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PubMed2006

Evolutionary predictions should be based on individual-level traits.

Recent theoretical studies have analyzed the evolution of habitat specialization using either the logistic or the Ricker equation. These studies have implemented evolutionary change directly in population-level parameters such as habitat-specific intrinsic growth rates r or carrying capacities K. This approach is a shortcut to a more detailed analysis where evolutionary change is studied in underlying morphological, physiological, or behavioral traits at the level of the individual that contribute to r or K. Here we describe two pitfalls that can occur when such a shortcut is employed. First, population-level parameters that appear as independent variables in a population dynamical model might not be independent when derived from processes at the individual level. Second, patterns of covariation between individual-level traits are usually not conserved when mapped to the level of demographic parameters. Nonlinear mappings constrain the curvature of trade-offs that can sensibly be assumed at the population level. To illustrate these results, we derive a two-habitat version of the logistic and Ricker equations from individual-level processes and compare the evolutionary dynamics of habitat-specific carrying capacities with those of underlying individual-level traits contributing to the carrying capacities. Finally, we sketch how our viewpoint affects the results of earlier studies.

Animals↗
PubMed1997

Clonal selection of HIV type 1 variants associated with resistance to foscarnet in vitro: confirmation by molecular evolutionary analysis.

Foscarnet (trisodium phosphonoformate, PFA) is an effective inhibitor of retroviral reverse transcriptase (RT) and is known to block the replication of human immunodeficiency virus type 1 (HIV-1). In this article we analyzed the evolutionary process in generating HIV-1 strains related to drug resistance, using PFA as a selective pressure. PFA inhibited virus replication and protected the virus-induced cell killing, but it did not completely eliminate HIV-1 during the course of 7 weeks of treatment. The nucleotide sequence of the 859-bp DNA fragment spanning the core region of the HIV-1 pol gene was determined for 51 clones obtained from genomic DNA of the HIV-1-infected cells at different time points during PFA treatment. The nucleotide sequence analysis documented the presence of a minor HIV-1 variant prior to the PFA treatment. Molecular evolutionary techniques were utilized to analyze how the minor HIV-1 clones became predominant during this evolutionary process under the selective pressure of PFA. A phylogenetic tree analysis divided these 51 HIV-1 clones into 3 groups. One of the groups consisted of the clones associated with the resistance to PFA. The clones belonging to this group became predominant over time during the course of PFA treatment. Thus, the acquisition of PFA resistance by HIV-1 was considered to be due to clonal selection. Furthermore, among the various amino acid substitutions observed, the substitution of arginine at position 172 by lysine (Arg172Lys) clearly distinguished this group from the others. Since the consistent amino acid substitution observed here has not been identified in the HIV-1 strains resistant to other RT inhibitors, PFA in combination with other RT inhibitors is considered to be a feasible candidate for a convergent combined chemotherapy against HIV-1 in the treatment of patients with AIDS and related conditions.

Amino Acid Sequence↗
PubMed2006

How evolutionary thinking affects people's ideas about aging interventions.

Evolutionary theory has guided the development of antiaging interventions in some conscious and some unconscious ways. It is a standard assumption that the body's health has been optimized by natural selection, and that the most benign and promising medical strategies should support the body's efforts to maintain itself. The very concept of natural healing is a reflection of evolutionary thinking about health. Meanwhile, a developing body of experimental evidence points to the startling hypothesis that aging is a metabolic program, under genetic control we are programmed for death. Evolution has provided that the aging program can be abated in times of stress, e.g., caloric restriction. CR mimetics are already recognized as a promising avenue for antiaging research. Beyond this, there are two ancient mechanisms of programmed death in protists that have survived half a billion years of evolution, and still figure in the aging of vertebrates today. These are apoptosis and replicative senescence via telomere truncation. Most researchers have been wary of modifying these mechanisms because they are known to play a stopgap role in cancer prevention. But intriguing evidence suggests that, despite some counter-carcinogenic function, the net result of both these mechanisms may be to shorten lifespan. Thus, interventions that suppress apoptosis and that preserve telomeres may be promising avenues for life extension research. A third element of the body's self-destruction program co-opts the inflammation response. Epidemiological evidence suggests that NSAIDs including aspirin protect against atherosclerosis, arthritis, and some forms of cancer. It may be that aging engages an autoimmune response that can be modified by drugs acting more narrowly on this same pathway. The existence of an evolutionary program that controls aging from the top down supports a new optimism concerning the types of antiaging interventions that are possible, and the likelihood that simple strategies may have dramatic results without dramatic side-effects.

