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PubMed1997

Evolution of sex and the molecular clock in RNA viruses.

Although there exist many hypotheses for the advantage of sexual reproduction, Muller's ratchet is one that has received recent attention as an explanation for the evolution of sex in RNA viruses. Muller's ratchet provides for an advantage of sex when the rate of deleterious mutations is high and population size is small. A small population size intensifies genetic drift, which can lead to the random loss of genomes that are free of deleterious mutations. Sex becomes advantageous because it can re-create, through genetic exchange, genomes with fewer or no mutations. RNA viruses may be subject to Muller's ratchet because they have very high mutation rates and they may experience genetic drift if their populations are forced through small bottlenecks during infection. This review discusses the results of laboratory studies examining the possibility of an advantage of sex through Muller's ratchet in RNA viruses. Data from studies of wild populations of RNA viruses are also considered, and a model is presented for how an observed pattern of molecular evolution (or the molecular clock) in wild populations may be explained by Muller's ratchet (or a similar process) and the addition of compensatory mutations to Ohta's model of evolution by slightly deleterious mutations.

Evolution, Molecular↗
PubMed2000

Trophic-dynamic considerations in relating species diversity to ecosystem resilience.

Complexity in the networks of interactions among and between the living and abiotic components forming ecosystems confounds the ability of ecologists to predict the economic consequences of perturbations such as species deletions in nature. Such uncertainty hampers prudent decision making about where and when to invest most intensively in species conservation programmes. Demystifying ecosystem responses to biodiversity alterations may be best achieved through the study of the interactions allowing biotic communities to compensate internally for population changes in terms of contributing to ecosystem function, or their intrinsic functional redundancy. Because individual organisms are the biologically discrete working components of ecosystems and because environmental changes are perceived at the scale of the individual, a mechanistic understanding of functional redundancy will hinge upon understanding how individuals' behaviours influence population dynamics in the complex community setting. Here, I use analytical and graphical modelling to construct a conceptual framework for predicting the conditions under which varying degrees of interspecific functional redundancy can be found in dynamic ecosystems. The framework is founded on principles related to food web successional theory, which provides some evolutionary insights for mechanistically linking functional roles of discrete, interacting organisms with the dynamics of ecosystems because energy is the currency both for ecological fitness and for food web commerce. Net productivity is considered the most contextually relevant ecosystem process variable because of its socioeconomic significance and because it ultimately subsumes all biological processes and interactions. Redundancy relative to productivity is suggested to manifest most directly as compensatory niche shifts among adaptive foragers in exploitation ecosystems, facilitating coexistence and enhancing ecosystem recovery after disturbances which alter species' relative abundances, such as extinctions. The framework further explicates how resource scarcity and environmental stochasticity may constitute 'ecosystem legacies' influencing the emergence of redundancy by shaping the background conditions for foraging behaviour evolution and, consequently, the prevalence of compensatory interactions. Because it generates experimentally testable predictions for a priori hypothesis testing about when and where varying degrees of functional redundancy are likely to be found in food webs, the framework may be useful for advancing toward the reliable knowledge of biodiversity and ecosystem function relations necessary for prudent prioritization of conservation programmes. The theory presented here introduces explanation of how increasing diversity can have a negative influence on ecosystem sustainability by altering the environment for biotic interactions and thereby changing functional compensability among biota--under particular conditions.

Animals↗
PubMed2006

Compensatory relationship between splice sites and exonic splicing signals depending on the length of vertebrate introns.

BACKGROUND: The signals that determine the specificity and efficiency of splicing are multiple and complex, and are not fully understood. Among other factors, the relative contributions of different mechanisms appear to depend on intron size inasmuch as long introns might hinder the activity of the spliceosome through interference with the proper positioning of the intron-exon junctions. Indeed, it has been shown that the information content of splice sites positively correlates with intron length in the nematode, Drosophila, and fungi. We explored the connections between the length of vertebrate introns, the strength of splice sites, exonic splicing signals, and evolution of flanking exons. RESULTS: A compensatory relationship is shown to exist between different types of signals, namely, the splice sites and the exonic splicing enhancers (ESEs). In the range of relatively short introns (approximately, < 1.5 kilobases in length), the enhancement of the splicing signals for longer introns was manifest in the increased concentration of ESEs. In contrast, for longer introns, this effect was not detectable, and instead, an increase in the strength of the donor and acceptor splice sites was observed. Conceivably, accumulation of A-rich ESE motifs beyond a certain limit is incompatible with functional constraints operating at the level of protein sequence evolution, which leads to compensation in the form of evolution of the splice sites themselves toward greater strength. In addition, however, a correlation between sequence conservation in the exon ends and intron length, particularly, in synonymous positions, was observed throughout the entire length range of introns. Thus, splicing signals other than the currently defined ESEs, i.e., potential new classes of ESEs, might exist in exon sequences, particularly, those that flank long introns. CONCLUSION: Several weak but statistically significant correlations were observed between vertebrate intron length, splice site strength, and potential exonic splicing signals. Taken together, these findings attest to a compensatory relationship between splice sites and exonic splicing signals, depending on intron length.

