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Long-term saline-alkaline selection rewires the growth-survival trade-off in Priestia megaterium.

Saline-alkaline soils impose persistent osmotic, ionic, pH, and nutrient stress on soil microorganisms, but the evolutionary routes by which beneficial bacteria adapt to such conditions remain poorly resolved. We performed adaptive laboratory evolution to examine the adaption of the plant growth-promoting rhizobacterium Priestia megaterium HA22 to long-term oligotrophic saline-alkaline selection. After 175 serial transfers, the evolved lineage proliferated stably at 40 g L-1 Na2SO4 at pH 10.0, whereas the wild-type strain failed to proliferate. Genome resequencing and allelic replacement revealed a 5-bp insertion in spo0A, the master sporulation regulator, as a major adaptive mutation. This mutation abolished sporulation; shortened the lag phase; and enhanced vegetative growth, nutrient uptake, and expression of tricarboxylic acid cycle and nitrogen metabolism gene under saline-alkaline stress. According to untargeted metabolomics, adaptation was accompanied by increased amino acid metabolism and aminoacyl-tRNA biosynthesis, with proline, isoleucine and pantothenic acid functionally promoting growth. A point mutation in ugpB enhanced glycerol-3-phosphate uptake, increased peptidoglycan and wall teichoic acid levels, and partially rescued the survival cost of the spo0A mutation. In greenhouse assays under combined saline-alkaline stress, the evolved strain increased soybean shoot dry weight and root dry weight by 56.08% and 27.02%, respectively. These results indicate that prolonged, predictable saline-alkaline selection can favor active growth rather than dormancy when compensatory cell envelope reinforcement buffers survival costs.

Adaptive laboratory evolution↗

Meat-adaptive genes and the evolution of slower aging in humans.

The chimpanzee life span is shorter than that of humans, which is consistent with a faster schedule of aging. We consider aspects of diet that may have selected for genes that allowed the evolution of longer human life spans with slower aging. Diet has changed remarkably during human evolution. All direct human ancestors are believed to have been largely herbivorous. Chimpanzees eat more meat than other great apes, but in captivity are sensitive to hypercholesterolemia and vascular disease. We argue that this dietary shift to increased regular consumption of fatty animal tissues in the course of hominid evolution was mediated by selection for "meat-adaptive" genes. This selection conferred resistance to disease risks associated with meat eating also increased life expectancy. One candidate gene is apolipoprotein E (apoE), with the E3 allele evolved in the genus Homo that reduces the risks for Alzheimer's and vascular disease, as well as influencing inflammation, infection, and neuronal growth. Other evolved genes mediate lipid metabolism and host defense. The timing of the evolution of apoE and other candidates for meat-adaptive genes is discussed in relation to key events in human evolution.

Adaptation, Biological↗

The evolution of anisogamy: the adaptive significance of damage, repair and mortality.

Classic theory on the evolution of anisogamy focuses on the trade-off between gamete productivity and provisioning and mechanisms associated with post-zygotic survival. In this article, the role of mortality acting on both zygotes and gametes is explored as a factor influencing the evolution of different sized gametes. In particular, variable mortality through differential survival or metabolic damage is shown to affect the persistence of isogamy, the evolution of more than two sexes and the evolution of anisogamy. Evolutionary stable isogamous states are shown to be locally unstable and disruptive selection can induce the evolution of anisogamy. Analysis of both the isogamous and anisogamous ESS points reveals that the persistence of either of these conditions is not always assured. The implications of variable survival on the evolution of anisogamy are discussed.

Adaptation, Physiological↗

Directed evolution study of temperature adaptation in a psychrophilic enzyme.

We have used laboratory evolution methods to enhance the thermostability and activity of the psychrophilic protease subtilisin S41, with the goal of investigating the mechanisms by which this enzyme can adapt to different selection pressures. A combined strategy of random mutagenesis, saturation mutagenesis and in vitro recombination (DNA shuffling) was used to generate mutant libraries, which were screened to identify enzymes that acquired greater thermostability without sacrificing low-temperature activity. The half-life of seven-amino acid substitution variant 3-2G7 at 60 degrees C is approximately 500 times that of wild-type and far surpasses those of homologous mesophilic subtilisins. The dependence of half-life on calcium concentration indicates that enhanced calcium binding is largely responsible for the increased stability. The temperature optimum of the activity of 3-2G7 is shifted upward by approximately 10 degrees C. Unlike natural thermophilic enzymes, however, the activity of 3-2G7 at low temperatures was not compromised. The catalytic efficiency, k(cat)/K(M), was enhanced approximately threefold over a wide temperature range (10 to 60 degrees C). The activation energy for catalysis, determined by the temperature dependence of k(cat)/K(M) in the range 15 to 35 degrees C, is nearly identical to wild-type and close to half that of its highly similar mesophilic homolog, subtilisin SSII, indicating that the evolved S41 enzyme retained its psychrophilic character in spite of its dramatically increased thermostability. These results demonstrate that it is possible to increase activity at low temperatures and stability at high temperatures simultaneously. The fact that enzymes displaying both properties are not found in nature most likely reflects the effects of evolution, rather than any intrinsic physical-chemical limitations on proteins.

