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The diversification of Halenia (Gentianaceae): ecological opportunity versus key innovation.

The plant genus Halenia (Gentianaceae) consists of herbs growing in temperate and tropical alpine habitats and most species possess flowers in which nectar is produced in spurs. This probably helps reward only specialized long-tongued pollinators, and a narrow pollinator/flower relationship is thought to accelerate diversification rates (a key innovation). To test the pattern of diversification of Halenia against the unspurred sister group we reconstructed phylogenetic relationships among 22 species plus outgroups using nuclear ITS and chloroplast rpl16 intron sequence data. We show that Halenia originated in East Asia and migrated via North America into Central America. From there, it colonized South America three times independently, probably within the last million years. Significant changes in diversification rates were found during the evolution of Halenia using a sister group method, a likelihood method, and a diversity-through-time plot. In contrast to other studies, we could not observe a direct speciation rate effect of the evolution of nectar spurs in comparison with the unspurred sister group of Halenia. Rather, increases in diversification occurred following the colonization of Central and South America by spurred progenitor taxa. This later switch in diversification may have resulted from the availability of new geographical and ecological opportunities, or from the availability of more and different pollinators in these regions. Following the latter hypothesis, the nectar spurs were a preadaption and functioned as a key innovation only in this new biotic environment. After an initial rapid increase, a reduction in diversification rate was observed in Central America, probably illustrating density dependence of speciation rates. Finally, we found preliminary evidence for the key innovation hypothesis in geologically young spurred and unspurred lineages of Halenia in South America.

Adaptation, Biological↗

Directed evolution of Lactiplantibacillus plantarum for utilizing ethanol to produce postbiotics.

Alcohol is a recognized carcinogen worldwide. In this study, we aimed to utilize probiotics to metabolize ethanol and produce postbiotics. Initially, we identified a lactic acid bacteria community in kimchi with excellent probiotic activity. By employing our previously developed directed evolution techniques, a Lactiplantibacillus plantarum mutant with safe characteristics and an ethanol utilization capacity of 40 g/L and 0.15 g/L/OD was obtained. Genome sequencing and RT-qPCR analysis revealed the up-regulated expression of alcohol dehydrogenase and aldehyde dehydrogenase genes greatly contributed to ethanol utilization. Furthermore, the mutant strain demonstrated marked superiority in producing postbiotics, including antimicrobial peptides and beneficial organic acids such as lactic acid, phenyllactic acid, succinic acid, and indole-3-lactic acid. In the ethanol-fed fermentation process, the mutant strain achieved a lactic acid yield of 8.47 g/L and a carbon conversion rate of 21.8%. In vivo testing further validated its safety and ability to assist alcohol metabolism.

Adaptive laboratory evolution↗

Cell cycle control in bacteria and yeast: a case of convergent evolution?

Superficially similar traits in phylogenetically unrelated species often result from adaptation to common selection pressures. Examples of convergent evolution are known at the levels of whole organisms, organ systems, gene networks and specific proteins. The phenotypic properties of living things, on the other hand, are determined in large part by complex networks of interacting proteins. Here we present a mathematical model of the network of proteins that controls DNA synthesis and cell division in the alpha-proteobacterium, Caulobacter crescentus. By comparing the protein regulatory circuits for cell reproduction in Caulobacter with that in budding yeast (Saccharomyces cerevisiae), we suggest that convergent evolution may have created similar molecular reaction networks in order to accomplish the same purpose of coordinating DNA synthesis to cell division. Although the genes and proteins involved in cell cycle regulation in prokaryotes and eukaryotes are very different and (apparently) phylogenetically unrelated, they seem to be wired together in similar regulatory networks, which coordinate cell cycle events by identical dynamical principles.

Biological Evolution↗

A chicken consultation with ramifications.

