<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Bioinformática, Genómica y Evolución. Una alianza estratégica para la biología de este siglo.</style></title><secondary-title><style face="normal" font="default" size="100%">Ciencia Hoy</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year></dates><number><style face="normal" font="default" size="100%">113</style></number><volume><style face="normal" font="default" size="100%">19</style></volume><pages><style face="normal" font="default" size="100%">88-93</style></pages><language><style face="normal" font="default" size="100%">eng</style></language></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>6</ref-type><contributors><secondary-authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Navarro, A.</style></author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Evolución y Adaptación.150 años después del Origen de las Especies</style></title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year></dates><publisher><style face="normal" font="default" size="100%">Obrapropia.</style></publisher><pub-location><style face="normal" font="default" size="100%">Valencia. España</style></pub-location><pages><style face="normal" font="default" size="100%">510</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;Evoluci&amp;oacute;n y Adaptaci&amp;oacute;n: 150 a&amp;ntilde;os despu&amp;eacute;s del Origen de las Especies&lt;/b&gt; es un homenaje a la figura de Charles Darwin al cumplirse 200 a&amp;ntilde;os de su nacimiento y 150 a&amp;ntilde;os de la publicaci&amp;oacute;n que lo hiciese mundialmente famoso. En esta edici&amp;oacute;n 101 autores convocados por la Sociedad Espa&amp;ntilde;ola de Biolog&amp;iacute;a Evolutiva han resumido su trabajo de investigaci&amp;oacute;n en 51 art&amp;iacute;culos. Estos se han agrupado en tem&amp;aacute;ticas que abarcan los problemas de la evoluci&amp;oacute;n molecular,&amp;nbsp;el cambio morfol&amp;oacute;gico, la evoluci&amp;oacute;n del desarrollo,&amp;nbsp;el origen de las especies y su interacci&amp;oacute;n, la diversidad biol&amp;oacute;gica, la evoluci&amp;oacute;n del comportamiento, la paleobiolog&amp;iacute;a, la evoluci&amp;oacute;n experimental, la evoluci&amp;oacute;n cultural y la evoluci&amp;oacute;n en la filosof&amp;iacute;a y la docencia. Muchos de estos trabajos representan d&amp;eacute;cadas de constante investigaci&amp;oacute;n en el laboratorio y en el campo. El com&amp;uacute;n denominador de los art&amp;iacute;culos que contiene este libro es el esfuerzo por transmitir a un p&amp;uacute;blico no necesariamente experto la actualidad de las investigaciones que en el campo de la adaptaci&amp;oacute;n y la evoluci&amp;oacute;n se desarrolla en diferentes laboratorios. Esta obra resume por lo tanto, gran parte de las investigaciones que &amp;nbsp;en materia de evoluci&amp;oacute;n biol&amp;oacute;gica se realiza en Espa&amp;ntilde;a. Esta edici&amp;oacute;n deja constancia entonces del &amp;quot;Hecho de la Evoluci&amp;oacute;n&amp;quot;, y de la actualidad de teor&amp;iacute;a evolutiva moderna como cuerpo explicativo del mundo biol&amp;oacute;gico 150 a&amp;ntilde;os despu&amp;eacute;s del origen de las especies.&amp;nbsp;&lt;/p&gt;</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>5</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Serra, François</style></author><author><style face="normal" font="default" size="100%">Arbiza, L.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author></authors><secondary-authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Navarro, A.</style></author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Genómica Comparativa y Selección Natural. Aplicaciones en el Genoma Humano. Capítulo 1.6</style></title><secondary-title><style face="normal" font="default" size="100%">Evolución y Adaptacón. 150 años después del Origen de las Especies</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year></dates><publisher><style face="normal" font="default" size="100%">Obrapropia.</style></publisher><pub-location><style face="normal" font="default" size="100%">Valencia</style></pub-location><pages><style face="normal" font="default" size="100%">51-59</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;La b&amp;uacute;squeda de los eventos adaptativos a nivel molecular que ha diferenciado el genoma humano del de nuestro pariente vivo m&amp;aacute;s cercano, el chimpanc&amp;eacute;, ha sido una de las &amp;aacute;reas de mayor investigaci&amp;oacute;n en gen&amp;oacute;mica comparativa. Paralelamente, la predicci&amp;oacute;n funcional de variantes gen&amp;eacute;ticas en nuestra especie ha sido un &amp;aacute;rea de intenso desarrollo en bioinform&amp;aacute;tica. En este trabajo discutiremos resultados previos y otros m&amp;aacute;s recientes que dan cuenta de estos desarrollos. Veremos que en todos los casos la estimaci&amp;oacute;n de las presiones selectivas a nivel de los genes individuales o de los residuos de las prote&amp;iacute;nas son el denominador com&amp;uacute;n para discutir ambos aspectos. Finalmente mostraremos c&amp;oacute;mo el an&amp;aacute;lisis de estas presiones selectivas por grupos funcionales de genes resulta una alternativa viable y con suficiente poder estad&amp;iacute;stico para el an&amp;aacute;lisis de la adaptaci&amp;oacute;n y de las restricciones evolutivas a nivel gen&amp;oacute;mico.