SEARCH · PubMed Health

Results for “evolution”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,405 records · Page 78Linked to original sources

PubMed2002

Mechanisms influencing the evolution of resistance to Qo inhibitor fungicides.

Fungicides inhibiting the mitochondrial respiration of plant pathogens by binding to the cytochrome bc1 enzyme complex (complex III) at the Qo site (Qo inhibitors, QoIs) were first introduced to the market in 1996. After a short time period, isolates resistant to QoIs were detected in field populations of a range of important plant pathogens including Blumeria graminis Speer f sp tritici, Sphaerotheca fuliginea (Schlecht ex Fr) Poll, Plasmopara viticola (Berk & MA Curtis ex de Bary) Berl & de Toni, Pseudoperonospora cubensis (Berk & MA Curtis) Rost, Mycosphaerella fijiensis Morelet and Venturia inaequalis (Cooke) Wint. In most cases, resistance was conferred by a point mutation in the mitochondrial cytochrome b (cyt b) gene leading to an amino-acid change from glycine to alanine at position 143 (G143A), although additional mutations and mechanisms have been claimed in a number of organisms. Transformation of sensitive protoplasts of M fijiensis with a DNA fragment of a resistant M fijiensis isolate containing the mutation yielded fully resistant transformants, demonstrating that the G143A substitution may be the most powerful transversion in the cyt b gene conferring resistance. The G143A substitution is claimed not to affect the activity of the enzyme, suggesting that resistant individuals may not suffer from a significant fitness penalty, as was demonstrated in B graminis f sp tritici. It is not known whether this observation applies also for other pathogen species expressing the G143A substitution. Since fungal cells contain a large number of mitochondria, early mitotic events in the evolution of resistance to QoIs have to be considered, such as mutation frequency (claimed to be higher in mitochondrial than nuclear DNA), intracellular proliferation of mitochondria in the heteroplasmatic cell stage, and cell to cell donation of mutated mitochondria. Since the cyt b gene is located in the mitochondrial genome, inheritance of resistance in filamentous fungi is expected to be non-Mendelian and, therefore, in most species uniparental. In the isogamous fungus B graminis f sp tritici, crosses of sensitive and resistant parents yielded cleistothecia containing either sensitive or resistant ascospores and the segregation pattern for resistance in the F1 progeny population was 1:1. In the anisogamous fungus V inaequalis, donation of resistance was maternal and the segregation ratio 1:0. In random mating populations, the sex ratio (mating type distribution) is generally assumed to be 1:1. Therefore, the overall proportion of sensitive and resistant individuals in unselected populations is expected to be 1:1. Evolution of resistance to QoIs will depend mainly on early mitotic events; the selection process for resistant mutants in populations exposed to QoI treatments may follow mechanisms similar to those described for resistance controlled by single nuclear genes in other fungicide classes. It will remain important to understand how the mitochondrial nature of QoI resistance and factors such as mutation, recombination, selection and migration might influence the evolution of QoI resistance in different plant pathogens.

Biological Evolution↗

PubMed2005

Rapid asymmetrical evolution of Saccharomyces cerevisiae wine yeasts.

Genetic instability causes very rapid asymmetrical loss of heterozygosity (LOH) at the cyh2 locus and loss of killer K2 phenotype in some wine yeasts under the usual laboratory propagation conditions or after long freeze-storage. The direction of this asymmetrical evolution in heterozygous cyh2(R)/CYH2(S) hybrids is determined by the mechanism of asymmetrical LOH. However, the speed of the process is affected by the differences in cell viability between the new homozygous yeasts and the original heterozygous hybrid cells. The concomitant loss of ScV-M2 virus in the LOH process may increase cell viability of cyh2(R)/cyh2(R) yeasts and so favour asymmetrical evolution. The presence of active killer K2 toxin, however, abolishes the asymmetrical evolution of the hybrid populations. This phenomenon may cause important sudden phenotype changes in industrial and pathogenic yeasts.

Crosses, Genetic↗

PubMed2000

Rates of evolution of pyridoxal-5'-phosphate-dependent enzymes.