Animals↗
PubMed2004

Bicoherence analysis of new cardiovascular spectral components observed in heart-transplant patients: statistical approach for bicoherence thresholding.

Following heart transplant (HT), the patient's heart functions under complete cardiac denervation. As a result, the variability in physiologic signals is extremely reduced. We have previously reported that in addition to the typical spectral components (of very low amplitude), part of the HT patients (above 50%) demonstrated unexpected additional peaks in their heart rate and blood pressure spectra. These peaks may be a result of the development of compensatory mechanism induced by loss of parasympathetic control, or of increased importance of nonlinear control interactions. It is important to quantify these strange, unexpected very-high frequency (VHF) peaks, to understand their origin and their contribution to cardiac control in transplant patients. In this paper, we chose to examine these VHF peaks by applying the bicoherence approach. The reduced signal to noise ratio, occurring in these patients, results, however, in an extremely noisy bicoherence. We, therefore, developed several statistical tools in order to distinguish between "true" bicoherence peaks (reflecting true phase coupling) and spurious peaks. The outcome of these methods was an efficient and sensitive bicoherence thresholding procedure, able to identify most of the spurious peaks. Applying these tools to the bicoherence of cardiovascular signals which display VHF peaks, revealed several significant bicoherence peaks. Interestingly, these peaks consisted of two different types. The first type of VHF peaks simply reflects nonlinear cardiac-respiratory coupling, imposed by nonsinusoidal breathing. The second type, however, is clearly not induced by the respiratory system. We believe that these type-2 VHF peaks reflect the evolution of a new, yet unexplained, compensatory mechanism.

Adult↗
PubMed2006

Acute vascular events and electrolytes variations in elderly patients.

Alterations in electrolyte balance have been claimed to play a role in the pathophysiology of coronary heart disease; however, the relationship between the electrolyte pattern and other clinical variables immediately after an acute vascular event is unclear. The aim of the present study was to test whether electrolyte and microelement changes characterize the acute phase in patients with different degrees of glucose tolerance admitted to the hospital shortly after an acute cardiovascular or cerebrovascular ischemic event. Two hundred consecutive patients with either myocardial infarction or stroke (SP group), stratified by degree of glucose tolerance, were studied within six hours of admission, and compared against 125 patients admitted for conditions other than acute vascular ischemia (CP). Routine laboratory parameters and serum Na, K, Cl, Mg and Ca concentrations were determined in all patients and compared to those recorded within six months before the admission. Relative to CP and independently of confounding factors including glucose tolerance status, the SP group showed significantly higher plasma glucose and insulin concentrations, higher creatinine and a modified serum electrolyte pattern characterized by significantly lower potassium and magnesium levels and by hypercalcemia and hyperphosphatemia. Irrespective of glucose tolerance, the first hours following an acute vascular event are characterized by marked insulin resistance with a consistent shift in the serum electrolyte pattern. This pattern is the physiological consequence of the attendant compensatory hyperinsulinemia. Its significance for the evolution of ischemic damage remains to be established.

Aged↗
PubMed1980

Brain center correlations among Chiroptera.

Correlations between progression indices of five categories of nuclei and brain centers indicate that Megachiroptera rely primarily on vision and olfaction while Microchiroptera rely primarily on audition. Among Microchiroptera, some rely more heavily on olfaction than on vision as a secondary sense, and vice-versa. There may have been compensatory effects, in the course of evolution, regarding the choice of the primary and secondary information channels.

Animals↗
PubMed2001

[Contribution of positron emission tomography to functional neuroimaging in Alzheimer's disease].

When combined with cognitive investigations, functional neuroimaging methods such as positron emission tomography allow to depict the neural substrates that underlie the neuropsychological alterations in Alzheimer's disease. Capitalising on the variance in both cognitive performances and resting cerebral metabolic rate of glucose (CMRGlc) in Alzheimer's disease, it is possible to correlate these two quantitative variables on a pixel-by-pixel basis and to generate maps showing the significant correlations in stereotaxic space. Some examples using this approach in the domain of memory disorders are presented in this brief review. We notably show that the localisation of the significant correlations differs from one memory system to another, as evaluated by clinical memory tasks. This approach also unravels the compensatory mechanisms that take place with evolution of the disease. Over and above its interest in clinical neuropsychology, this method constitutes a new source of inferences complementary to the classic activation paradigm in normal subjects, as the latter identifies the cerebral structures that are involved with, but not necessarily indispensable for, the normal execution of the task. This approach highlights the interest of combining functional neuroimaging and neuropsychology to better understand the neural substrates of cognitive deficits in both patients with memory disorders and elderly normal subjects.