&amp;nbsp;&lt;/p&gt;</style></abstract><section><style face="normal" font="default" size="100%">19</style></section></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Reiss, JO</style></author><author><style face="normal" font="default" size="100%">Burke, A C</style></author><author><style face="normal" font="default" size="100%">Archer, C</style></author><author><style face="normal" font="default" size="100%">De Renzi, M</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Etxeberria, A</style></author><author><style face="normal" font="default" size="100%">Gale, E A</style></author><author><style face="normal" font="default" size="100%">Hinchliffe, J R</style></author><author><style face="normal" font="default" size="100%">Nuño de la Rosa, L</style></author><author><style face="normal" font="default" size="100%">Rose, C S</style></author><author><style face="normal" font="default" size="100%">Rasskin-Gutman, D</style></author><author><style face="normal" font="default" size="100%">Müller, G</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pere Alberch: Originator of EvoDevo</style></title><secondary-title><style face="normal" font="default" size="100%">Biological Theory</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year></dates><number><style face="normal" font="default" size="100%">4</style></number><volume><style face="normal" font="default" size="100%">3</style></volume><pages><style face="normal" font="default" size="100%">351-353</style></pages><language><style face="normal" font="default" size="100%">eng</style></language></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Martin-Coello, J.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Arbiza, L.</style></author><author><style face="normal" font="default" size="100%">Ausio, J.</style></author><author><style face="normal" font="default" size="100%">Roldan, E. R.</style></author><author><style face="normal" font="default" size="100%">Gomendio, M.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Sexual selection drives weak positive selection in protamine genes and high promoter divergence, enhancing sperm competitiveness</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Biol Sci</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adaptation</style></keyword><keyword><style  face="normal" font="default" size="100%">positive selection</style></keyword><keyword><style  face="normal" font="default" size="100%">sperm competition</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2009</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=19364735</style></url></web-urls></urls><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Phenotypic adaptations may be the result of changes in gene structure or gene regulation, but little is known about the evolution of gene expression. In addition, it is unclear whether the same selective forces may operate at both levels simultaneously. Reproductive proteins evolve rapidly, but the underlying selective forces promoting such rapid changes are still a matter of debate. In particular, the role of sexual selection in driving positive selection among reproductive proteins remains controversial, whereas its potential influence on changes in promoter regions has not been explored. Protamines are responsible for maintaining DNA in a compacted form in chromosomes in sperm and the available evidence suggests that they evolve rapidly. Because protamines condense DNA within the sperm nucleus, they influence sperm head shape. Here, we examine the influence of sperm competition upon protamine 1 and protamine 2 genes and their promoters, by comparing closely related species of Mus that differ in relative testes size, a reliable indicator of levels of sperm competition. We find evidence of positive selection in the protamine 2 gene in the species with the highest inferred levels of sperm competition. In addition, sperm competition levels across all species are strongly associated with high divergence in protamine 2 promoters that, in turn, are associated with sperm swimming speed. We suggest that changes in protamine 2 promoters are likely to enhance sperm swimming speed by making sperm heads more hydrodynamic. Such phenotypic changes are adaptive because sperm swimming speed may be a major determinant of fertilization success under sperm competition. Thus, when species have diverged recently, few changes in gene-coding sequences are found, while high divergence in promoters seems to be associated with the intensity of sexual selection.&lt;/p&gt;</style></abstract><notes><style face="normal" font="default" size="100%">&lt;p&gt;Journal article Proceedings. Biological sciences / The Royal Society Proc Biol Sci. 2009 Apr 8.&lt;/p&gt;</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>5</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Selective Constraints and Human Disease Genes: Evolutionary and Bioinformatic Approaches</style></title><secondary-title><style face="normal" font="default" size="100%">Encyclopedia of Life Science</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year></dates><publisher><style face="normal" font="default" size="100%">John Wiley &amp; Sons, Ltd.