In Madison I once worked with two postdoctoral fellows who had spent their youth in New York City and who, when asked what birds they knew both responded "why, pigeons and LBJ's!" (little brown jobbies). Despite their undoubted brilliance, they clearly had an educational deficiency not fixed by buying eggs and poultry at a grocery store. Though of enormous economic and nutritional importance to humans, turkeys and chickens constitute only a minute fraction of the disappearing avian life in our ecology. One could easily teach an entire middle or high school biology course around the reproduction, embryology, evolution, genetics, anatomy, special adaptations, virology, bacteriology, taxonomy, behavior, and extinctions of birds, as paradigmatic of all of life. Where would developmental or evolutionary biology be without the Galapagos finches, chick embryo, or neurobiology without the Zebra Finch? The modifications of the original red jungle fowl of India and South East Asia into hundreds of races through artificial selection and breeding practices provide as beautiful an example of developmental plasticity, well-known to Darwin, as the domestic dog, cat, laboratory mice, and guinea pigs. In what follows I have begun to repay my indebtedness to my mentor Emil Witschi who introduced me to developmental biology, physiology, and genetics and its historical study on the basis of birds (and amphibians); and to Mark Leppert, Professor of Human Genetics at the University of Utah for collaborative support, and bird-watching fieldtrips.

Animals↗

Manduca sexta recognition and resistance among allopolyploid Nicotiana host plants.

Allopolyploid speciation occurs instantly when the genomes of different species combine to produce self-fertile offspring and has played a central role in the evolution of higher plants, but its consequences for adaptive responses are unknown. We compare herbivore-recognition and -resistance responses of the diploid species and putative ancestral parent Nicotiana attenuata with those of the two derived allopolyploid species Nicotiana clevelandii and Nicotiana bigelovii. Manduca sexta larvae attack all three species, and in N. attenuata attack is recognized when larval oral secretions are introduced to wounds during feeding, resulting in a jasmonate burst, a systemic amplification of trypsin inhibitor accumulation, and a release of volatile organic compounds, which function as a coordinated defense response that slows caterpillar growth and increases the probability of their being attacked. Most aspects of this recognition response are retained with modifications in one allotetraploid (N. bigelovii) but lost in the other (N. clevelandii). Differences between diploid and tetraploid species were apparent in delays (maximum 1 and 0.5 h, respectively) in the jasmonate burst, the elicitation of trypsin inhibitors and release of volatile organic compounds, and the constitutive levels of nicotine, trypsin inhibitors, diterpene glycosides, rutin, and caffeoylputrescine in the leaves. Resistance to M. sexta larvae attack was most strongly associated with diterpene glycosides, which were higher in the diploid than in the two allotetraploid species. Because M. sexta elicitors differentially regulate a large proportion of the N. attenuata transcriptome, we propose that these species are suited for the study of the evolution of adaptive responses requiring trans-activation mechanisms.

Animals↗

Four hypotheses on mitochondria's role in the development and regulation of oxidative stress in the normal state, cell pathology and reversion of tumor cells.