The pyridoxal-5'-phosphate-dependent enzymes (B(6) enzymes), that operate in the metabolism of amino acids, are of multiple evolutionary origin. To estimate their rates of evolution, a total of 180 sequences of 21 B(6) enzymes from distantly related eukaryotic species were compared. The enzymes belong to all four evolutionarily independent families of B(6) enzymes with different folds, i.e., the large alpha family, the beta family, the d-alanine aminotransferase family, and the alanine racemase family. Their unit evolutionary periods, i.e., the time for a 1% sequence difference to accumulate between branches, ranged from 4.6 to 45.1 million years. Both, fastest changing serine pyruvate aminotransferase and most slowly changing glutamate decarboxylase are members of the alpha family. The evolutionary rates of the few enzymes belonging to the other three families were interspersed among those of the alpha family members. Enzymes that catalyze the same reaction, e.g., transamination or amino acid decarboxylation, with different substrates show widely varying rates. The absence of correlations of the rate of evolution with either protein fold or type of catalyzed reaction suggests that individual functional constraints have determined the differential rates of evolution of B(6) enzymes.

Animals↗

PubMed1997

Artificial evolution: a new path for artificial intelligence?

Recently there have been a number of proposals for the use of artificial evolution as a radically new approach to the development of control systems for autonomous robots. This paper explains the artificial evolution approach, using work at Sussex to illustrate it. The paper revolves around a case study on the concurrent evolution of control networks and visual sensor morphologies for a mobile robot. Wider intellectual issues surrounding the work are discussed, as is the use of more abstract evolutionary simulations as a new potentially useful tool in theoretical biology.

Artificial Intelligence↗

PubMed2000

On the evolution of handedness: a speculative analysis of Darwin's views and a review of early studies of handedness in "the nearest allies of man".

Scientists today who seek clues into the evolutionary origins of human handedness make extensive use of evidence from comparative studies, that is, studies that ask whether handedness occurs in other species, especially apes and monkeys, as the Darwinian principle of continuity would seem to imply, or whether it is uniquely human. Early investigations had the same goal and drew on much the same kind of evidence. In this article, I review studies of animal handedness in the period before 1859, when Darwin published On the Origin of Species, and afterward, through the 1st decade of the 20th century. Inasmuch as Darwin's published writings contain hardly any statements about handedness and none at all about its evolution and continuity across species, I also speculate about what Darwin himself might have said on the subject. To do this, I draw on his statements on related matters, such as the form and structure of the hand and the transition from a quadrupedal to bipedal stance, on other writers' reports and opinions about handedness with which he was familiar or likely to have been familiar, and finally, on clues from his own and only statement about animal handedness in an unpublished letter. I conclude by asking whether and how early investigators, lacking any statement by Darwin on the evolution of handedness, invoked his theory of evolution and his views on related matters in the interpretation of their findings.

Animals↗

PubMed2002

Concerted evolution in the ribosomal RNA genes of an Epichloë endophyte hybrid: comparison between tandemly arranged rDNA and dispersed 5S rrn genes.

We examined ribosomal RNA concerted evolution in an Epichloë endophyte interspecific hybrid (Lp1) and its progenitors (Lp5 and E8). We show that the 5S rrn genes are organized as dispersed copies. Cloned 5S gene sequences revealed two subfamilies exhibiting 12% sequence divergence, with substitutions forming coevolving pairs that maintain secondary structure and presumably function. Observed sequence patterns are not fully consistent with either concerted or classical evolution. The 5S rrn genes are syntenic with the tandemly arranged rDNA genes, despite residing outside the rDNA arrays. We also examined rDNA concerted evolution. Lp1 has rDNA sequence from only one progenitor and contains multiple rDNA arrays. Using 5S rrn genes as chromosomal markers, we propose that interlocus homogenization has replaced all Lp5 rDNA sequence with E8 sequence in the hybrid. This interlocus homogenization appears to have been rapid and efficient and is the first demonstration of hybrid interlocus homogenization in the Fungi.

Ascomycota↗

PubMed1999

Grandmothering and the evolution of homo erectus.