</style></publisher><pub-location><style face="normal" font="default" size="100%">UK</style></pub-location><language><style face="normal" font="default" size="100%">eng</style></language></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>5</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Selective Constraints on Human Disease Mutations and Polymorphisms</style></title><secondary-title><style face="normal" font="default" size="100%">Handbook of Human Molecular Evolution</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://eu.wiley.com/WileyCDA/WileyTitle/productCd-0470517468,descCd-description.html</style></url></web-urls></urls><publisher><style face="normal" font="default" size="100%">Hildegard Kehrer-Sawatzki &amp; David N. Cooper. John Wiley &amp; Sons, Ltd</style></publisher><pub-location><style face="normal" font="default" size="100%">UK</style></pub-location><language><style face="normal" font="default" size="100%">eng</style></language></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">E. Capriotti</style></author><author><style face="normal" font="default" size="100%">Arbiza, L.</style></author><author><style face="normal" font="default" size="100%">Casadio, R.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">M. A. Marti-Renom</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Use of estimated evolutionary strength at the codon level improves the prediction of disease-related protein mutations in humans</style></title><secondary-title><style face="normal" font="default" size="100%">Hum Mutat</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Algorithms Codon/genetics Computational Biology/*methods *DNA Mutational Analysis Databases</style></keyword><keyword><style  face="normal" font="default" size="100%">Human Humans Iduronic Acid/analogs &amp; derivatives/metabolism *Point Mutation Polymorphism</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular *Genetic Predisposition to Disease Genetic Variation Genome</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein *Evolution</style></keyword><keyword><style  face="normal" font="default" size="100%">Single Nucleotide Proteins/chemistry/*genetics Tumor Suppressor Protein p53/genetics</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17935148</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">1</style></number><volume><style face="normal" font="default" size="100%">29</style></volume><pages><style face="normal" font="default" size="100%">198-204</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Predicting the functional impact of protein variation is one of the most challenging problems in bioinformatics. A rapidly growing number of genome-scale studies provide large amounts of experimental data, allowing the application of rigorous statistical approaches for predicting whether a given single point mutation has an impact on human health. Up until now, existing methods have limited their source data to either protein or gene information. Novel in this work, we take advantage of both and focus on protein evolutionary information by using estimated selective pressures at the codon level. Here we introduce a new method (SeqProfCod) to predict the likelihood that a given protein variant is associated with human disease or not. Our method relies on a support vector machine (SVM) classifier trained using three sources of information: protein sequence, multiple protein sequence alignments, and the estimation of selective pressure at the codon level. SeqProfCod has been benchmarked with a large dataset of 8,987 single point mutations from 1,434 human proteins from SWISS-PROT. It achieves 82% overall accuracy and a correlation coefficient of 0.59, indicating that the estimation of the selective pressure helps in predicting the functional impact of single-point mutations. Moreover, this study demonstrates the synergic effect of combining two sources of information for predicting the functional effects of protein variants: protein sequence/profile-based information and the evolutionary estimation of the selective pressures at the codon level. The results of large-scale application of SeqProfCod over all annotated point mutations in SWISS-PROT (available for download at http://sgu.bioinfo.cipf.es/services/Omidios/; last accessed: 24 August 2007), could be used to support clinical studies.</style></abstract><notes><style face="normal" font="default" size="100%">Capriotti, Emidio Arbiza, Leonardo Casadio, Rita Dopazo, Joaquin Dopazo, Hernan Marti-Renom, Marc A Evaluation Studies Research Support, Non-U.S. Gov’t United States Human mutation Hum Mutat. 2008 Jan;29(1):198-204.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Fatima Al-Shahrour</style></author><author><style face="normal" font="default" size="100%">Arbiza, L.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Huerta-Cepas, J.</style></author><author><style face="normal" font="default" size="100%">Minguez, P.