The biological evolution has resulted in adaptation of both unicellular and multicellular organisms to negative effect of excessive O2 in reply to gradual increase of free oxygen (O2) contents in the earth atmosphere. This adaptation has led to formation of various antioxidant systems in the organism. Such system within the cell has hierarchic structure and is represented by at least than three levels of protection: antioxygene, antiradical and antiperoxide. The first and most effective antioxidant level is represented as mitochondrial respiration able to perform several functions. One of these functions is antioxygene since the very the mitochondria's capability to be a main O2 consumer in the cell provides for low but sufficient for respiration and energy supply levels of O2 partial pressure and dependent concentrations of active O2 forms. The latters, being signal molecules at certain values, modify regular and synthetic processes in the cells either directly or indirectly. This is the possibility for mitochondria to more extensively affect the intracellular processes than simply produce ATP. In case of defective of the cell first protection line the hyperoxia starts due to poor utilization of the incoming O2. Change in mitochondria's "capacity" (quantity, size and maturity level of mitochondria) anyway occurring in the cells are an efficient way of regulation of the oxy-peroxide condition (oxidative stress) and related signal channels. The relationship between changes in the condition of cells, i.e. from their normal state to different pathologic forms, and growing disbalance Delta(PO-AO) between its pro-oxygen (PO) and anti-oxygen (AO) components has been assumed. It is expected that during the evolution the cell could have supposedly acquired a sequence of "specialized" Delta(PO-AO) disbalances. Each sequence needs to implement a certain set of biochemical processes. The probability of Delta(PO-AO) disbalance gradation with specification of their value ranges has been determined. These ranges identify or impact certain cell state, namely proliferation of normal cell (oxidative mitogenesis), ageing, A1 apoptosis, carcinogenesis, A2 apoptosis, and oxidative cytolysis. The cited assumption allows us to: (1) explain reverse dependence of cell proliferation due to the level of their differentiation, increase in the amount and activity of mitochondria as an indispensable condition for the disbalance shift towards differentiation, (2) bring up the idea that regress of the cells, and in particular tumour cells, directly results from the Delta(PO-AO) disbalance decrease to certain levels under the influence of reverse inductors, (3) explain relatively easy and frequent embryonic and stem cells malignancy, and also their reversal normalization. These phenomena occur due to small number and/or size of mitochondria in the designated cells. To verify the above mentioned hypotheses it is primarily necessary to be able to stimulate and slow down the mitochondria biogenesis in the embryonic, stem, ageing, cancer and other cells.

Animals↗

Adaptation to Plant Defence in an Agricultural Insect Pest: Integrating Genome Scans and Gene Expression in the Soybean Aphid Reveals Multi-Genic Pathways.

In agroecosystems, intense selection pressures cause species to adapt and spread, often leading to the evolution and persistence of pests. Understanding how pests rapidly adapt can help develop sustainable strategies for their management and improve agroecosystem health. Pest adaptation involves stable variations in DNA sequence, as well as dynamic shifts in gene expression, often mediated by non-coding regulatory elements. We examined adaptation to plant defences in the soybean aphid, Aphis glycines, in which virulent aphids have overcome plant defences and avirulent aphids have not. Previous data with laboratory colonies suggested that virulent aphids have higher overall gene expression, including transposable elements, some of which influence gene regulation. However, we lack information on how genetic variation in natural populations impacts adaptation and potentially gene regulation. We integrated population genome scans of field-collected, soybean aphid populations with gene expression profiles of virulent and avirulent laboratory colonies to uncover connections between genetic differentiation and gene regulation for virulence. Genome scan methods found 2144 single nucleotide polymorphisms (SNPs) with significant genetic differentiation (i.e., outliers) in field-collected populations. These SNPs were near 1004 genes, representing 5.16% of the effective number of genes. Based on previous RNA-Seq data with laboratory colonies, we found 3160 genes and 147 long non-coding RNAs (lncRNAs) with differential expression among virulent and avirulent biotypes. By integrating both data sets, we identified 16 genes and 5 long non-coding RNAs with differential expression and that were associated with an outlier SNP (within 10 kbp). We validated SNPs with additional field collected aphids and found an aphid clone with stronger virulence than our laboratory virulent colony, surviving on 2 different aphid-resistant soybean varieties. This new virulent clone had fixed allele differences at 9 SNPs compared to our avirulent and other virulent colony. Field collected soybean aphids matching the phenotype of this new virulent clone had significant genetic differentiation with 3 outlier SNPs near genes related to zinc transport and lachesin compared to field collected avirulent aphids. Our entire data reinforced the importance of a potential multi-genetic response to overcome plant defence and generates new insights into complex genetic and regulatory mechanisms involved in insect-plant interactions.

Animals↗

Mechanism, origin, and evolution of anoxia tolerance in animals.

