Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “compensatory evolution”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 163 records · Page 9Linked to original sources
PubMed2003

Phylogeny of the photosynthetic euglenophytes inferred from the nuclear SSU and partial LSU rDNA.

Previous studies using the nuclear SSU rDNA have indicated that the photosynthetic euglenoids are a monophyletic group; however, some of the genera within the photosynthetic lineage are not monophyletic. To test these results further, evolutionary relationships among the photosynthetic genera were investigated by obtaining partial LSU nuclear rDNA sequences. Taxa from each of the external clades of the SSU rDNA-based phylogeny were chosen to create a combined dataset and to compare the individual LSU and SSU rDNA datasets. Conserved areas of the aligned sequences for both the LSU and SSU rDNA were used to generate parsimony, log-det, maximum-likelihood and Bayesian trees. The SSU and LSU rDNA consistently generated the same seven terminal clades; however, the relationship among those clades varied depending on the type of analysis and the dataset used. The combined dataset generated a more robust phylogeny, but the relationships among clades still varied. The addition of the LSU rDNA dataset to the euglenophyte phylogeny supports the view that the genera Euglena, Lepocinclis and Phacus are not monophyletic and substantiates the existence of several well-supported clades. A secondary structural model for the D2 region of the LSU rDNA was proposed on the basis of compensatory base changes found in the alignment.

Animals↗
PubMed1998

Experimental models of Parkinson's disease: from the static to the dynamic.

The experimental models of Parkinson's disease (PD) available today can be divided into two categories according to the mode of action of the compound used: transient pharmacological impairment of dopaminergic transmission along the nigrostriatal pathway or selective destruction by a neurotoxic agent of the dopaminergic neurons of the substantia nigra pars compacta. The present article looks at the relative merits of each model, the clinical symptoms and neuronal impairment it induces, and the contribution it could make to the development of a truly dynamic model. It is becoming more and more clear that there is an urgent need for a chronic model integrating all the clinical features of PD including resting tremor, and reproducing the gradual but continuous nigral degeneration observed in the human pathology. Discrepancies have been reported several times between results obtained in classic animal models and those described in PD, and it would seem probable that such contradictions can be ascribed to the fact that animal models do not, as yet, reproduce the continuous evolution of the human disease. Dynamic experimental models which come closer to the progressive neurodegeneration and gradual intensification of motor disability so characteristic of human PD will enable us to investigate crucial aspects of the disease, such as compensatory mechanisms and dyskinesia.

Animals↗
PubMed1998

Competition among body parts in the development and evolution of insect morphology.

Changes in form during ontogeny and evolution depend in large measure on changes in the relative growth of the various parts of the body. The current consensus in developmental biology is that the final size of appendages and internal organs is regulated autonomously, within the structure itself. Size regulation of body parts typically requires no external control and is thought to be relatively insensitive to signals from the developmental environment. We show in two very different systems, butterfly wings and beetle horns, that experimentally induced changes in the allocation of developmental resources to one trait produces compensatory changes in the relative sizes of other traits. These findings illustrate that interaction among body parts in development is part of the mechanism of size regulation of those parts. Furthermore, in the case of beetle horns, we show that the tradeoff in size is manifest as a significant negative genetic correlation among the involved body parts and, therefore, constitutes a developmental source of genetic constraint on the evolution of body form.

Animals↗
PubMed1990

An undecamer DNA sequence directs termination of human ribosomal gene transcription.

Previously we have shown that a repetitive 18 bp sequence motif, the Sal box (AGGTCGACCAGA/TT/ANTCCG), present in the 3' terminal spacer of mouse rDNA constitutes a termination signal for RNA polymerase I (pol I). Similar sequence elements which are functionally analogous to the murine terminator are present in the spacer of human rDNA. However, the human termination signal is shorter encompassing only 11 bp (GGGTCGACCAG) which correspond to the proximal part of the mouse sequence. Two out of the five human Sal box elements are functionally inactive due to natural point mutations which damage factor binding. A similar sequence motif with a 10 of 11 base identity with the downstream terminators is located upstream of the human transcription initiation site. The upstream element interacts with the same factor(s) as the downstream terminators and is also capable to stop elongating human RNA polymerase I. Despite the human and mouse factors exert different electrophoretic mobilities in gel retardation assays, UV-crosslinking and proteolytic clipping experiments indicate that both the sizes and the tertiary structure of the Sal box binding proteins of both species are very similar. When bound to DNA, both the human and the mouse factor terminate transcription of pol I from the heterologous species. The results implicate that changes in signal sequences necessary for termination have been accompanied by compensatory changes in the DNA binding domain of the protein(s) interacting with the termination signal. In contrast, the protein-protein interactions between the termination factor and the transcribing RNA polymerase I appear to have been conserved during evolution.