Alzheimer Disease↗
PubMed1998

High apparent rate of simultaneous compensatory base-pair substitutions in ribosomal RNA.

We present a model for the evolution of paired bases in RNA sequences. The new model allows for the instantaneous rate of substitution of both members of a base pair in a compensatory substitution (e.g., A-U-->G-C) and expands our previous work by allowing for unpaired bases or noncanonical pairs. We implemented the model with distance and maximum likelihood methods to estimate the rates of simultaneous substitution of both bases, alphad, vs. rates of substitution of individual bases, alphas in rRNA. In the rapidly evolving D2 expansion segments of Drosophila large subunit rRNA, we estimate a low ratio of alphad/alphas, indicating that most compensatory substitutions involve a G-U intermediate. In contrast, we find a surprisingly high ratio of alphad/alphas in the core small subunit rRNA, indicating that the evolution of the slowly evolving rRNA sequences is modeled much more accurately if simultaneous substitution of both members of a base pair is allowed to occur approximately as often as substitution of individual bases. Using simulations, we have ruled out several potential sources of error in the estimation of alphad/alphas. We conclude that in the core rRNA sequences compensatory substitutions can be fixed so rapidly as to appear to be instantaneous.

Animals↗
PubMedDate not supplied

Bihemispheric contribution to motor recovery after stroke: A longitudinal study with transcranial doppler ultrasonography.

BACKGROUND: Both cerebral hemispheres seem to contribute to motor recovery after stroke. We studied the effect of motor activity on cerebral blood flow in both hemispheres at different stages of stroke evolution. METHODS: Thirty patients with hemiplegic stroke and 30 controls were included. Patients were examined within the first week (T1), 1 month (T2) and 6 months after stroke (T3). All subjects performed a 2-min sequential thumb-to-finger opposition task while blood flow velocities in both middle cerebral arteries were measured with transcranial Doppler ultrasonography (TCD). RESULTS: Contralateral movement caused a higher increase in blood flow velocity than ipsilateral movement in controls (p < 0.0001). On the healthy side, patients showed a striking increase with ipsilateral movement (affected hand), which was similar to the increase with contralateral movement (normal hand) at all stages. On the damaged side, the increase with contralateral movement (affected hand) was low and was similar to the increase with ipsilateral movement (normal hand) at T1 and T2; however, at T3 the increase with contralateral movement was higher and the pattern of response was similar to that found in controls. CONCLUSIONS: TCD can trace the evolution of brain motor output following stroke. Compensatory activation of the healthy side of the brain may be already present soon after stroke, whereas function of the damaged side may improve during several months.

Aged↗
PubMed1991

Lack of correlation between cardiac mass and arteriolar structural changes in mild-to-moderate hypertension.

A morphological restructuring of cardiac and arteriolar tissue is common in hypertension. The parallel evolution of these two processes as a compensatory response to pressure overload is a frequently assumed but unsubstantiated hypothesis. To evaluate this possibility, we have concomitantly measured left ventricular mass (LVM; two-dimensional echo) and minimal forearm vascular resistance (FVR; derived from the ratio of intra-arterial blood pressure: forearm blood flow by venous plethysmography) at maximal postischemic (13 min ischemia + 1 min hand exercise) reactive hyperemia. The study was performed on 29 essential hypertensive patients (15 males, 14 females, aged 50 +/- 10 years) who had not been undergoing treatment for hypertension for at least 15 days at the time of study. Minimum FVR was taken as a hemodynamic index of the integrated arteriolar lumen at the forearm level. LVM index and minimum FVR ranged from normal to clearly altered values. In spite of a wide spread of values, no correlation existed between the individual values of the two variables. Systemic mean blood pressure correlated with minimum FVR and tended to correlate with LVMI. Thus, morphological restructing of cardiac and arteriolar tissue does not seem to evolve in parallel in human hypertension. Pressure overload may contribute to cardiovascular hypertrophy, but other unrelated mechanisms may also underlie the development of cardiac and arteriolar abnormalities of human hypertension.

Arterioles↗
PubMed1993

[Morphologic classification of vascular changes in the microcirculation].