Aging↗
PubMed2000

Using traveling salesman problem algorithms for evolutionary tree construction.

MOTIVATION: The construction of evolutionary trees is one of the major problems in computational biology, mainly due to its complexity. RESULTS: We present a new tree construction method that constructs a tree with minimum score for a given set of sequences, where the score is the amount of evolution measured in PAM distances. To do this, the problem of tree construction is reduced to the Traveling Salesman Problem (TSP). The input for the TSP algorithm are the pairwise distances of the sequences and the output is a circular tour through the optimal, unknown tree plus the minimum score of the tree. The circular order and the score can be used to construct the topology of the optimal tree. Our method can be used for any scoring function that correlates to the amount of changes along the branches of an evolutionary tree, for instance it could also be used for parsimony scores, but it cannot be used for least squares fit of distances. A TSP solution reduces the space of all possible trees to 2n. Using this order, we can guarantee that we reconstruct a correct evolutionary tree if the absolute value of the error for each distance measurement is smaller than f2.gif" BORDER="0">, where f3.gif" BORDER="0">is the length of the shortest edge in the tree. For data sets with large errors, a dynamic programming approach is used to reconstruct the tree. Finally simulations and experiments with real data are shown.

Algorithms↗
PubMed2001

MEGA2: molecular evolutionary genetics analysis software.

UNLABELLED: We have developed a new software package, Molecular Evolutionary Genetics Analysis version 2 (MEGA2), for exploring and analyzing aligned DNA or protein sequences from an evolutionary perspective. MEGA2 vastly extends the capabilities of MEGA version 1 by: (1) facilitating analyses of large datasets; (2) enabling creation and analyses of groups of sequences; (3) enabling specification of domains and genes; (4) expanding the repertoire of statistical methods for molecular evolutionary studies; and (5) adding new modules for visual representation of input data and output results on the Microsoft Windows platform. AVAILABILITY: http://www.megasoftware.net. CONTACT: s.kumar@asu.edu

DNA↗
PubMed2003

Using guide trees to construct multiple-sequence evolutionary HMMs.

MOTIVATION: Score-based progressive alignment algorithms do dynamic programming on successive branches of a guide tree. The analogous probabilistic construct is an Evolutionary HMM. This is a multiple-sequence hidden Markov model (HMM) made by combining transducers (conditionally normalised Pair HMMs) on the branches of a phylogenetic tree. METHODS: We present general algorithms for constructing an Evolutionary HMM from any Pair HMM and for doing dynamic programming to any Multiple-sequence HMM. RESULTS: Our prototype implementation, Handel, is based on the Thorne-Kishino-Felsenstein evolutionary model and is benchmarked using structural reference alignments.

Algorithms↗
PubMed2003

STRUCLA: a WWW meta-server for protein structure comparison and evolutionary classification.

MOTIVATION: Evolutionary relationships of proteins have long been derived from the alignment of protein sequences. But from the view of function, most restraints of evolutionary divergence operate at the level of tertiary structure. It has been demonstrated that quantitative measures of dissimilarity in families of structurally similar proteins can be applied to the construction of trees from a comparison of their three-dimensional structures. However, no convenient tool is publicly available to carry out such analyses. RESULTS: We developed STRUCLA (STRUcture CLAssification), a WWW tool for generation of trees based on evolutionary distances inferred from protein structures according to various methods. The server takes as an input a list of PDB files or the initial alignment of protein coordinates provided by the user (for instance exported from SWISS PDB VIEWER). The user specifies the distance cutoff and selects the distance measures. The server returns series of unrooted trees in the NEXUS format and corresponding distance matrices, as well as a consensus tree. The results can be used as an alternative and a complement to a fixed hierarchy of current protein structure databases. It can complement sequence-based phylogenetic analysis in the 'twilight zone of homology', where amino acid sequences are too diverged to provide reliable relationships.

Algorithms↗
PubMed2005

Predicting protein-protein interaction by searching evolutionary tree automorphism space.