</style></author><author><style face="normal" font="default" size="100%">Montaner, D.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">From genes to functional classes in the study of biological systems</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Bioinformatics</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Algorithms Chromosome Mapping/*methods Computer Simulation Gene Expression Profiling/methods *Models</style></keyword><keyword><style  face="normal" font="default" size="100%">babelomics</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Multigene Family/*physiology Signal Transduction/*physiology *Software Systems Biology/*methods *User-Computer Interface</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2007</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17407596</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">114</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;BACKGROUND: With the popularization of high-throughput techniques, the need for procedures that help in the biological interpretation of results has increased enormously. Recently, new procedures inspired in systems biology criteria have started to be developed. RESULTS: Here we present FatiScan, a web-based program which implements a threshold-independent test for the functional interpretation of large-scale experiments that does not depend on the pre-selection of genes based on the multiple application of independent tests to each gene. The test implemented aims to directly test the behaviour of blocks of functionally related genes, instead of focusing on single genes. In addition, the test does not depend on the type of the data used for obtaining significance values, and consequently different types of biologically informative terms (gene ontology, pathways, functional motifs, transcription factor binding sites or regulatory sites from CisRed) can be applied to different classes of genome-scale studies. We exemplify its application in microarray gene expression, evolution and interactomics. CONCLUSION: Methods for gene set enrichment which, in addition, are independent from the original data and experimental design constitute a promising alternative for the functional profiling of genome-scale experiments. A web server that performs the test described and other similar ones can be found at: http://www.babelomics.org.&lt;/p&gt;</style></abstract><notes><style face="normal" font="default" size="100%">&lt;p&gt;Al-Shahrour, Fatima Arbiza, Leonardo Dopazo, Hernan Huerta-Cepas, Jaime Minguez, Pablo Montaner, David Dopazo, Joaquin Research Support, Non-U.S. Gov’t England BMC bioinformatics BMC Bioinformatics. 2007 Apr 3;8:114.&lt;/p&gt;</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Huerta-Cepas, J.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">Gabaldón, T.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The human phylome</style></title><secondary-title><style face="normal" font="default" size="100%">Genome Biol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals *Evolution Evolution</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Gene Duplication *Genome Humans *Phylogeny Proteins/genetics Sequence Analysis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2007</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17567924</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">6</style></number><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">R109</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">BACKGROUND: Phylogenomics analyses serve to establish evolutionary relationships among organisms and their genes. A phylome, the complete collection of all gene phylogenies in a genome, constitutes a valuable source of information, but its use in large genomes still constitutes a technical challenge. The use of phylomes also requires the development of new methods that help us to interpret them. RESULTS: We reconstruct here the human phylome, which includes the evolutionary relationships of all human proteins and their homologs among 39 fully sequenced eukaryotes. Phylogenetic techniques used include alignment trimming, branch length optimization, evolutionary model testing and maximum likelihood and Bayesian methods. Although differences with alternative topologies are minor, most of the trees support the Coelomata and Unikont hypotheses as well as the grouping of primates with laurasatheria to the exclusion of rodents. We assess the extent of gene duplication events and their relationship with the functional roles of the protein families involved. We find support for at least one, and probably two, rounds of whole genome duplications before vertebrate radiation. Using a novel algorithm that is independent from a species phylogeny, we derive orthology and paralogy relationships of human proteins among eukaryotic genomes. CONCLUSION: Topological variations among phylogenies for different genes are to be expected, highlighting the danger of gene-sampling effects in phylogenomic analyses. Several links can be established between the functions of gene families duplicated at certain phylogenetic splits and major evolutionary transitions in those lineages. The pipeline implemented here can be easily adapted for use in other organisms.