Despite recent, compelling challenge, the evolution of Homo erectus is still commonly attributed to big game hunting and/or scavenging and family provisioning by men. Here we use a version of the "grandmother" hypothesis to develop an alternative scenario, that climate-driven adjustments in female foraging and food sharing practices, possibly involving tubers, favored significant changes in ancestral life history, morphology, and ecology leading to the appearance, spread and persistence of H. erectus. Available paleoclimatic, environmental, fossil and archaeological data are consistent with this proposition; avenues for further critical research are readily identified. This argument has important implications for widely-held ideas about the recent evolution of long human lifespans, the prevalence of male philopatry among ancestral hominids, and the catalytic role of big game hunting and scavenging in early human evolution.

Animals↗

PubMed2000

The evolution of human skin coloration.

Skin color is one of the most conspicuous ways in which humans vary and has been widely used to define human races. Here we present new evidence indicating that variations in skin color are adaptive, and are related to the regulation of ultraviolet (UV) radiation penetration in the integument and its direct and indirect effects on fitness. Using remotely sensed data on UV radiation levels, hypotheses concerning the distribution of the skin colors of indigenous peoples relative to UV levels were tested quantitatively in this study for the first time. The major results of this study are: (1) skin reflectance is strongly correlated with absolute latitude and UV radiation levels. The highest correlation between skin reflectance and UV levels was observed at 545 nm, near the absorption maximum for oxyhemoglobin, suggesting that the main role of melanin pigmentation in humans is regulation of the effects of UV radiation on the contents of cutaneous blood vessels located in the dermis. (2) Predicted skin reflectances deviated little from observed values. (3) In all populations for which skin reflectance data were available for males and females, females were found to be lighter skinned than males. (4) The clinal gradation of skin coloration observed among indigenous peoples is correlated with UV radiation levels and represents a compromise solution to the conflicting physiological requirements of photoprotection and vitamin D synthesis. The earliest members of the hominid lineage probably had a mostly unpigmented or lightly pigmented integument covered with dark black hair, similar to that of the modern chimpanzee. The evolution of a naked, darkly pigmented integument occurred early in the evolution of the genus Homo. A dark epidermis protected sweat glands from UV-induced injury, thus insuring the integrity of somatic thermoregulation. Of greater significance to individual reproductive success was that highly melanized skin protected against UV-induced photolysis of folate (Branda & Eaton, 1978, Science201, 625-626; Jablonski, 1992, Proc. Australas. Soc. Hum. Biol.5, 455-462, 1999, Med. Hypotheses52, 581-582), a metabolite essential for normal development of the embryonic neural tube (Bower & Stanley, 1989, The Medical Journal of Australia150, 613-619; Medical Research Council Vitamin Research Group, 1991, The Lancet338, 31-37) and spermatogenesis (Cosentino et al., 1990, Proc. Natn. Acad. Sci. U.S.A.87, 1431-1435; Mathur et al., 1977, Fertility Sterility28, 1356-1360).As hominids migrated outside of the tropics, varying degrees of depigmentation evolved in order to permit UVB-induced synthesis of previtamin D(3). The lighter color of female skin may be required to permit synthesis of the relatively higher amounts of vitamin D(3)necessary during pregnancy and lactation. Skin coloration in humans is adaptive and labile. Skin pigmentation levels have changed more than once in human evolution. Because of this, skin coloration is of no value in determining phylogenetic relationships among modern human groups.

Adaptation, Physiological↗

PubMed2001

Evolution of activity patterns and chromatic vision in primates: morphometrics, genetics and cladistics.

Hypotheses for the adaptive origin of primates have reconstructed nocturnality as the primitive activity pattern for the entire order based on functional/adaptive interpretations of the relative size and orientation of the orbits, body size and dietary reconstruction. Based on comparative data from extant taxa this reconstruction implies that basal primates were also solitary, faunivorous, and arboreal. Recently, primates have been hypothesized to be primitively diurnal, based in part on the distribution of color-sensitive photoreceptor opsin genes and active trichromatic color vision in several extant strepsirrhines, as well as anthropoid primates (Tan & Li, 1999 Nature402, 36; Li, 2000 Am. J. phys. Anthrop. Supple.30, 318). If diurnality is primitive for all primates then the functional and adaptive significance of aspects of strepsirrhine retinal morphology and other adaptations of the primate visual system such as high acuity stereopsis, have been misinterpreted for decades. This hypothesis also implies that nocturnality evolved numerous times in primates. However, the hypothesis that primates are primitively diurnal has not been analyzed in a phylogenetic context, nor have the activity patterns of several fossil primates been considered. This study investigated the evolution of activity patterns and trichromacy in primates using a new method for reconstructing activity patterns in fragmentary fossils and by reconstructing visual system character evolution at key ancestral nodes of primate higher taxa. Results support previous studies that reconstruct omomyiform primates as nocturnal. The larger body sizes of adapiform primates confound inferences regarding activity pattern evolution in this group. The hypothesis of diurnality and trichromacy as primitive for primates is not supported by the phylogenetic data. On the contrary, nocturnality and dichromatic vision are not only primitive for all primates, but also for extant strepsirrhines. Diurnality, and possibly X-linked polymorphic trichromacy, evolved at least in the stem lineage of Anthropoidea, or the stem lineage of all haplorhines.

