionary change that Darwin never had a clue about, namely the immense genomic potential of the collective viral genome. Given the approximately 1031 bacteriophage particles on planet Earth and their role in horizontal gene transfer, phage-driven microbial evolution represents a major driving force in evolution.
For students wondering if there are still new worlds to discover, Sallie Chisholm‘s essay “Unveiling Prochlorococcus: the Life and Times of the World’s Smallest Photosynthetic Cell” is reassuring. This smallest inhabitantof the world’s oceans was recognized a mere 25 years ago. It is ubiquitous in the ocean—shallow, deep, east, west, tropical, or cold. It has adapted to all these environments over millions of years but has only recently been discovered.
John Roth (“How Bacteria Revealed Darwin’s Mistake”) is concerned with the pesky question of the origins of mu- tations. Did the classic Luria-Delbruck experiment answer the question? And did the later Cairns experiment raise the issue anew? Roth points out that Darwin’s idea of stress-induced mutation was wrong, that the Luria-Del-bruck experiment was incomplete, and that Cairns’ experiment was flawed. He emphasizes the powerful and often overlooked role of common small effect mutations on evolution.
For those who may fınd themselves seduced by the Circe of irreducible complexity, the essays of Andres Moyas (“Minimal Genomes and Reducible Compexity”) which discusses the minimal genome and motility apparatus of the aphid symbiont Buchnera, plus the discussion of flagellar assembly by Blair and Hughes (“Irreducible Complexity? Not!”) will provide a persuasive antidote.
We have all read that conventional sampling techniques provide us with only a tiny glimpse of the true spectrum of microbial diversity. Mitch Sogin (“Trying to Make Sense of the Microbial Census”) discusses this challenge and suggests that based on statistical analyses and new approaches “. . . theory predicts that diversity in the microbial world might be too great to fully measure.”
It is also fun to watch the transition made by Jessica Green, aka “Thumper” Green, a microbial biogeographer and a blocker in the Flat Track Furies, a Roller Derby team, as she moves from the spatial dynamics of her teammate Lady Lump’s mouthguard flora to bio-geography.
Philippe Sansonetti (“On the Origin of Bacterial Pathogenic Species by Means of Natural Selection: A Tale of Coevolution”) discusses the conversion to virulence resulting from the rapid acquisition, via horizontal transfer of genome sequences, often followed by massive genome reduction. Equally interesting are the genetic “black holes” that either are responsible for genome reduction or may result in decreases in virulence.
In some of the essays, e.g. Tom Schmidt’s “Bacteria Battling for Survival” and Dianne Newman’s “In Pursuit of Billion-Year-Old Rosetta Stones,” we are privileged to learn the answer to ”And just how did you get to do this fascinating stuff that you do?”
Darwin placed heavy emphasis on geographic divergence as a determining factor in the evolution of diversity and speciation. A number of essays in the book examine this precept from a microbial point of view. Rachel Whitaker (“A New Age of Naturalists”) examines the role of bacteriophage as determinants of the adaptation of the extremophilic Archaon Sulfolobus. Paul Rainey (“The Evolution of Diversity and the Emergence of Rules Governing Phenotypic Evolution”) describes the adaptive radiation of Pseudomonas fluorescens in static and shaken lab cultures, and found their evolution strikingly similar to Darwin’s description of adaptive radiation of fınches in the Galapagos. And Johannes Sikorski (“A Glimpse Into Microevolution in Nature. Adaptation and Speciation of Bacillus simplex from Evolution Canyon”) not only recounts his own evolution from a creationist Christian to an evolutionary microbiologist, but also describes the existence of phenotypic and genetic diversity in 1,000 stains of Bacillus simplex isolated from two geographically separated canyons in Israel, each with two facing slopes of widely different environments.
Each of the essays is preceded by an often ideosyncratic mini-biography of its author. As I read them I longed to meet each of their authors. It often astonishes me that not everyone wants to be a biologist—a puzzlement that is reinforced by this wonderful book—and what a bargain it is at $14.95.
Microbe Magazine
Reviewer: Martin Dworkin, Microbe Reviews Editor, University of Minnesota, Minneapolis
Review Date: August 2012
Journal of Microbiology and Biology Education (JMBE)
MICROORGANISMS ENHANCE UNDERSTANDING OF EVOLUTION
Microbes and Evolution: The World That Darwin Never Saw is a paperback collection of essays written by eminent researchers. Very short essays provide compelling reading with substantial factual and hypothetical information. The authors cover a broad diversity of interesting and useful topics, revealing personal interests and how their scientific research fits into and, in some cases, changed their lives. The authors write passionately and with excitement inviting everyone to join in their research journeys. The book is a great reference source of expertly written essays with detailed, succinct background information, most with additional readings, and some with figures and illustrations. There is also a helpful index for navigating to topics of interest. The collection of short essays can easily be used by educators in many disciplines. For example, it can be used to prepare students for discussions about how evolution relates to DNA, and allows them to compare Darwin’s phenotypic studies to a modern view of genotypic research, now made easy using bioinformatics and genomic techniques. Many authors use simple analogies to explain the workings of evolution, comparing it to a software program continually being upgraded, and overuse of antibiotics to running too quickly and too soon, instead of setting a slow, consistent pace. The essays bring up many important questions posed by authors concerning evolutionary processes related to their research.