Animals↗
PubMed1995

Brain size and morphology in miniaturized plethodontid salamanders.

In six miniaturized salamanders of the family Plethodontidae, including one of the smallest tetrapod vertebrates. Thorius pennatulus, the anatomical consequences of miniaturization for the brain were investigated. We determined (1) absolute and relative size of the brain, major parts of the brain, the tectum and tectal gray matter, (2) nerve cell size and density, and (3) the number of cells within the visual and visuomotor centers (thalamus, tectum/praetectum and tegmentum). No common compensatory strategy for the brain among the miniaturized salamanders was found. Except for the smallest species, T. pennatulus, only some of the expected compensatory processes (increase in relative size of the brain, relative size of visual centers, relative amount of gray matter or relative density of cell packing density) are found in any species, and these occur in different combinations and degrees. The most decisive factor for maximizing cell number was cell size. Miniaturized species with small cells also have many visual cells, regardless of the other factors. In contrast, the minimum number of visual neurons is found in miniaturized salamanders with large cells. It is concluded that the neuroanatomical traits investigated exert different degrees of resistance to adaptive compensatory processes. Cell size seems to be the most resistant parameter and is strictly dependent on genome size.

Animals↗
PubMed1993

[Theoretical analysis of some features of compensatory substitution in stem regions of transport RNA].

Some families of isoacceptor tRNAs were studies using VOSTORG software package for phylogenetic analysis. While analysing the evolutionary trees in was shown that the fixation of double substitutions AU<-->GC in spiral double-stranded regions passes two stages with intermediate station, such as non-canonical base pairs. In all the families studied double substitutions can be explained not only by passages through slightly deleterious GU pairs. Comparative analysis of B2-like repeats shown the absence of compensatory substitutions in the parts which are homologous to RNA stem regions. The data obtained let us assume that compensatory substitutions in the RNA helical regions represent an expressive example of non-directed adaptive molecular coevolution.

Animals↗
PubMedDate not supplied

[The magnocellular hypothalamus (the main and accessory nuclei): the evolutionary, molecular biological and morphofunctional aspects].

In the hypothalamus of high vertebrates apart major magnocellular nuclei, accessory nuclei have been described. The review is devoted to evolution of the accessory nuclei and to some questions of molecular biology and histophysiology of neuroendocrine neurones composed these nuclei. On the basis of literary and original data author put forward the speculation that the accessory nuclei (dorsolateral, circular, forniceal, and anterior commissural) are evolutionary stable. These "untraditional" formations have a peculiarities of cell compositions and projections to neurohaemal regions (posterior pituitary, external zone of median eminence). In rats accessory nuclei might play a compensatory role in the osmotic stress condition as well as during ageing. One from accessory nuclei (forniceal nucleus) is involved in the neurogenic stress realization, another one (dorsolateral nucleus) participates in the regulation of endocrine pancrease and erection. The idea about functional differences among magnocellular hypothalamic nuclei is discussed.

Aging↗
PubMed2002

Resistance to extinction of low fitness virus subjected to plaque-to-plaque transfers: diversification by mutation clustering.

Plaque-to-plaque transfers of RNA viruses lead to accumulation of mutations and fitness decrease. To test whether continuing plaque-to-plaque transfers would lead to viral extinction, we have subjected several low fitness foot-and-mouth disease virus (FMDV) clones to up to 130 successive plaque transfers, and have analyzed the evolution of plaque titers and genomic nucleotide sequences. No case of viral extinction could be documented. Some low fitness clones that posses an internal poly(A) tract evaded extinction by modifying the length or base composition of the poly(A) tract. The comparison of entire genomic sequences of FMDV clones at increasing plaque transfer number revealed that mutations accumulated at a uniform rate, and that they were distributed unevenly along the genome. Clusters of mutations were identified at different genomic sites in two plaque transfer lineages. Mutation clustering appears to occur stochastically and could not be related to fixation of compensatory mutations. The results document resistance of viral clones to extinction, and suggest that mutation clustering may be a mechanism of genetic diversification of low fitness virus.

Animals↗
PubMed1999

Evolution by small steps and rugged landscapes in the RNA virus phi6.