Organisms vary widely in their tolerance to conditions of limiting oxygen supply to their cells and tissues. A unifying framework of hypoxia tolerance is now available that is based on information from cell-level models from highly anoxia-tolerant species, such as the aquatic turtle, and from other more hypoxia-sensitive systems. The response of hypoxia-tolerant systems to oxygen lack occurs in two (defense and rescue) phases. The first lines of defense against hypoxia include a drastic, if balanced, suppression of ATP demand and supply pathways; this regulation allows ATP levels to remain constant, even while ATP turnover rates greatly decline. The ATP requirements of ion pumping are down-regulated by generalized 'channel' arrest in hepatocytes and by the arrest of specific ion channels in neurons. In hepatocytes, the ATP demands of protein synthesis are down-regulated on exposure to hypoxia by an immediate global blockade of the process (probably through translational arrest caused by complexing between polysomes and elongation factors). In hypoxia-sensitive cells, this translational arrest seems irreversible, but hypoxia-tolerant systems activate 'rescue' mechanisms if the period of oxygen lack is extended by preferentially regulating the expression of several proteins. In these cells, a cascade of processes underpinning hypoxia rescue and defense begins with an oxygen sensor (a heme protein) and a signal transduction pathway that leads to the specific activation of some genes (increased expression of several proteins) and to specific down-regulation of other genes (decreased expression of several other proteins). The functional roles of the oxygen-sensing and signal-transduction system include significant gene-based metabolic reprogramming - the rescue process - with maintained down-regulation of energy demand and supply pathways in metabolism throughout the hypoxic period. We consider that, through this recent work, it is becoming evident how normoxic-maintenance ATP turnover rates can be down-regulated by an order of magnitude or more - to a new hypometabolic steady state, which is prerequisite for surviving prolonged hypoxia or anoxia. Because the phylogenies of the turtles and of fishes are well known, we are now in an excellent position to assess conservative vs. adaptable features in the evolution of the above hypoxia-response physiology in these two specific animal lineages.

Adenosine Triphosphate↗

Contrast nephropathy may be partly mediated by autonomic dysfunction: renal failure considered as a modern maladaptation of the prehistoric trauma response.

The mechanism behind iodinated radiocontrast nephropathy remains elusive. Direct oxidative damage is the prevailing hypothesis, but the apparent protective effect of iodine against oxidation contradicts this view. We propose that autonomic dysfunction participates in the pathogenesis of radiocontrast nephropathy and may account for other contrast-associated reactions previously attributed to allergy. Iodine, through its effects on thyroid function and chemoreceptor response to metabolic acidosis, may induce hyperadrenergia and consequently diminish renovascular flow and urine output. The renal response to adrenergia likely served an adaptive function during prehistoric evolution when trauma was a dominant source of hypovolemia and adrenergia, but the response may behave maladaptively today as evolutionarily nai ve triggers for adrenergia have emerged. Autonomic dysfunction can further impair renal function by deranging renovascular autoregulation and inducing oxidative reperfusion injury as a secondary phenomenon. Many other causes of acute renal failure such as drug toxicity, surgery, hospitalization, and diabetes may operate through hyperadrenergia, impaired renovascular autoregulation, and oxidative reperfusion injury. Dialysis, a volume reduction therapy for renal failure, can counterintuitively worsen renal dysfunction by exacerbating adrenergia, which may explain its association with accelerated atherosclerosis, inflammation, and cancer. Other examples of vicious cycles that perpetuate renal dysfunction may include renal artery stenosis, carotid stenosis, and atherosclerosis as well as the cardio-renal, hepato-renal, and pulmonary-renal syndromes. The benefits of hydration and bicarbonate in protecting renal function may operate in part through baroreceptor- and chemoreceptor-mediated reduction of sympathovagal ratio, respectively. New treatment paradigms for renal failure including pharmacologic and electro-mechanical therapies are envisioned based on autonomic remodeling, reduced sympathovagal ratio, and neuromodulation of pathways typically associated with trauma such as renin, angiotensin, vasopressin, and aldosterone.