MOTIVATION: Uncovering the protein-protein interaction network is a fundamental step in the quest to understand the molecular machinery of a cell. This motivates the search for efficient computational methods for predicting such interactions. Among the available predictors are those that are based on the co-evolution hypothesis "evolutionary trees of protein families (that are known to interact) are expected to have similar topologies". Many of these methods are limited by the fact that they can handle only a small number of protein sequences. Also, details on evolutionary tree topology are missing as they use similarity matrices in lieu of the trees. RESULTS: We introduce MORPH, a new algorithm for predicting protein interaction partners between members of two protein families that are known to interact. Our approach can also be seen as a new method for searching the best superposition of the corresponding evolutionary trees based on tree automorphism group. We discuss relevant facts related to the predictability of protein-protein interaction based on their co-evolution. When compared with related computational approaches, our method reduces the search space by approximately 3 x 10(5)-fold and at the same time increases the accuracy of predicting correct binding partners.

Algorithms↗
PubMed2005

Using evolutionary Expectation Maximization to estimate indel rates.

MOTIVATION: The Expectation Maximization (EM) algorithm, in the form of the Baum-Welch algorithm (for hidden Markov models) or the Inside-Outside algorithm (for stochastic context-free grammars), is a powerful way to estimate the parameters of stochastic grammars for biological sequence analysis. To use this algorithm for multiple-sequence evolutionary modelling, it would be useful to apply the EM algorithm to estimate not only the probability parameters of the stochastic grammar, but also the instantaneous mutation rates of the underlying evolutionary model (to facilitate the development of stochastic grammars based on phylogenetic trees, also known as Statistical Alignment). Recently, we showed how to do this for the point substitution component of the evolutionary process; here, we extend these results to the indel process. RESULTS: We present an algorithm for maximum-likelihood estimation of insertion and deletion rates from multiple sequence alignments, using EM, under the single-residue indel model owing to Thorne, Kishino and Felsenstein (the 'TKF91' model). The algorithm converges extremely rapidly, gives accurate results on simulated data that are an improvement over parsimonious estimates (which are shown to underestimate the true indel rate), and gives plausible results on experimental data (coronavirus envelope domains). Owing to the algorithm's close similarity to the Baum-Welch algorithm for training hidden Markov models, it can be used in an 'unsupervised' fashion to estimate rates for unaligned sequences, or estimate several sets of rates for sequences with heterogenous rates. AVAILABILITY: Software implementing the algorithm and the benchmark is available under GPL from http://www.biowiki.org/

Algorithms↗
PubMed2005

The inference of protein-protein interactions by co-evolutionary analysis is improved by excluding the information about the phylogenetic relationships.

MOTIVATION: The prediction of protein-protein interactions is currently an important issue in bioinformatics. The mirror tree method uses evolutionary information to predict protein-protein interactions. However, it has been recognized that predictions by the mirror tree method lead to many false positives. The incentive of our study was to solve this problem by improving the method of extracting the co-evolutionary information regarding the protein pairs. RESULTS: We developed a novel method to predict protein-protein interactions from co-evolutionary information in the framework of the mirror tree method. The originality is the use of the projection operator to exclude the information about the phylogenetic relationships among the source organisms from the distance matrix. Each distance matrix was transformed into a vector for the operation. The vector is referred to as a 'phylogenetic vector'. We have proposed three ways to extract the phylogenetic information: (1) using the 16S rRNA from the same source organisms as the proteins under consideration, (2) averaging the phylogenetic vectors and (3) analyzing the principal components of the phylogenetic vectors. We examined the performance of the proposed methods to predict interacting protein pairs from Escherichia coli, using experimentally verified data. Our method was successful, and it drastically reduced the number of false positives in the prediction. AVAILABILITY: The R script for the prediction of protein-protein interactions reported in this manuscript is available at http://timpani.genome.ad.jp/~proj/ CONTACT: sato@kuicr.kyoto-u.ac.jp SUPPLEMENTARY INFORMATION: The information is also available at the same site as the R script.

Algorithms↗
PubMed2006

Evolutionary trace report_maker: a new type of service for comparative analysis of proteins.