Morphological vascular alterations in microhemocirculation are classified into those connected with the age (evolutional and involutional), functional, pathologic, regenerative and compensatory. Age and functional transformations of vascular terminals are related to the physiological processes. Manifestations of reparative regeneration and compensatory restructuring of the microcirculatory bed vessels are characterized. It is noted that compensatory transformations of vascular terminals are frequently combined with regenerative changes which, on the whole, represent the morphology of adaptive responses of microvessels.

Adolescent↗
PubMed2004

Adaptive amplification and point mutation are independent mechanisms: evidence for various stress-inducible mutation mechanisms.

"Adaptive mutation" denotes a collection of processes in which cells respond to growth-limiting environments by producing compensatory mutants that grow well, apparently violating fundamental principles of evolution. In a well-studied model, starvation of stationary-phase lac(-)Escherichia coli cells on lactose medium induces Lac(+)revertants at higher frequencies than predicted by usual mutation models. These revertants carry either a compensatory frameshift mutation or a greater than 20-fold amplification of the leaky lac allele. A crucial distinction between alternative hypotheses for the mechanisms of adaptive mutation hinges on whether these amplification and frameshift mutation events are distinct, or whether amplification is a molecular intermediate, producing an intermediate cell type, in colonies on a pathway to frameshift mutation. The latter model allows the evolutionarily conservative idea of increased mutations (per cell) without increased mutation rate (by virtue of extra gene copies per cell), whereas the former requires an increase in mutation rate, potentially accelerating evolution. To resolve these models, we probed early events leading to rare adaptive mutations and report several results that show that amplification is not the precursor to frameshift mutation but rather is an independent adaptive outcome. (i) Using new high-resolution selection methods and stringent analysis of all cells in very young (micro)colonies (500-10,000 cells), we find that most mutant colonies contain no detectable lac-amplified cells, in contrast with previous reports. (ii) Analysis of nascent colonies, as young as the two-cell stage, revealed mutant Lac(+)cells with no lac-amplified cells present. (iii) Stringent colony-fate experiments show that microcolonies of lac-amplified cells grow to form visible colonies of lac-amplified, not mutant, cells. (iv) Mutant cells do not overgrow lac-amplified cells in microcolonies fast enough to mask the lac-amplified cells. (v)lac-amplified cells are not SOS-induced, as was proposed to explain elevated mutation in a sequential model. (vi) Amplification, and not frameshift mutation, requires DNA polymerase I, demonstrating that mutation is separable from amplification, and also illuminating the amplification mechanism. We conclude that amplification and mutation are independent outcomes of adaptive genetic change. We suggest that the availability of alternative pathways for genetic/evolutionary adaptation and clonal expansion under stress may be exploited during processes ranging from the evolution of drug resistance to cancer progression.

Adaptation, Biological↗
PubMed1981

Ontophyletics of the nervous system: eyeless mutants illustrate how ontogenetic buffer mechanisms channel evolution.

Genetics and molecular biology have shown the mechanisms that allow the genome to provide both the continuity and the variation from generation to generation within a phylogeny. Embryology and developmental biology show the mechanisms that turn the genome into an organism. Mutations, the basis for evolutionary change, cannot in themselves ensure concordance between their products and the products of unchanged genes. Thus, mutations will not necessarily produce a viable organism. On the other hand, ontogenetic buffer mechanisms normally maintain concordance in the developing organism. In addition, ontogenetic buffer mechanisms can integrate discordant mutations into viable organisms that can then be perpetuated during evolution. The evolutionary role of one ontogenetic buffer mechanism, compensatory innervation, is well illustrated in the anopthalmic mutant mouse. In the anopthalmic mouse, a single gene mutation removes afferent axons of the dorsal lateral geniculate nucleus, and compensatory innervation by another population of axons ensures that the dorsal lateral geniculate remains integrated into the central nervous system. Within each organism's ontogeny is a hierarchy of sources of compensatory innervation, and this hierarchy will determine how any particular deafferentating mutation will be buffered. In this way, an ontogeny can channel the phylogeny of which it is a member.

Animals↗
PubMed2006

Complex parameter landscape for a complex neuron model.

The electrical activity of a neuron is strongly dependent on the ionic channels present in its membrane. Modifying the maximal conductances from these channels can have a dramatic impact on neuron behavior. But the effect of such modifications can also be cancelled out by compensatory mechanisms among different channels. We used an evolution strategy with a fitness function based on phase-plane analysis to obtain 20 very different computational models of the cerebellar Purkinje cell. All these models produced very similar outputs to current injections, including tiny details of the complex firing pattern. These models were not completely isolated in the parameter space, but neither did they belong to a large continuum of good models that would exist if weak compensations between channels were sufficient. The parameter landscape of good models can best be described as a set of loosely connected hyperplanes. Our method is efficient in finding good models in this complex landscape. Unraveling the landscape is an important step towards the understanding of functional homeostasis of neurons.