Animals↗

PubMed2002

Leopard predation and primate evolution.

Although predation is an important driving force of natural selection its effects on primate evolution are still not well understood, mainly because little is known about the hunting behaviour of the primates' various predators. Here, we present data on the hunting behaviour of the leopard (Panthera pardus), a major primate predator in the Tai; forest of Ivory Coast and elsewhere. Radio-tracking data showed that forest leopards primarily hunt for monkeys on the ground during the day. Faecal analyses confirmed that primates accounted for a large proportion of the leopards' diet and revealed in detail the predation pressure exerted on the eight different monkey and one chimpanzee species. We related the species-specific predation rates to various morphological, behavioural and demographic traits that are usually considered adaptations to predation (body size, group size, group composition, reproductive behaviour, and use of forest strata). Leopard predation was most reliably associated with density, suggesting that leopards hunt primates according to abundance. Contrary to predictions, leopard predation rates were not negatively, but positively, related to body size, group size and the number of males per group, suggesting that predation by leopards did not drive the evolution of these traits in the predicted way. We discuss these findings in light of some recent experimental data and suggest that the principal effect of leopard predation has been on primates' cognitive evolution.

Adaptation, Physiological↗

PubMed1993

Empirical and structural models for insertions and deletions in the divergent evolution of proteins.

The exhaustive matching of the protein sequence database makes possible a broadly based study of insertions and deletions (indels) during divergent evolution. In this study, the probability of a gap in an alignment of a pair of homologous protein sequences was found to increase with the evolutionary distance measured in PAM units (number of accepted point mutations per 100 amino acid residues). A relationship between the average number of amino acid residues between indels and evolutionary distance suggests that a unit 30 to 40 amino acid residues in length remains, on average, undisrupted by indels during divergent evolution. Further, the probability of a gap was found to be inversely proportional to gap length raised to the 1.7 power. This empirical law fits closely over the entire range of gap lengths examined. Gap length distribution is largely independent of evolutionary distance. These results rule out the widely used linear gap penalty as a satisfactory formula for scoring gaps when constructing alignments. Further, the observed gap length distribution can be explained by a simple model of selective pressures governing the acceptance of indels during divergent evolution. Finally, this model provides theoretical support for using indels as part of "parsing algorithms", important in the de novo prediction of the folded structure of proteins from the sequence data.

Amino Acid Sequence↗

PubMed2002

Concerted evolution between duplicated genetic elements in Helicobacter pylori.

The Helicobacter pylori genome includes a family of outer membrane proteins (OMPs) with substantial N and C-terminal identity. To better understand their evolution, the nucleotide sequences for two members, babA and babB, were determined from a worldwide group of 23 strains. The geographic origin of each strain was found to be the major determinant of phylogenetic structure, with strains of Eastern and Western origin showing greatest divergence. For strains 96-10 (Japan) and 96-74 (USA), the 5' regions of babB are replaced with babA sequences, demonstrating that recombination occurs between the two loci. babA and babB have nearly equivalent variation in nucleotide and amino acid identity, and frequencies of synonymous and non-synonymous substitutions. Both genes have segmental conservation but within the 3' segment, substitution patterns are nearly identical. Although babA and babB 5' and midregion segment phylogenies show strong interstrain similarity, the 3' segments show strong intrastrain similarity, indicative of concerted evolution. Within these 3' segments, the lower intrastrain than interstrain frequencies of nucleotide substitutions, which are below mean background H. pylori substitution frequencies, indicate selection against intrastrain diversification. Since babA/babB gene conversions likely underlie the concerted evolution of the 3' segments, in an experimental system, we demonstrate that gene conversions can frequently (10(-3)) occur in H. pylori. That these events are recA-dependent and DNase-resistant indicates their likely cause is intragenomic recombination.

