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Dramatic progress has been made in the past ten years in the development of statistical and experimental techniques for investigating features of molecular evolution. Applied to coding regions, these techniques have produced remarkable advances in our understanding of selection for codon usage but, ironically, have had little impact on our understanding of protein evolution. That may be about to change.
How species evolve depends on the communities in which they are embedded. Here, we briefly review the ideas underlying concepts of diffuse coevolution, evolution, and selection. We discuss criteria to identify when evolution will be diffuse. We advocate a more explicitly trait-oriented approach to diffuse (co)evolution, and discuss how considering effects of interacting species on fitness alone tells us little about evolution. We endorse the view that diffuse evolution occurs whenever the response to selection by one interacting species on a given trait is altered by the presence of a second interacting species. Building on the work of others, we clarify and expand the criteria for diffuse evolution and present a simple experimental design that will allow the detection of diffuse selection. We argue that a greater focus on selection on specific traits and the evolutionary response to that selection will improve our conceptual understanding of how communities affect the evolution of species embedded within them.
Random drift, while indifferent to the functionality of the molecular features on which it acts, may nevertheless affect evolving molecular mechanisms. It can lead to functional novelty in either gene structure or regulation. In particular, a nearly neutral (in the sense of Ohta), somewhat deleterious mutation can result in a loss of efficiency in gene regulation, and this loss is expected at times to be compensated by a selected event of a particular type: the use of an additional regulatory factor. An accumulation of additional regulatory factors, implying a combination of events of drift and selection, can permit regulatory systems to achieve an increase in both specificity and complexity as mere byproducts of a particular repair process. Nearly neutral mutations thus may, at times, constitute a required pathway for increases in gene interaction complexity. The process seems to point to an inbuilt drive-built into the gene interaction system itself-toward the evolution of higher organisms. This is a matter worthy of experimental exploration, since the general foundations for the evolution of "higher" from "lower" organisms seems so far to have largely eluded analysis.
RNA viruses are the most common viruses of plants, and the evolution of these viruses has been studied both experimentally and phylogenetically. The basic molecular mechanisms for plant virus evolution are similar to those of other viruses, with some notable exceptions. Recent advances include new insights into the origins of plant viruses, analyses of quasispecies and mutation frequencies, population studies on field isolates and practical studies on the importance of virus evolution to agriculture.
By controlling the irradiance of an extended quasimonochromatic, spatially incoherent source, an optical field is generated that exhibits spatial coherence with phase singularities, called coherence vortices. A simple optical geometry for direct visualization of coherence vortices is proposed, and the local properties and the spatial evolution of coherence vortex are experimentally investigated. To our knowledge, this is the first direct and quantitative experimental measurement of a generic coherence vortex.
On 200 Wistar white rats the authors experiment the effects of an original solution administered by the mouth on the evolution of a chronic gastric ulcer experimentally induced. This solution tuning for the prevention or the treatment of the stress ulcer seems to aggravate the chronic ulcers in the way of formation but on the contrary accelerates in a way highly significant the cicatrization of constituted chronic ulcers. The local and general effects of different components of this solution produce these double actions and do not contraindicate its clinic utilisation.
Over the last 15 years, interest in plant virus evolution has re-emerged, as shown by the increasing number of papers published on this subject. In recent times, research in plant virus evolution has been viewed from a molecular, rather than populational, standpoint, and there is a need for work aimed at understanding the processes involved in plant virus evolution. However, accumulated data from analyses of experimental and natural populations of plant viruses are beginning to delineate some trends that often run contrary to accepted opinion: (1) high mutation rates are not necessarily adaptive, as a large fraction of the mutations are deleterious or lethal; (2) in spite of high potential for genetic variation, populations of plant viruses are not highly variable, and genetic stability is the rule rather than the exception; (3) the degree of constriction of genetic variation in virus-encoded proteins is similar to that in their eukaryotic hosts and vectors; and (4) in spite of huge census sizes of plant virus populations, selection is not the sole factor that shapes their evolution, and genetic drift may be important. Here, we review recent advances in understanding plant virus evolution, and describe the experimental and analytical methods most suited to this purpose.