Fisher's geometric model of adaptive evolution argues that adaptive evolution should generally result from the substitution of many mutations of small effect because advantageous mutations of small effect should be more common than those of large effect. However, evidence for both evolution by small steps and for Fisher's model has been mixed. Here we report supporting results from a new experimental test of the model. We subjected the bacteriophage phi6 to intensified genetic drift in small populations and caused viral fitness to decline through the accumulation of a deleterious mutation. We then propagated the mutated virus at a range of larger population sizes and allowed fitness to recover by natural selection. Although fitness declined in one large step, it was usually recovered in smaller steps. More importantly, step size during recovery was smaller with decreasing size of the recovery population. These results confirm Fisher's main prediction that advantageous mutations of small effect should be more common. We also show that the advantageous mutations of small effect are compensatory mutations whose advantage is conditional (epistatic) on the presence of the deleterious mutation, in which case the adaptive landscape of phi6 is likely to be very rugged.

Bacteriophage phi 6↗
PubMed1992

Ventricular remodeling following myocardial infarction.

Ventricular remodeling denotes structural changes that occur in ventricular chamber size, wall thickness, and composition following myocardial damage. Following acute coronary occlusion, there are various factors to consider at different times that may contribute to subsequent ventricular dilation. Early infarct expansion and later healing may be accompanied by compensatory hypertrophy in the noninfarcted region and progressive global dilation, that may progress long term, the major stimulus being increased wall stress. The 2 major factors influencing ventricular remodeling following myocardial infarction are infarct artery patency and the ventricular loading conditions. Thrombolytic therapy may produce coronary reperfusion and limit infarct size. Patency of the infarct-related artery may also provide later benefits for ventricular remodeling. Following infarct evolution, pharmacologic intervention provides the potential to minimize the sequelae of infarct expansion and ventricular dilation. Clinical studies indicate that treatment of symptomless left ventricular dysfunction with angiotensin-converting enzyme inhibition at greater than or equal to 1 week following myocardial infarction may prevent further ventricular dilation and reduce the probability of progression to heart failure. Earlier intervention, at 24-48 hours following Q-wave myocardial infarction, is also practicable and effective. Even earlier intervention, in combination with or immediately following thrombolysis, is being assessed in other studies. The timing of treatment is of considerable importance because blockade of compensatory mechanisms activated at the time of infarction may not be desirable immediately, even though these mechanisms may be deleterious later. The results of large-scale mortality studies are awaited to indicate the benefit of this type of treatment in terms of heart failure prevention and survival long term.

Humans↗
PubMed1999

Concerted regulation and molecular evolution of the duplicated SNRPB'/B and SNRPN loci.

The human small nuclear ribonucleoprotein SNRPB ' /B gene is alternatively spliced to produce the SmB or SmB' spliceosomal core proteins. An ancestral duplication gave rise to the closely related SNRPN paralog whose protein product, SmN, replaces SmB'/B in brain. However, the precise evolutionary and functional relationship between these loci has not been clear. Genomic, cDNA and protein analyses presented here in chicken, two marsupials (South American opossum and tammar wallaby), and hedgehog, suggest that the vertebrate ancestral locus produced the SmB' isoform. Interestingly, three eutherians exhibit radically distinct splice choice expression profiles, producing either exclusively SmB in mouse, both SmB and SmB' in human, or exclusively SmB' in hedgehog. The human SNRPB ' /B locus is biallelically unmethylated, unlike the imprinted SNRPN locus which is unmethyl-ated only on the expressed paternal allele. Western analysis demonstrates that a compensatory feedback loop dramatically upregulates SmB'/B levels in response to the loss of SmN in Prader-Willi syndrome brain tissue, potentially reducing the phenotypic severity of this syndrome. These findings imply that these two genes encoding small nuclear ribonucleoprotein components are subject to dosage compensation. Therefore, a more global regulatory network may govern the maintenance of stoichiometric levels of spliceosomal components and may constrain their evolution.

Alternative Splicing↗
PubMed1989

Sequence conservation in Alu evolution.