Adaptation, Physiological↗

The evolution of female orgasm: adaptation or byproduct?

Do women experience orgasm because this trait was shaped by natural selection to augment female fitness? Or are women merely the lucky recipients of developmental patterns favored by selection to produce orgasm in males? A recent and widely publicized book by Elisabeth Lloyd (2005a) contends that there is insufficient evidence to validate any of the adaptive explanations yet proposed for female orgasm. We agree. But our reading of the data differs from Lloyd's. In this essay, we outline why, unlike Caton (2006), whose review of Lloyd's book appeared previously in this journal, we are not persuaded by Lloyd's argument that female orgasm is a nonadaptive byproduct of orgasm in men. We hold this view because we disagree with the criteria Lloyd uses to evaluate evolutionary hypotheses, and because we believe Lloyd defines female orgasm too narrowly, ignoring critical information about its affective aspects.

Adaptation, Physiological↗

Response to Puts and Dawood's 'the evolution of female orgasm: adaptation or byproduct?'--Been there.

David Puts and Khytam Dawood's recent critique of my book, The Case of the Female Orgasm: Bias in the Science of Evolution, attempts to make plausible an adaptive account of female orgasm based on a hypothesized mechanism of uterine upsuck and sperm competition. Yet the authors fail to respond to the criticisms of such accounts that I detailed previously in my book. They raise a further concern about my definition of adaptation--a red herring--and manufacture a conceptual error regarding heritability that they then attribute to me. Most seriously, they fail to address the glaring failure of sperm competition accounts to accord with evidence from sexology. Specifically, the distribution curve of orgasm-with-intercourse--according to Dawood et al.'s own data, as well as others'--is relatively flat across the various classes. This curve needs to be tested against a well-formed multistrategy adaptive hypothesis; it cannot be explained by the adaptive account defended by Puts and Dawood in their critique.

Adaptation, Physiological↗

Adaptive divergence and the evolution of reproductive isolation in the wild: an empirical demonstration using introduced sockeye salmon.

Populations exposed to different ecological environments should diverge for phenotypic traits that influence survival and reproduction. This adaptive divergence should reduce gene flow between populations because immigrants become less fit than residents and because hybrids perform poorly in either environment (i.e., ecologically-dependent reproductive isolation). Here I demonstrate adaptive divergence and the evolution of reproductive isolation in populations of sockeye salmon (Oncorhynchus nerka) introduced from a common ancestral source into a new lake system (Lake Washington, Washington). The introduced fish founded several new populations, two of which experience very different environments during breeding and early development (Cedar River v.s. Pleasure Point beach). Over 13 generations, the two populations diverged for adult traits (female body size, male body depth; measured in the wild) and embryo traits (survival to hatching, development rate, size at emergence; measured in a common environment). The rates of divergence for these characters were similar to those observed in other examples of 'rapid evolution', and can best be attributed to natural selection. Partial reproductive isolation has evolved in concert with adaptive divergence: the rate of exchange of adults between the populations (determined using natural tags) is higher than the rate of gene flow (determined using DNA microsatellites). The demonstration that adaptive divergence can initiate reproductive isolation in less than 13 generations suggests that the first signs of 'ecological speciation' may appear soon after new environments are first colonized.

Adaptation, Biological↗

Menstruation: a nonadaptive consequence of uterine evolution.

Although adaptive explanations for menstruation go back at least twenty-five hundred years, in the last decade two new hypotheses have been advanced. The first suggests that menstruation evolved to cleanse the uterus of pathogens introduced by sperm, and the second argues that the function of endometrial regression (with the associated menstruation in humans) is to save energy by getting rid of tissue, rather than maintaining it in the absence of an available blastocyst. Both these suggestions may be questioned on the grounds that they do not take into account the physiology of the reproductive processes involved. Menstruation is not an independent physiological process and is unlikely to have been selected for independently of the evolutionary events that led to it. Furthermore, most primitive menstruating animals would have menstruated infrequently, and many may have reproduced or died without ever menstruating. In order to provide a context for understanding how menstruation may have come about, the evolution of the female vertebrate reproductive tract is briefly reviewed. In later stages, the coevolution of the embryo and uterus resulted in an intimate association between the trophoblast and the uterine blood vessels. As the embryo became more invasive, the uterus responded with increased cellular growth and differentiation of the endometrium to accommodate it. This reached its peak in mammals (such as rodents and humans), where the embryo passes through the epithelium into the endometrial stroma, which responds with differentiation of cells and blood vessels. Progesterone, secreted after ovulation, plays a crucial role in preparation for pregnancy. In addition to its well-known effects on the uterus, progesterone may be important in suppressing the inflammatory reaction that would be expected in response to the presence of a foreign body, such as an embryo. It is also suggested that vascular and cellular differentiation of the endometrial stroma has evolved by adaptation of the inflammatory (granulation tissue) reaction. When progesterone levels fall at the end of the cycle, there is tissue breakdown and bleeding. The uterus then reforms for the next ovulatory cycle. It is shown that the female reproductive tract has multiple functions that must occur in sequence. The coevolution of the embryo and maternal tract thus led to the close contact of two genetically different tissues, and problems such as the inflammatory reaction had to be overcome. Menstruation is a necessary consequence of these evolutionary changes, and needed no adaptive value in order to evolve.