We used the temporal evolution of the bubble radius in single-bubble sonoluminescence to estimate the water liquid-vapor accommodation coefficient. The rapid changes in the bubble radius that occur during the bubble collapse and rebounds are a function of the actual value of the accommodation coefficient. We selected bubble radius measurements obtained from two different experimental techniques in conjunction with a robust parameter estimation strategy and we obtained that for water at room temperature the mass accommodation coefficient is in the confidence interval [0.217,0.329].
Objectives of this work were as follows: 1. to establish a laboratory experimental system utilizable in a biophysical approach to molecular evolution; and 2. to provide real world parameters to theories of molecular evolution, especially to Eigen's theory of quasi-species. Secretion type bacteriophage fd of E. coli, closely related phages and artificial chimera phages of fd, and a virulent phage Q beta of E. coli were cultured continuously in a specially designed fermenter called a "cellstat". A phage is cultured in a flow of host bacterial cells. Due to its high dilution rate, the mutant cell could not be selected in the cellstat. It was therefore recognized that the cellstat is suitable for study of the selection and evolution process of a bacteriophage under well-defined environmental conditions without interference from host cell mutations. Population dynamics of bacteriophages of various types in the cellstat were studied theoretically by computer simulation and experimentally. A genetically invariable pure population of phage behaves like an open non-linear chemical reaction system. An invariable mixed population shows a selection process, while a variable population generates an evolution process. Kinetic constants describing the dynamics were determined by curve fitting between the theoretical and the experimental curve obtained from competition experiments and from biological relaxation experiments. One of the most important kinetic parameters thus obtained was the selection coefficient, and its dependence on the base sequence of phage DNA. We drew a local landscape of the selection coefficient near the fd sequence on the base sequence space. From this landscape we were able to confirm the importance of slightly deleterious mutants in molecular evolution. We also confirmed the possibility of developing an evolutionary molecular engineering using a cellstat as an evolution reactor and fd phage as a working replicon. Novelties of this work were as follows: 1. the first stable continuous culture of a bacteriophage was achieved with a cellstat; 2. a local landscape of selection coefficient near the fd sequence on the sequence space was the first experimental drawing of such a map; 3. a biological relaxation method was realized to measure kinetic constants of a biological kinetic process, or molecular evolution; and 4. a practical engineering process of evolutionary molecular engineering was proposed.
A host of ecological, anatomical, and physiological selective pressures are hypothesized to have played a role in the evolution of hominid bipedalism. A referential model, based on the chimpanzee (Pan troglodytes) and bonobo (Pan paniscus), was used to test through experimental manipulation four hypotheses on the evolution of hominid bipedalism. The introduction of food piles (Carry hypothesis) increased locomotor bipedality in both species. Neither the introduction of branches (Display hypothesis) nor the construction of visual barriers (Vigilance hypothesis) altered bipedality in either species. Introduction of raised foraging structures (Forage hypothesis) increased postural bipedality in chimpanzees. These experimental manipulations provided support for carrying of portable objects and foraging on elevated food-items as plausible mechanisms that shaped bipedalism in hominids.
Recent studies of long-term experimental populations of bacteria have revealed the actual progression of evolutionary change and how rates of phenotypic evolution can be decoupled from rates of genomic evolution.