Adaptation, Physiological↗

Adaptive divergence vs. environmental plasticity: tracing local genetic adaptation of metamorphosis traits in salamanders.

In order to assess the significance of local adaptation relative to environmental plasticity on the evolution of life history traits, we analysed the possible genetic basis of differences between pond- and stream-breeding fire salamanders (Salamandra salamandra) in Germany. These salamanders typically deposit their larvae in small streams, where they grow until they are sufficiently large to metamorphose. However, some populations in Western Germany use ponds as larval habitat. Because habitat quality of streams differs from that of ponds one expects life history differences in the pond animals, which may result either from a plastic response or through genetic differentiation (i.e. local adaptation). Using a phylogeographical analysis of mitochondrial D-loop sequences, we show that both stream and pond populations in Western Germany are derived from a single lineage that recolonized following the last glaciation. This finding suggests that pond breeding originated very recently. Our studies of habitat quality and metamorphic behaviour of larvae in natural ponds and streams disclosed that pond larvae experience a significantly reduced food supply and greater risk of drying than do stream larvae. Pond larvae metamorphose earlier at the cost of reduced mass. Common-environment experiments with pond and stream larvae show that metamorphic behaviour of pond larvae under limited-food conditions is determined genetically and is not simply a plastic response to the differing habitat conditions. These results show that phenotypic plasticity is less important than local adaptation in explaining differences in ecological diversification within this species and suggests the possibility of rapid evolution of genetic adaptations when new habitats are exploited.

Adaptation, Physiological↗

Solar cycles and their relationship to human disease and adaptability.

In this paper, we show that 11-year solar cycle peaks predispose humans to disease, but also endow creativity and adaptability. We give several examples of diseases that are modulated by light and present evidence for an effect of intensity and variation in sunlight, primarily ultraviolet radiation (UVR), on the human genome. The birth dates of nearly 237,000 unique clients in the Maine Medicaid database collected from 1995 to 2004, inclusive, were related to solar cycle irradiance for the past seventy-one years, encompassing seven solar cycles. The sample was divided into four general categories of disease: mental/behavioral illnesses; metabolic diseases; autoimmune diseases; neoplasms. The birth months for those clients born in any given year were arranged in the form of a winter/summer ratio in order to more clearly appreciate the seasonality inherent in each disease category. Solar cycles were separated into chaotic (approximately three times as irradiant) or non-chaotic according to the Gutenberg-Richter power law and the uncertainty inherent in predicting solar storms. The results show that radiation peaks in solar cycles and particularly in chaotic solar cycles (CSCs) are associated with a higher incidence of mental disorders, suggesting the sensitivity of ectodermal embryonic tissues to UVR. Autoimmune diseases have intermediate sensitivity, while the neoplasms in the study, primarily of endoderm, appear suppressed by peak UVR intensity. The ratio of the number of clients born in CSC cycles to non-CSC cycles was highest for the more genetic mental diseases, like schizophrenia and bipolar disorder, but as that ratio decreased, the clients with diseases like multiple sclerosis and rheumatoid arthritis showed more environmental features manifested as a greater winter/summer birth month ratio that was significantly different than that of the average client in the whole data set. The paper presents evidence that latitude, e.g., variation in light, is an added stress to the immune system (especially at 53-54 degrees N. latitude) that is involved in nearly all human disease. We hypothesize that introns, the presumptive engenderers of gene control, modulate the effects of UVR, particularly for the neoplasms studied. We conclude that intermittent and largely unpredictable peak solar cycle radiation has been the fundamental engine of evolution, forcing organisms to adapt to mutagenic UVR and producing enough damage to instigate genetic variation. Probably a chance genetic mutation over 80,000 years ago produced a human brain capable of abstract thought and consciousness. The slight genetic instability that favored an adaptable, creative brain also produced other somatic variations that present phenotypically as disease, but largely expressed after natural selection (reproduction) and associated with the inexorable entropy of aging.