Adaptation, Physiological↗

Evolution: informational constraints on adaptation.

Many species adaptively alter offspring sex ratios, yet little is known about how they obtain relevant environmental information. New work on the parasitoid wasp Nasonia vitripennis reveals that the presence of eggs on hosts provides a reliable cue allowing females to determine the degree of local mate competition and adaptively adjust offspring sex ratios.

Adaptation, Physiological↗

Evolution of innate and adaptive immunity: can we draw a line?

Several recent findings in the field of comparative immunology have reinforced the importance of examining the molecular and functional features of immune systems in a variety of organisms. Particularly exciting are the discoveries of a new gene rearrangement mechanism in lampreys and a somatic diversification of mollusk immune genes. These immune features being found in animals previously believed only to have innate immunity, as well as the flood of information on immune genes, molecules and mechanisms in many different creatures, have prompted us to revisit the artificial dichotomy between adaptive and innate immune systems. Although we draw no startling conclusions, we hope to encourage different thought patterns when viewing immune systems.

Adaptation, Physiological↗

Co-evolution of parasites and adaptive immune responses.

The interplay between evolving host populations and evolving parasite populations is dominated by two key genetically based elements, namely the virulence of parasites and the resistance of their hosts. Here, Graham Mitchell gives a personal overview of ideas on the coevolution of parasite-host relationships and the contributions to immunology that are likely to emerge from systematic studies on this relationship.

Adaptation, Biological↗

Disease consequences of pathogen adaptation.

Experimental evolution studies demonstrate that pathogens evolve rapidly, have a large capacity for increased virulence and cause disease in many different ways. A large proportion of genetic diversity for host susceptibility to infectious, autoimmune and 'genetic' diseases, and to cancer, is probably caused by pathogens and/or host counteradaptations. Recent advances in diverse fields support this claim and suggest many underused approaches for identifying and experimentally dissecting the complicated host-pathogen interactions that often lead to disease.

Adaptation, Physiological↗

A cold-adapted protease engineered by experimental evolution system.

A new cold-adapted protease subtilisin BPN' mutant, termed m-51, was successfully isolated by use of an evolutionary program consisting of two-step in vitro random mutagenesis, which we developed for the screening of mutant subtilisins with increased activity at low temperature. The m-51 mutant showed 70% higher catalytic efficiency, expressed by the k(cat)/K(m) value, than the wild-type at 10 degrees C against N-succinyl-L-Ala-L-Ala-L-Pro-L-Phe-p-nitroanilide as a synthetic substrate. This cold-adaptation was achieved mainly by the increase in the k(cat) value in a temperature-dependent manner. Genetic analysis revealed that m-51 had three mutations, Ala-->Thr at position -31 (A-31T) in the prodomain, Ala-->Val at position 88 (A88V), and Ala-->Thr at position 98 (A98T). From kinetic parameters of the purified mutant enzymes, it was found that the A98T mutation led to 30% activity increase, which was enhanced up to 70% by the accompanying neutral mutation A88V. The A-31T mutation severely constrained the autoprocessing-mediated maturation of the pro-subtilisin in the Escherichia coli expression system, thus probably causing an activity-non-detectable mutation in the first step of mutagenesis. No distinct change was observed in the thermal stability of any mutant or in the substrate specificity for m-51. In the molecular models of the two single mutants (A88V and A98T), relatively large displacements of alpha carbon atoms were found around the mutation points. In the model of the double mutant (A88V/A98T), on the other hand, the structural changes around the mutation point counterbalanced each other, and thus no crucial displacements occurred. This mutual effect may be related to the enhanced activity of the double mutant.

Base Sequence↗

Host-plant adaptation drives the parallel evolution of reproductive isolation.

Parallel evolution of similar traits in independent populations that inhabit ecologically similar environments strongly implicates natural selection as the cause of evolution. Parallel speciation is a special form of parallel evolution where traits that determine reproductive isolation evolve repeatedly, in closely related populations, as by-products of adaptation to ecological conditions. The outcome of such parallel evolution is that ecologically divergent pairs of populations exhibit greater levels of reproductive isolation than ecologically similar pairs of populations of a similar or younger age. The parallel evolution of reproductive isolation provides strong evidence for natural selection in the process of speciation, but only one conclusive example from nature is known. Populations of the walking-stick insect Timema cristinae that use different host-plant species have diverged in body size and shape, host preference, behaviour and the relative frequency of two highly cryptic colour-pattern morphs. Here we report that divergent selection for host adaptation, and not genetic drift, has promoted the parallel evolution of sexual isolation in this species. Our findings represent a clear demonstration that host-plant adaptation can play a crucial and repeatable role in the early stages of speciation.

Adaptation, Physiological↗