The study of post-reproductive lifespan has been of interest primarily with regard to the extended post-menopausal lifespan seen in humans. This unusual feature of human demography has been hypothesized to have evolved because of the "grandmother" effect, or the contributions that post-reproductive females make to the fitness of their children and grandchildren. While some correlative analyses of human populations support this hypothesis, few formal, experimental studies have addressed the evolution of post-reproductive lifespan. As part of an ongoing study of life history evolution in guppies, we compared lifespans of individual guppies derived from populations that differ in their extrinsic mortality rates. Some of these populations co-occur with predators that increase mortality rate, whereas other nearby populations above barrier waterfalls are relatively free from predation. Theory predicts that such differences in extrinsic mortality will select for differences in the age at maturity, allocation of resources to reproduction, and patterns of senescence, including reproductive declines. As part of our evaluation of these predictions, we quantified differences among populations in post-reproductive lifespan. We present here the first formal, comparative study of the evolution of post-reproductive lifespan as a component of the evolution of the entire life history. Guppies that evolved with predators and that experienced high extrinsic mortality mature at an earlier age but also have longer lifespans. We divided the lifespan into three non-overlapping components: birth to age at first reproduction, age at first reproduction to age at last reproduction (reproductive lifespan), and age at last reproduction to age at death (post-reproductive lifespan). Guppies from high-predation environments live longer because they have a longer reproductive lifespan, which is the component of the life history that can make a direct contribution to individual fitness. We found no differences among populations in post-reproductive lifespan, which is as predicted since there can be no contribution of this segment of the life history to an individual's fitness. Prior work on the evolution of post-reproductive lifespan has been dominated by speculation and correlative analyses. We show here that this component of the life history is accessible to formal study as part of experiments that quantify the different segments of an individual's life history. Populations of guppies subject to different mortality pressures from predation evolved differences in total lifespan, but not in post-reproductive lifespan. Rather than showing the direct effects of selection characterizing other life-history traits, post-reproductive lifespan in these fish appears to be a random add-on at the end of the life history. These findings support the hypothesis that differences in lifespan evolving in response to selection are confined to the reproductive lifespan, or those segments of the life history that make a direct contribution to fitness. We also show, for the first time, that fish can have reproductive senescence and extended post-reproductive lifespans despite the general observation that they are capable of producing new primary oocytes throughout their lives.
Did senescence evolve as a direct result of natural selection in order to limit the life-span or did increases in longevity evolve in the face of random events that ordinarily limit the life-span? The adaptive hypothesis is that senescence is a programmed process which appeared in evolution because a limited life-span has selective advantages for certain species. Non-adaptive theorists hold that evolution has acted to lengthen the life-span and maximize reproduction and that senescence is only an evolutionary by-product since natural selection does not act directly on postreproductive events. The assumptions and arguments underlying these hypotheses are examined critically in the light of experimental evidence. While theoretical study of the evolution of ageing may advance our understanding of the nature of ageing itself, it is likely that further clarification of the relationship between evolution and ageing will depend on experimental approaches that are now becoming possible.
This paper describes a new approach to the radiological worker allocation problem using a multiple objective genetic algorithm. The worker allocation problem in radiological facilities involves various types of constraints and even mutually conflicting ones, such as individual dose limits, working time limits, etc. A major difficulty of this highly working time limits, etc. A major difficulty of this highly constrained problem is the way of finding an optimal solution in the huge search space where a large proportion of solutions are not feasible because some of the constraints cannot be satisfied. The paper proposes a model of evolution to establish an optimal assignment efficiently, based on the biological insights into the evolutionary process and heuristic ideas. The experimental results show a very rapid evolution to produce feasible solutions, and the application of multiple evaluation functions converges the feasible solutions to good ones. The genetic algorithm approach was found to be superior to the goal programming and simplex methods.
We have studied both the frequency and biogeographical distribution of the transposable DNA element mariner in natural populations of Drosophila simulans and the short-term evolutionary characteristics of mariner in experimental populations. The mariner element has been identified in natural populations of D. simulans from Africa, Europe, the Middle East, Japan, Australia, several Pacific islands, North America, and South America. Only four lines out of 296 were devoid of active mariner elements, as measured by the presence of functional mariner transposase. A slight correlation was found between the latitudinal coordinate of the collection sites and the level of mariner activity in the populations; this correlation became highly significant in Australia where a cline in mariner activity was observed along the eastern coast of the continent. We also observed that wild-type laboratory strains kept for several years as small populations might lose mariner activity over time. Using experimental populations, we modeled what might happen when naturally occurring populations exhibiting high and low levels of mariner activity encounter one another. We found that active mariner elements either will tend to lose their activity over time and gradually become inactive or possibly will be lost from the population; in either case, this will lead to the pattern seen in this experiment of a significant loss of mariner activity over time.