Adhesins, Bacterial↗

PubMed2001

Gene duplication and the evolution of group II chaperonins: implications for structure and function.

Chaperonins are multisubunit protein-folding assemblies. They are composed of two distinct structural classes, which also have a characteristic phylogenetic distribution. Group I chaperonins (called GroEL/cpn60/hsp60) are present in Bacteria and eukaryotic organelles while group II chaperonins are found in Archaea (called the thermosome or TF55) and the cytoplasm of eukaryotes (called CCT or TriC). Gene duplication has been an important force in the evolution of group II chaperonins: Archaea possess one, two, or three homologous chaperonin subunit-encoding genes, and eight distinct CCT gene families (paralogs) have been described in eukaryotes. Phylogenetic analyses indicate that while the duplications in archaeal chaperonin genes have occurred numerous times independently in a lineage-specific fashion, the eight different CCT subunits found in eukaryotes are the products of duplications that occurred early and very likely only once in the evolution of the eukaryotic nuclear genome. Analyses of CCT sequences from diverse eukaryotic species reveal that each of the CCT subunits possesses a suite of invariant subunit-specific amino acid residues ("signatures"). When mapped onto the crystal structure of the archaeal chaperonin from Thermoplasma acidophilum, these signatures are located in the apical, intermediate, and equatorial domains. Regions that were found to be variable in length and/or amino acid sequence were localized primarily to the exterior of the molecule and, significantly, to the extreme tip of the apical domain (the "helical protrusion"). In light of recent biochemical and electron microscopic data describing specific CCT-substrate interactions, our results have implications for the evolution of subunit-specific functions in CCT.

Animals↗

PubMed1993

A model for the evolution of networks of genes.

An organism persists through the activity of structural genes, which is co-ordinated by clusters of coupled regulatory genes. During evolution, changes of coupling within a cluster can increase the reliability with which its structural genes perform a task. To study the evolution of coupling, we have simulated and analyzed a stochastic model for a simple problem. The assumptions of the model are these: A network of regulatory genes co-ordinates the synthesis of four structural proteins, which associate in distinct heterodimers that form a heterotetramer. Mutation in cis-regulatory regions produces transitions among 64 types of network. In a population, each network reproduces in proportion to its fitness, which depends on its probability (reliability) of synthesizing the tetramer. Fitness-dependent attrition keeps the size of the population constant. Regulatory genes occur in a sequence of levels; each level is associated with a different family of transcription factors. The following results emerge: Because different messengers within a family can give networks with the same connectivity, the 64 types of networks cluster into eight equivalence classes. During evolution with a low mutation rate, high-fitness classes can be approached through various paths on a fitness landscape. With a higher mutation rate, networks remain more uniformly distributed among the 64 types, and lower-fitness networks remain preponderant. An initially homogeneous population becomes more heterogeneous through mutation, but selection according to fitness later reduces its diversity. During this process the dispersion of the population over the possible networks increases, then decreases as the population approaches a unique steady state.

Animals↗

PubMed1994

Let there be life. Thermodynamic reflections on biogenesis and evolution.

The question of how life emerged from inanimate matter is closely related to the more fundamental question, namely: What is life? Both issues yield novel insights when discussed in the light of thermodynamics. The model proposed here is based on a simple assumption, namely, that life began with the accidental assembly of a self-replicating molecule. From this assumption the emergence of life naturally follows, enabling a new understanding of evolution as a whole. The evolution of any type of self-replicating systems, even the simplest ones, is shown to be highly efficient in extracting, recording and processing information about the environment. A variety of related issues yield some surprising conclusions when discussed in the thermodynamic context. New processes of order-increase are pointed out, a novel measure of information is proposed, and Lamarckianism is proved to be inconsistent with thermodynamics. Recent works on biogenesis and evolution are critically reviewed.

Animals↗

PubMed1994

Superinfection, metapopulation dynamics, and the evolution of diversity.