: Evolutionary trace report_maker offers a new type of service for researchers investigating the function of novel proteins. It pools, from different sources, information about protein sequence, structure and elementary annotation, and to that background superimposes inference about the evolutionary behavior of individual residues, using real-valued evolutionary trace method. As its only input it takes a Protein Data Bank identifier or UniProt accession number, and returns a human-readable document in PDF format, supplemented by the original data needed to reproduce the results quoted in the report.

Algorithms↗
PubMed2006

Imprint of evolutionary conservation and protein structure variation on the binding function of protein tyrosine kinases.

MOTIVATION: According to the models of divergent molecular evolution, the evolvability of new protein function may depend on the induction of new phenotypic traits by a small number of mutations of the binding site residues. Evolutionary relationships between protein kinases are often employed to infer inhibitor binding profiles from sequence analysis. However, protein kinases binding profiles may display inhibitor selectivity within a given kinase subfamily, while exhibiting cross-activity between kinases that are phylogenetically remote from the prime target. The emerging insights into kinase function and evolution combined with a rapidly growing number of publically available crystal structures of protein kinases complexes have motivated structural bioinformatics analysis of sequence-structure relationships in determining the binding function of protein tyrosine kinases. RESULTS: In silico profiling of Imatinib mesylate and PD-173955 kinase inhibitors with protein tyrosine kinases is conducted on kinome scale by using evolutionary analysis and fingerprinting inhibitor-protein interactions with the panel of all publically available protein tyrosine kinases crystal structures. We have found that sequence plasticity of the binding site residues alone may not be sufficient to enable protein tyrosine kinases to readily evolve novel binding activities with inhibitors. While evolutionary signal derived solely from the tyrosine kinase sequence conservation can not be readily translated into the ligand binding phenotype, the proposed structural bioinformatics analysis can discriminate a functionally relevant kinase binding signal from a simple phylogenetic relationship. The results of this work reveal that protein conformational diversity is intimately linked with sequence plasticity of the binding site residues in achieving functional adaptability of protein kinases towards specific drug binding. This study offers a plausible molecular rationale to the experimental binding profiles of the studied kinase inhibitors and provides a theoretical basis for constructing functionally relevant kinase binding trees.

Amino Acid Sequence↗
PubMed2006

ECRbase: database of evolutionary conserved regions, promoters, and transcription factor binding sites in vertebrate genomes.

Evolutionary conservation of DNA sequences provides a tool for the identification of functional elements in genomes. We have created a database of evolutionary conserved regions (ECRs) in vertebrate genomes, entitled ECRbase, which is constructed from a collection of whole-genome alignments produced by the ECR Browser. ECRbase features a database of syntenic blocks that recapitulate the evolution of rearrangements in vertebrates and a comprehensive collection of promoters in all vertebrate genomes generated using multiple sources of gene annotation. The database also contains a collection of annotated transcription factor binding sites (TFBSs) in evolutionary conserved and promoter elements. ECRbase currently includes human, rhesus macaque, dog, opossum, rat, mouse, chicken, frog, zebrafish and fugu genomes. It is freely accessible at http://ecrbase.dcode.org.

Animals↗
PubMed2026

Lack of Evidence for Gene-Level Convergence Linked to Evolutionary Shifts in Torpor Among Placental Mammals.

Torpor is a key survival strategy that many avian and mammalian lineages evolved in response to challenging environmental conditions. Whether the independent evolution of torpor in different lineages involved changes in the same genes remains poorly understood. Here, we performed comparative screens across 190 placental mammal genomes to comprehensively examine associations between loss, positive selection, and evolutionary rate shifts in individual protein-coding genes and evolutionary shifts in torpor use. We find that gene-torpor associations are highly clade-specific, with no gene being able to explain the majority of torpor shifts across the phylogeny of placental mammals. In contrast, there is more evidence, albeit still limited, for evolutionary convergence at the pathway level. Our results suggest that torpor emerged through several genetic routes in placental mammals, which likely explains the vast diversity of torpor use patterns that can be observed among torpor-capable species today.

Animals↗
PubMed1997

Bottleneck effect on evolutionary rate in the nearly neutral mutation model.