A statistical analysis of a set of genomic human Alu elements is based on a published alignment and a recent classification of these sequences. After separation of the Alu sequences into families, the consensus sequences of these families are determined, using the correct weighting of the unidirectional decay of CG-dinucleotides. For, the tenfold greater mutation rate at CG's requires separate consideration of an independent clock at every stage of analysis. The distributions of the substitutions with respect to the new consensus sequences, taking the CG and the non-CG-nucleotide positions separately, lie far closer to the expected distributions than the total diversity. Computer analysis of the folding of RNAs derived from these sequences indicates that RNA secondary structure is conserved among Alu families, suggesting its importance for Alu proliferation and/or function. The folding pattern, further substantiated by a number of compensatory mutations, includes secondary structure domains which are homologous to those observed in 7SL RNA and a defined region of interaction between the two Alu subunits. These results are consistent with a model in which a small number of conserved Alu master genes give rise via retroposition to the numerous copies of Alu pseudogenes, that then diversify by random substitution. The master genes appeared at different periods during evolution giving rise to different families of Alu sequences.

Base Composition↗
PubMed1996

Secondary structure and patterns of evolution among mammalian mitochondrial 12S rRNA molecules.

Forty-nine complete 12S ribosomal RNA (rRNA) gene sequences from a diverse assortment of mammals (one monotreme, 11 marsupials, 37 placentals), including 11 new sequences, were employed to establish a "core" secondary structure model for mammalian 12S rRNA. Base-pairing interactions were assessed according to the criteria of potential base-pairing as well as evidence for base-pairing in the form of compensatory mutations. In cases where compensatory evidence was not available among mammalian sequences, we evaluated evidence among other vertebrate 12S rRNAs. Our results suggest a core model for secondary structure in mammalian 12S rRNAs with deletions as well as additions to the Gutell (1994: Nucleic Acids Res. 22) models for Bos and Homo. In all, we recognize 40 stems, 34 of which are supported by at least some compensatory evidence within Mammalia. We also investigated the occurrence and conservation in mammalian 12S rRNAs of nucleotide positions that are known to participate in the decoding site in E. coli. Twenty-four nucleotide positions known to participate in the decoding site in E. coli also occur among mammalian 12S rRNAs and 17 are invariant for the same base as in E. coli. Patterns of nucleotide substitution were assessed based on our secondary structure model. Transitions in loops become saturated by approximately 10-20 million years. Transitions in stems, in turn, show partial saturation at 20 million years but divergence continues to increase beyond 100 million years. Transversions accumulate linearly beyond 100 million years in both stems and loops although the rate of accumulation of transversions is three- to fourfold higher in loops. Presumably, this difference results from constraints to maintain pairing in stems.

Animals↗
PubMed1995

Coevolution of RNA helix stability and Shine-Dalgarno complementarity in a translational start region.

The initiation region of the coat-protein gene of RNA bacteriophage MS2 adopts a well-defined hairpin structure with the start codon occupying the loop position, while the Shine-Dalgarno (SD) sequence is part of the stem. In a previous study, we introduced mutations in this hairpin that changed its thermodynamic stability. The resulting phages evolved to regain the wild-type stability by second-site compensatory substitutions. Neither the original nor the suppressor mutations were in the SD region. In the present analysis, we have made changes in the SD region that shorten or extend its complementarity to the 3' end of 16S rRNA and monitored their evolution to a stable pseudorevertant species. Phages in which the SD complementarity was decreased evolved an initiator hairpin of lower stability than wild type while those in which the complementarity was extended evolved a hairpin with an increased stability. We conclude that weaker SD sequences still allow maximal translation if the secondary structure of the ribosome-landing site is destabilized accordingly. Alternatively, translation-initiation regions with a stronger secondary structure still allow maximal expression, if the SD complementarity is extended. These findings support a previously published model in which the SD interaction helps the ribosome to melt the structure in a translation-initiation region.

Base Sequence↗
PubMed2002

Quantitative analysis of gametic incompatibility between closely related species of neotropical sea urchins.

Species of the sea urchin genus Echinometra found on the two coasts of Panamá are recently diverged and only partially isolated by incomplete barriers to interspecific fertilization. This study confirms previous work that revealed incompatibility between the eggs of the Atlantic E. lucunter and the sperm of the other two neotropical species, whereas eggs of its sympatric congener E. viridis and allopatric E. vanbrunti are largely compatible with heterospecific sperm. Here we quantify fertilization using a range of sperm dilutions. We demonstrate a much stronger block to cross-species fertilization of E. lucunter eggs than was previously shown at fixed sperm concentrations, and mild incompatibility of the other two species' eggs where previous crosses between species were not distinguishable from within-species controls. Additionally, we present evidence for intraspecific variation in egg receptivity towards heterospecific sperm. Our findings here again discount the "reinforcement model" as a viable explanation for the pattern of prezygotic isolation. Gamete incompatibility in these Echinometra has appeared recently-within the last 1.5 million years-but is weaker in sympatry than in allopatry. Accidents of history may help explain why incompatibility of eggs emerged in one species and not in others. Compensatory sexual selection on sperm in this species could follow, and promote divergence of proteins mediating sperm-egg recognition.