Additionally, essays document the role of microbes as the first life form, initiating explosive development of aerobic organisms, and microbial roles in endosymbiosis. The authors pay homage to Darwin’s seminal work, pointing out questions Darwin could not answer but can now be answered. Students skeptical of macroevolution may understand essays on “test tube evolution” describing random mutation and selection in varied environmental conditions, and observing microevolution in short periods of time and not eons. Another essay addresses the power of reverse genetics to determine gene additions and deletions, providing pathways for commensals to evolve into pathogens. Writings cover core concepts such as how the species definition relates to prokaryotes, horizontal gene transfer and leaps in rapid diversification, and classifications in the tree of life, all of which Darwin did not discover.
While some essays may start discussion on practical topics such as increased antibiotic resistance, pathogenicity islands and virulence, and co-evolution of host/parasite and immune system, the collection may also serve to stimulate debate and hypothesis-generation. Essays on using metagenomics to study microbial interactions in unique natural environments and to catalogue entire ecosystems of microbes could preface debate about disrupting environmental microbial ecosystems, agriculture, biofilms, and the human microbiome. The role of viruses in evolution and the impact of their absence on the tree of life are presented, as well as the role of pseudogenes in driving co-evolution, genome reduction, and host restriction in parasitic relationships. Authors describe small core genomes of certain bacteria, such as E. coli or Prochlorococcus, and the large available gene pool resulting in diversification into new strains. Compelling essays discuss altruistic bacteria, the role of non-coding RNAs in multiple phenotypic expressions of the same genes, and long-term stationary-phase mutants that live continuously. Other essays bring forward the implications of interkingdom conjugation, and the role of transformation as means of obtaining nutrients rather than a need for new genetic material. In total, students are reminded that humans depend on microbial life for survival, and that these organisms live with us in continuous evolutionary flux and refinement. Authors point out that microbes have shown us it is better not to kill everything but to live together for survival—an important concept for students of any discipline. The collection suggests that our understanding of evolution might have been very different if Darwin had started studying microbes.
Journal of Microbiology & Biology Education (JMBE)
Reviewer: Deborah V. Harbour, College of Southern Nevada, Las Vegas, NV
Review Date: December 2012
Initially stimulated by the bicentenary of Darwin's birth, this collection of essays discusses how microbes fit evolution as Darwin would have understood it. There are good examples of classical Darwinian evolution and cases where we have to bend our ideas somewhat.
Metaphor is a powerful tool for conveying concepts to a lay audience. Unfortunately, it ends up being confusing when the metaphor shifts every few pages. This is not, then, a book to be read from cover to cover, at least not in one sitting. It is also unclear at whom this book is aimed. Many chapters would be clear to any intelligent reader, but others seem to be written for an audience of microbiologists or molecular biologists. That said, there are some excellent essays in this collection and I shall use ideas from it when teaching the concept of microbiology to general biologists.
Society for General Microbiology: Microbiology Today
Reviewer: David Roberts, The Natural History Museum
Review Date: 2012
Biologists have a long history of using the microbial world as a ready-made laboratory for the exploration and testing of evolutionary theory. The editors of this volume, inspired by the 200th anniversary of Darwin's birth and the 150th anniversary of the publication of The Origin of Species, have assembled a fascinating, entertaining, and informative collection of scientific essays that focuses on the burgeoning field of microbial ecology and evolution.
Written by leading researchers, the essays address the most current research, and they will certainly be of great use to other researchers in the field. However, the stated purpose of this book was to make microbial ecology and evolution more accessible to general readers, and in this, the editors have succeeded. Many of the essays have interesting, eye-catching titles, and most of the researchers/contributors include personal vignettes that relate how they arrived at their particular fields of research, including wrong turns and serendipitous events. Each essay is accompanied by a short but useful list of references for further reading, and the book includes a complete index.
Summing Up: Highly recommended. All readership levels.
CHOICE Current Reviews for Academic Libraries
SCIENCE AND TECHNOLOGY Biology
Vol. 50 No. 04
Reviewer: R. K. Harris, William Carey University
Review Date: December 2012
Reprinted with permission from CHOICE http://www.cro2.org, copyright by the American Library Association.
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