Using both analytic and numerical methods, we elucidate the dynamical properties of a class of metapopulation models in which many different species/strains contend for persistence, with local extinction of subpopulations being balanced by colonization of other patches. The species/strains have a strict competitive hierarchy with a given species/strain "taking over" any patch occupied by a lower-ranking species/strain; competitively inferior species/strains compensate by having higher colonization rates and/or lower patch death rates. New species/strains keep appearing, so that we can follow the evolution of the system. Such models may be metaphors for multispecies metapopulations, or for the evolution of virulence (where the patches are hosts, who are infected with various strains of a pathogen, and then die or recover at strain-dependent rates). Our emphasis is on a set of questions relating to the evolution of diversity. How many species/strains are present after a long time, t? Asymptotically, this number continues to increase very slowly, as ln t. What are the relative abundances of the species/strains? Under a broad range of assumptions about the mutations which produce new species/strains, the rank-abundance distribution is roughly geometric (as is commonly observed in early succession and other "ecologically one-dimensional" situations); some of our analysis here is based in part on an interesting but unproved mathematical conjecture about a new kind of probabilistic/combinatorial problem. If the number of patches/hosts is permanently reduced--by habitat destruction or vaccination--what happens? Characteristically, there is an initial sharp loss of species/strains (with selective removal of the competitive dominants), with subsequent slow recovery as new mutants continue to partition the now-diminished "niche space" (but the pristine levels of virulence are not regained).

Animals↗

PubMed1995

Learning and evolution: a quantitative genetics approach.

Recent models of the interactions between learning and evolution show that learning increases the rate at which populations find optima in fixed environments. However, learning ability is only advantageous in variable environments. In this study, quantitative genetics models are used to investigate the effects of individual learning on evolution. Two models of populations of learning individuals are constructed and analyzed. In the first model, the effect of learning is represented as an increase in the variance of selection. Dynamical equations and equilibrium conditions are derived for a population of learning individuals under fixed and variable environmental selection. In the second model, the amount of individual learning effort is regulated by a second gene specifying the duration of a critical learning period. The second model includes a model of the learning process to determine the individual fitness costs and benefits accrued during the learning period. Individuals are then selected for the optimal learning investment. The similarities of the results from these two models suggest that the net effects of learning on evolution are relatively independent of the mechanisms underlying the learning process.

Animals↗

PubMed1996

Population evolution on a multiplicative single-peak fitness landscape.

A theory for evolution of either gene sequences or molecular sequences must take into account that a population consists of a finite number of individuals with related sequences. Such a population will not behave in the deterministic way expected for an infinite population, nor will it behave as in adaptive walk models, where the whole of the population is represented by a single sequence. Here we study a model for evolution of population in a fitness landscape with a single fitness peak. This landscape is simple enough for finite size population effects to be studied in detail. Each of the N individuals in the population is represented by a sequence of L genes which may either be advantageous or disadvantageous. The fitness of an individual with k disadvantageous genes is Wk = (1-s)k, where s determines the strength of selection. In the limit L-->infinity, the model reduces to the problem of Muller's Ratchet: the population moves away from the fitness peak at a constant rate due to the accumulation of disadvantageous mutations. For finite length sequences, a population placed initially at the fitness peak will evolve away from the peak until a balance is reached between mutation and selection. From then on the population will wander through a spherical shell in sequence space at a constant mean Hamming distance from the optimum sequence. We give an approximate theory for the way depends on N, L, s, and the mutation rate u. This is found to agree well with numerical simulation. Selection is less effective on small populations, so increases as N decreases. Our simulations also show that the mean overlap between gene sequences separated by a time of t generations is of the form Q(t) = Q infinity + (Q0-Q infinity)exp(-2ut), which means that the rate of evolution within the spherical shell is independent of the selection strength. We give a simplified model which can be solved exactly for which Q(t) has precisely this form. We then consider the limit L-->infinity keeping U = uL constant. We suppose that each mutation may be favourable with probability p, or unfavourable with probability 1-p. We show that for p less than a critical value pc, the population decreases in fitness for all values of U, whereas for pc < p < 1/2, the population increases in fitness for small U and decreases in fitness for large U. In this case there is an optimum non-zero value of U at which the fitness increases most rapidly, and natural selection will favour species with non-zero mutation rates.

Animals↗