Animals↗
PubMed1990

Direct sequencing of the activation peptide and the catalytic domain of the factor IX gene in six species.

By means of RNA amplification with transcript sequencing (RAWTS) under low stringency conditions, sequence was obtained directly without cloning for the activation peptide and the catalytic domain of factor IX from six species--sheep, pig, rabbit, guinea pig, rat, and mouse. The data presented demonstrate that, by the appropriate design of oligonucleotides and by performance of a nested PCR under appropriate conditions, it is possible to obtain sequence on a battery of species with a minimum of oligonucleotide primers. A total of 5.2 kb of cross-species sequence was generated with RAWTS. The results indicate that (1) 69% of the amino acids in the catalytic domain, but only 23% of the amino acids in the activation peptide, are identical in humans and the six species; (2) the catalytic domain evolves at a slower rate, but the extent and pattern of conservation of amino acids in the activation peptide suggest that the peptide functions as more than a cleavage spacer that separates the heavy and light chains in the catalytically inactive zymogen; (3) 37% of the amino acids in the activation peptide and 34% of the amino acids in the catalytic domain are factor IX-specific; i.e., they are either identical or changed in a highly conservative fashion in factor IX, but not in other related coagulation proteases; (4) these conserved factor IX-specific amino acids fall into three clusters, which are candidates for involvement in the protein interactions specific to factor IX; (5) there is a human-specific deletion after lysine 142 and a rodent-specific insertion after alanine 161; (6) in guinea pig, the insertion is associated with a seven-amino-acid repeat that corresponds to a perfect repeat of a 21-bp sequence; (7) humans have lost a potential N-glycosylation site that is conserved in the other species; (8) in each species, a few nonconservative changes occur in amino acids that are otherwise completely conserved, suggesting that compensatory mutations may have occurred; and (9) when compared to that of mouse, the amino acid identity with guinea pig factor IX is no greater than that found for the non-rodent species, a result compatible with the postulated increased rate of evolution in rodents.

Amino Acid Sequence↗
PubMed2000

The faint young Sun paradox: an observational test of an alternative solar model.

We report the results of deep observations at radio (3.6 cm) wavelengths of the nearby solar-type star pi 01 Ursa Majoris with the Very Large Array (VLA) intended to test an alternative theory of solar luminosity evolution. The standard model predicts a solar luminosity only 75% of the present value and surface temperatures below freezing on Earth and Mars at 4 Ga, seemingly in conflict with geologic evidence for liquid water on these planets. An alternative model invokes a compensatory mass loss through a declining solar wind that results in a more consistent early luminosity. The free-free emission from an enhanced wind around nearby young Sun-like stars should be detectable at microwave frequencies. Our observations of pi 01 UMa, a 300 million year-old solar-mass star, place an upper limit on the mass loss rate of 4-5 x 10(-11) M(solar) yr-1. Total mass loss from such a star over 4 Gyr would be less than 6%. If this star is indeed an analog of the early Sun, it casts doubt on the alternative model as a solution to the faint young Sun paradox, particularly for Mars.

Astronomy↗
PubMed1988

Evidence of natural selection to maintain a functional domain outside of the 'core' in a large subclass of group I introns.

Comparison of three closely-related, homologous Group I introns reveals conservation of RNA secondary structure and some primary sequence outside of the characteristic Group I core structure. Further examination of forty Group I introns showed that all can be placed into one of two categories based on the length of the "loop L5" region (subtended by the base-paired sequences P and Q): short (21 to 38 bases) or long (59 to 295 bases). Despite the large variation in size and sequence, all nineteen of the long L5 introns share a common structure whose features include an adenine-rich bulge at a fixed distance from the P-Q pairing. This bulge is flanked by base-paired regions of greater than or equal to 6 base pairs on the core-proximal side and greater than or equal to 3 base pairs on the distal side. In the core-proximal helix there are a large number and high proportion of deviations from the consensus sequence that maintain base-pairing. These naturally-occurring compensatory base substitutions provide compelling phylogenetic support for the existence of this pairing and indicate that the conserved structure has a function in vivo.

Aspergillus↗