Variances of evolutionary rates among lineages in some proteins are larger than those expected from simple Poisson processes. This phenomenon is called overdispersion of the molecular clock. If population size N is constant, the overdispersion is observed only in a limited range of 2N sigma under the nearly neutral mutation model, where sigma represents the standard deviation of selection coefficients of new mutants. In this paper, we investigated effects of changing population size on the evolutionary rate by computer simulations assuming the nearly neutral mutation model. The size was changed cyclically between two numbers, N1 and N2 (N1 > N2), in the simulations. The overdispersion is observed if 2N2 sigma is less than two and the state of reduced size (bottleneck state) continues for more than approximately 0.1/u generations, where u is the mutation rate. The overdispersion results mainly because the average fitnesses of only a portion of populations go down when the population size is reduced and only in these populations subsequent advantageous substitutions occur after the population size becomes large. Since the fitness reduction after the bottleneck is stochastic, acceleration of the evolutionary rate does not necessarily occur uniformly among loci. From these results, we argue that the nearly neutral mutation model is a candidate mechanism to explain the overdispersed molecular clock.

Biological Evolution↗
PubMed1981

A model of evolutionary base substitutions and its application with special reference to rapid change of pseudogenes.

A model of evolutionary base substitutions that can incorporate different substitutional rates between the four bases and that takes into account unequal composition of bases in DNA sequences is proposed. Using this model, we derived formulae that enable us to estimate the evolutionary distances in terms of the number of nucleotide substitutions through comparative studies of nucleotide sequences. In order to check the validity of various formulae, Monte Carlo experiments were performed. These formulae were applied to analyze data on DNA sequences from diverse organisms. Particular attention was paid to problems concerning a globin pseudogene in the mouse and the time of its origin through duplication. We obtained a result suggesting that the evolutionary rates of substitution in the first and second codon positions of the pseudogene were roughly 10 times faster than those in the normal globin genes; whereas, the rate in the third position remained almost unchanged. Application of our formulae to histone genes H2B and H3 of the sea urchin showed that, in each of these genes, the rate in the third codon position is tremendously higher than that in the second position. All of these observations can easily and consistently be interpreted by the neutral theory of molecular evolution.

Animals↗
PubMed1989

What evolutionary biology can do for gerontology.

Evolutionary biologists have shown mathematically that aging is an inevitable consequence of age-specific natural selection acting on species with somata separate from germ lines. Two specific genetic mechanisms are known which could underlie the evolution of aging under these conditions: age-specificity of gene effects and antagonistic pleiotropy between early and late ages. Comparative evidence indicates that senescence occurs only when the stipulations of the evolutionary theory are met. Laboratory experiments with Drosophila indicate that prolonging the action of natural selection leads to the evolution of postponed senescence. The genetic variation involved in such postponed senescence exhibits both age-specificity and antagonistic pleiotropy. These theories and empirical findings together suggest that the best general theory of aging now available is the evolutionary theory. In addition, this work has yielded Drosophila stocks with postponed senescence that are being used to unravel physiological mechanisms of senescence.

Aging↗
PubMed2003

Enrichment of segmental duplications in regions of breaks of synteny between the human and mouse genomes suggest their involvement in evolutionary rearrangements.

The sequence of the mouse genome allows one to compare the conservation of synteny between the human and mouse genome and exploration of regions that might have been involved in major rearrangements during the evolution of these two species (evolutionary genome rearrangements). Recent segmental duplications (or duplicons) are paralogous DNA sequences with high sequence identity that account for about 3.5-5% of the human genome and have emerged during the past approximately 35 million years of evolution. These regions are susceptible to illegitimate recombination leading to rearrangements that result in genomic disorders or genomic mutations. A catalogue of several hundred segmental duplications potentially leading to genomic rearrangements has been reported. The authors and others have observed that some chromosome regions involved in genomic disorders are shuffled in orientation and order in the mouse genome and that regions flanked by segmental duplications are often polymorphic. We have compared the human and mouse genome sequences and demonstrate here that recent segmental duplications correlate with breaks of synteny between these two species. We also observed that nine primary regions involved in human genomic disorders show changes in the order or the orientation of mouse/human synteny segments, were often flanked by segmental duplications in the human sequence. We found that 53% of all evolutionary rearrangement breakpoints associate with segmental duplications, as compared with 18% expected in a random location of breaks along the chromosome (P<0.0001). Our data suggest that segmental duplications have participated in the recent evolution of the human genome, as driving forces for evolutionary rearrangements, chromosome structure polymorphisms and genomic disorders.

Animals↗