The entorhinal cortex (ERC) has been implicated in the pathophysiology of Alzheimer's disease, schizophrenia and other disorders affecting cognitive functions. While powerful anatomical and histochemical methods (immunohistochemistry, in situ hybridization, etc.) may be applied (although with limitations) to postmortem human brain, each analysis should utilize a cytoarchitectonic approach to provide appropriate comparisons within the subdivisions of the ERC. Accordingly, we describe here the normal cyto- and myeloarchitecture of the human ERC as a prerequisite for the accompanying study of this region in schizophrenia. Our parcellation of this cortex differs from previous treatments in three ways. First, we adopted specific criteria of inclusion to define each subdivision of the region. Although distinctive ERC features are most prominent in the intermediate portion of this region, at least one of these features was considered the minimum necessary criterion to include adjacent tissue in the entorhinal area. Second, we used morphometric measurements (neuronal size and density as well as subdivisional volume and laminar thickness) to support our qualitative evaluation. Third, we have applied to the human ERC the conventional cytoarchitectonic nomenclature of the entorhinal cortex used previously in studies of non-human primates. This allows a more accurate extrapolation of the available numerous experimental anatomical, physiological and psychological data on this region to the human. As in the monkey, the five main subareas were recognized in the human (prorhinal, lateral, intermediate, sulcal and medial) but three required further subdivision (intermediate, sulcal and medial). The morphometric results obtained suggested a progression of the human entorhinal cortex from the peripheral to the central subareas, with the intermediate subarea (281) as the most complete entorhinal subdivision. Compared with non-human primates, the human ERC not only retains the basic periallocortical organization but also demonstrates further evolution. Taken together with available experimental data on the connectivity of this brain region, these results provide an anatomical basis for evaluating the ERC in human behavior.
Early ultrastructural changes and their progressive evolution were studied in rat epidermis following topical application of carcinogen (3-methylcholanthrene) and were compared to ultrastructural features of fully developed tumors (sebaceous epithelioma and basal cell epithelioma) in animals of the same group. Similar cytologic alterations were found, such as a marked increase in free ribosomes and polysomes, extensive endoplasmic reticulum, considerable increase of mitochondria, and dilated intercellular spaces, occupied by cytoplasmic projections. Predominance of dark cells, considered by us to be only phenotypically different from normal (light) cells, was also observed. A two-stage or multiple-stage of neoplastic evolution was suggested.
Myocardial infarction is a dynamic process that begins with the transition from reversible to irreversible ischemic injury and culminates in the replacement of dead myocardium by a fibrous scar. Many biochemical and metabolic changes have been observed early after the onset of ischemia, but the precise cause of the transition to irreversibility has not been elucidated. However, disruption of the plasmalemma of the sarcolemma is an early event, the presence of which indicates that the ischemic myocytes are dead. Not all ischemic myocytes become irreversibly injured simultaneously in experimental infarction in the canine heart; rather, myocytes die in a transmural wavefront of cell death proceeding from the subendocardial to the subepicardial myocardium with the subendocardial layer dying first and the subepicardial layer last. About 6 hours of ischemia are required to complete the wave-front. During the reversible phase of ischemic injury, reperfusion salvages all ischemic myocytes in all layers, but once lethal injury begins to develop, reperfusion salvages reversibly injured myocytes that are located chiefly in the subepicardial and midmyocardial layers and thereby limits the transmural extent of infarction. The gradual evolution of cell death in experimental acute ischemia provides a basis for limitation of infarct size by reperfusion with arterial blood in man. Many functions of myocardium subjected to reversible episodes of ischemia return to the control condition a few seconds or minutes after the onset of reperfusion. Others, such as repletion of the adenine nucleotide pool, require hours to days to repair. Reversibly injured myocardium exhibits reduced contractile efficiency, termed stunning, which is a form of reperfusion injury. Stunning is reversible; it disappears after hours or days of reperfusion. Finally, reversibly injured myocardium develops adaptive changes that protect it against subsequent episodes of ischemia. One such change, termed ischemic preconditioning, persists for 1-2 hours and serves to delay the development of cell death if the tissue is subjected to a new prolonged episode of ischemia. Another, heat shock protein synthesis, does not appear until the tissue has been reperfused for 12-24 hours; it also protects the myocardium against subsequent ischemic injury. The molecular mechanisms underlying stunning, ischemic preconditioning, and heat shock protein synthesis remain to be established.