Algorithms↗
PubMed2005

Parallel adaptive evolution cultures of Escherichia coli lead to convergent growth phenotypes with different gene expression states.

Laboratory evolution can be used to address fundamental questions about adaptation to selection pressures and, ultimately, the process of evolution. In this study, we investigated the reproducibility of growth phenotypes and global gene expression states during adaptive evolution. The results from parallel, replicate adaptive evolution experiments of Escherichia coli K-12 MG1655 grown on either lactate or glycerol minimal media showed that (1) growth phenotypes at the endpoint of evolution are convergent and reproducible; (2) endpoints of evolution have different underlying gene expression states; and (3) the evolutionary gene expression response involves a large number of compensatory expression changes and a smaller number of adaptively beneficial expression changes common across evolution strains. Gene expression changes initially showed a large number of differentially expressed genes in response to an environmental change followed by a return of most genes to a baseline expression level, leaving a relatively small set of differentially expressed genes at the endpoint that varied between evolved populations.

Biological Evolution↗
PubMedDate not supplied

Regeneration of skeletal and cardiac muscle in mammals: do nonprimate models resemble human pathology?

Most of the available information regarding the regenerative potential and compensatory remodeling of mammalian tissues has been obtained from nonprimate animals, mainly rodent experimental models. The increasing use of transgenic mice for studies of the mechanisms controlling organogenesis and regeneration also requires a clear understanding of their applicability as experimental models for studies of similar processes in humans and other mammals. Application of modern cell biology methods to studies of regenerative processes has provided new insights into similarity and differences in cellular responses to injury in the tissues of different mammalian species. During more than 200-million years of progressive divergent evolution of mammals, cellular mechanisms of tissue regeneration and compensatory remodeling evolved together with increasingly adaptive functional specialization and structural complexity of mammalian tissues and organs. Rodents represent a phylogenetically ancient order of mammals that has conservatively retained a number of morphofunctional characteristics of early representatives of this class, which include enhanced regenerative capacity of tissues. A comparative analysis of regenerative processes in skeletal and cardiac muscle, as well as in several other mammalian tissues, shows that time courses and intensities of regeneration in response to the same type of injury vary even within taxonomically related species (e.g., rat, mouse, and hamster). The warm bloodedness of mammals facilitated the development of more complex mechanisms of metabolic, immune, and neurohumoral regulation, which resulted in a stronger dependence of regenerative processes on vascularization and innervation. For this reason, interspecies modifications of regenerative responses are limited by the capacity of the animal to resorb rapidly the foci of necrosis and to revascularize and reinnervate the volume of the regenerating tissue. These differences, among other factors, result in significantly lower rates of reparative regeneration in mammals possessing larger body sizes than rodents. A review of these data strongly indicates that the phylogenetic age and biological differences between different species should be taken into account before extrapolation of regenerative properties of nonprimate tissues on the regenerative responses in the primates.

Animals↗
PubMed2003

Role of Baseline pol Genotype in HIV-1 Fitness Evolution.

Viral fitness can be modified upon development of antiretroviral drug resistance, usually by selection of compensatory mutations. In this study, we have used HIV-1 isolates from individuals receiving a protease inhibitor (PI)-based regimen to analyze the impact of basal genetic background on viral fitness evolution. Paired plasma samples and HIV-1 isolates were obtained from 10 PI-naive HIV-infected individuals enrolled in 2 different studies of combination antiretroviral therapy. Genomic regions from pol and env were sequenced. Viral fitness was measured using growth competition experiments followed by heteroduplex tracking analysis. Baseline genotypic analyses of pol showed that 9 of 10 viruses had a different degree of secondary mutations in the protease gene at codons associated with PI resistance (i.e., 10I, 36I, 63P, 71T, and 77I). After 48 weeks of PI-based therapy, a strong correlation was observed between protease genetic divergence and viral fitness difference (r = 0.78, P = 0.03), but not with reverse transcription or Env divergence, suggesting that genotypic changes in the protease gene were driving HIV-1 evolution in these patients. As expected, an inverse correlation was observed between the number of protease and reverse transcription primary mutations and viral fitness (r = -0.65, P < 0.0001). However, our results suggest that the preexistence of secondary mutations in protease genetic background may have implications in HIV-1 fitness evolution and virologic response to antiretroviral therapy.

Acquired Immunodeficiency Syndrome↗