Adaptation, Physiological↗

The evolution of the scrotum and testicular descent in mammals: a phylogenetic view.

The adaptive significance of the scrotum and the evolution of the descent of the testicles and epididymis have been a focus of interest among biologists for a long time. In this paper we use three anatomical character states of the scrotum and descensus: (1) testicles descended and scrotal; (2) testicles descended but ascrotal; (3) testicles not descended (testicondy). These states are then mapped on an up to date phylogeny of the Mammalia. Three main points arise out of this mapping procedure: (1) the presence of a scrotum is either primitive in extant Mammalia or primitive within eutherian mammals except Insectivora; (2) evolution has generally proceeded from a scrotal condition to progressively more ascrotal; (3) loss of testicular descensus is less common in mammalian evolution than is loss of the scrotum. In the light of these findings we discuss some current hypotheses regarding the origin and evolution of the scrotum. We find that these are all incomplete in so far as it is not the presence of the scrotum in various mammal groups that requires explaining. Instead, it is the reverse process, why the scrotum has been lost in so many groups, that should be explained. We suggest that the scrotum may have evolved before the origin of mammals, in concert with the evolution of endothermy in the mammalian lineage, and that the scrotum has been lost in many groups because descensus in many respects is a costly process that will be lost in mammal lineages as soon as an alternative solution to the problem of the temperature sensitivity of spermatogenesis is available.

Animals↗

Experimental adaptation of Salmonella typhimurium to mice.

Experimental evolution is a powerful approach to study the dynamics and mechanisms of bacterial niche specialization. By serial passage in mice, we evolved 18 independent lineages of Salmonella typhimurium LT2 and examined the rate and extent of adaptation to a mainly reticuloendothelial host environment. Bacterial mutation rates and population sizes were varied by using wild-type and DNA repair-defective mutator (mutS) strains with normal and high mutation rates, respectively, and by varying the number of bacteria intraperitoneally injected into mice. After <200 generations of adaptation all lineages showed an increased fitness as measured by a faster growth rate in mice (selection coefficients 0.11-0.58). Using a generally applicable mathematical model we calculated the adaptive mutation rate for the wild-type bacterium to be >10(-6)/cell/generation, suggesting that the majority of adaptive mutations are not simple point mutations. For the mutator lineages, adaptation to mice was associated with a loss of fitness in secondary environments as seen by a reduced metabolic capability. During adaptation there was no indication that a high mutation rate was counterselected. These data show that S. typhimurium can rapidly and extensively increase its fitness in mice but this niche specialization is, at least in mutators, associated with a cost.

Adaptation, Physiological↗

[Four year follow-up of social adjustment of a cohort of schizophrenic patients].

Sixty-seven first episode schizophrenic patients (PSE-Catego criteria) have been included in this study in order to evaluate their prognosis and the factors predictive of their evolution. Potential predictive factors consisted of anamnestic and demographic data, scores on the Disability Assessment Schedule (DAS-WHO) and relatives' Expressed Emotion index (EE), measured by the Camberwell Family Interview (CFI). The outcome was assessed monthly by the Global Assessment Scale (GAS/DSM III-R). At four years, 39 patients (58%) were still being followed. 33% of the patients presented a good evolution (EGF > or = 51) and 67% of the patients a bad evolution (EGF < 51). Four factors predictive of the psychosocial adaptation were extracted using regression analysis: premorbid psychosocial evolution, EE, sex and psychiatric family history. These 4 factors predicted correctly 85% of cases. Moreover, the monthly follow-up of these patients pointed to three types of evolution: the patients presenting a good and stable evolution (22%), those presenting a bad and stable evolution (33%) and those presenting an oscillating evolution which fluctuated between good and bad periods (44%). However, no predictive factors of the psychosocial adaptation of these oscillating patients could be identified through the statistical analysis. These results take all their importance regarding the treatment of schizophrenic patients, for whom the therapeutic plans which have to be settled should take into account their prognosis in the most precise manner. Moreover, the predictive value of EE on psychosocial adaptation for a 4 years period is confirmed.

Adolescent↗

Limits to adaptation in asexual populations.

In asexual populations, the rate of adaptation is basically limited by the frequency and properties of spontaneous beneficial mutations. Hence, knowledge of these mutational properties and how they are affected by particular evolutionary conditions is a precondition for understanding the process of adaptation. Here, we address how the rate of adaptation of asexual populations is limited by its population size and mutation rate, as well as by two factors affecting the fraction of mutations that confer a benefit, i.e. the initial adaptedness of the population and the variability of the environment. These factors both influence which mutations are likely to occur, as well as the probability that they will ultimately contribute to adaptation. We attempt to separate the consequences of these basic population features in terms of their effect on the rate of adaptation by using results from evolution experiments with microorganisms.

Adaptation, Physiological↗

Pathogen adaptation to seasonal forcing and climate change.

Many diverse infectious diseases exhibit seasonal dynamics. Seasonality in disease incidence has been attributed to seasonal changes in pathogen transmission rates, resulting from fluctuations in extrinsic climate factors. Multi-strain infectious diseases with strain-specific seasonal signatures, such as cholera, indicate that a range of seasonal patterns in transmission rates is possible in identical environments. We therefore consider pathogens capable of evolving their 'seasonal phenotype', a trait that determines the sensitivity of their transmission rates to environmental variability. We introduce a theoretical framework, based on adaptive dynamics, for predicting the evolution of disease dynamics in seasonal environments. Changes in the seasonality of environmental factors are one important avenue for the effects of climate change on disease. This model also provides a framework for examining these effects on pathogen evolution and associated disease dynamics. An application of this approach gives an explanation for the recent cholera strain replacement in Bangladesh, based on changes in monsoon rainfall patterns.

Adaptation, Physiological↗

Evolution of morphological integration: developmental accommodation of stress-induced variation.

Extreme environmental change during growth often results in an increase in developmental abnormalities in the morphology of an organism. The evolutionary significance of such stress-induced variation depends on the recurrence of a stressor and on the degree to which developmental errors can be accommodated by an organism's ontogeny without significant loss of function. We subjected populations of four species of soricid shrews to an extreme environment during growth and measured changes in the patterns of integration and accommodation of stress-induced developmental errors in a complex of mandibular traits. Adults that grew under an extreme environment had lower integration of morphological variation among mandibular traits and highly elevated fluctuating asymmetry in these traits, compared to individuals that grew under the control conditions. However, traits differed strongly in the magnitude of response to a stressor--traits within attachments of the same muscle (functionally integrated traits) had lower response and changed their integration less than other traits. Cohesiveness in functionally integrated complexes of traits under stress was maintained by close covariation of their developmental variation. Such developmental accommodation of stress-induced variation might enable the individual's functioning and persistence under extreme environmental conditions and thus provides a link between individual adaptation to stress and the evolution of stress resistance.

Adaptation, Physiological↗

Genomic adaptation to acidic environment: evidence from Helicobacter pylori.

The origin of new functions is fundamental in understanding evolution, and three processes known as adaptation, preadaptation, and exaptation have been proposed as possible evolutionary pathways leading to the origin of new functions. Here we examine the origin of an acid resistance mechanism in the mammalian gastric pathogen Helicobacter pylori, with reference to these three evolutionary pathways. The mechanism involved is that H. pylori, when exposed to the acidic environment in mammalian stomach, restricts the acute proton entry across its membrane by its increased usage of positively charged amino acids in the inner and outer membrane proteins. The results of our comparative genomic analysis between H. pylori, the two closely related species Helicobacter hepaticus and Campylobacter jejuni, and other relevant proteobacterial species are incompatible with the hypotheses invoking preadaptation or exaptation. The acid resistance mechanism most likely arose by selection favoring an increased usage of positively charged lysine in membrane proteins.

Adaptation, Biological↗