</style></abstract><notes><style face="normal" font="default" size="100%">Huerta-Cepas, Jaime Dopazo, Hernan Dopazo, Joaquin Gabaldon, Toni Research Support, Non-U.S. Gov’t England Genome biology Genome Biol. 2007;8(6):R109.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rico, D.</style></author><author><style face="normal" font="default" size="100%">Vaquerizas, J. M.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Bosca, L.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Identification of conserved domains in the promoter regions of nitric oxide synthase 2: implications for the species-specific transcription and evolutionary differences</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Genomics</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals Base Sequence Conserved Sequence Enhancer Elements</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic *Evolution</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Response Elements Species Specificity</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Humans Inflammation/metabolism Interferon-gamma/metabolism Mice NF-kappa B/metabolism Nitric Oxide Synthase Type II/*genetics *Promoter Regions</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2007</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17686182</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">271</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">BACKGROUND: The majority of the genes involved in the inflammatory response are highly conserved in mammals. These genes are not significantly expressed under normal conditions and are mainly regulated at the transcription and prost-transcriptional level. Transcription from the promoters of these genes is very dependent on NF-kappaB activation, which integrates the response to diverse extracellular stresses. However, in spite of the high conservation of the pattern of promoter regulation in kappaB-regulated genes, there is inter-species diversity in some genes. One example is nitric oxide synthase 2 (NOS-2), which exhibits a species-specific pattern of expression in response to infection or pro-inflammatory challenge. RESULTS: We have conducted a comparative genomic analysis of NOS-2 with different bioinformatic approaches. This analysis shows that in the NOS-2 gene promoter the position and the evolutionary divergence of some conserved regions are different in rodents and non-rodent mammals, and in particular in primates. Two not previously described distal regions in rodents that are similar to the unique upstream region responsible of the NF-kappaB activation of NOS-2 in humans are fragmented and translocated to different locations in the rodent promoters. The rodent sequences moreover lack the functional kappaB sites and IFN-gamma response sites present in the homologous human, rhesus monkey and chimpanzee regions. The absence of kappaB binding in these regions was confirmed by electrophoretic mobility shift assays. CONCLUSION: The data presented reveal divergence between rodents and other mammals in the location and functionality of conserved regions of the NOS-2 promoter containing NF-kappaB and IFN-gamma response elements.</style></abstract><notes><style face="normal" font="default" size="100%">Rico, Daniel Vaquerizas, Juan M Dopazo, Hernan Bosca, Lisardo Research Support, Non-U.S. Gov’t England BMC genomics BMC Genomics. 2007 Aug 8;8:271.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Tarraga, J.</style></author><author><style face="normal" font="default" size="100%">Medina, Ignacio</style></author><author><style face="normal" font="default" size="100%">Arbiza, L.</style></author><author><style face="normal" font="default" size="100%">Huerta-Cepas, J.</style></author><author><style face="normal" font="default" size="100%">Gabaldón, T.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Phylemon: a suite of web tools for molecular evolution, phylogenetics and phylogenomics</style></title><secondary-title><style face="normal" font="default" size="100%">Nucleic Acids Res</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals Computational Biology/*methods Databases</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Evolution</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Genetic Techniques Humans *Internet Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein Software User-Computer Interface</style></keyword><keyword><style  face="normal" font="default" size="100%">Statistical *Phylogeny Programming Languages Sequence Alignment Sequence Analysis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2007</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17452346</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">Web Server issue</style></number><volume><style face="normal" font="default" size="100%">35</style></volume><pages><style face="normal" font="default" size="100%">W38-42</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Phylemon is an online platform for phylogenetic and evolutionary analyses of molecular sequence data. It has been developed as a web server that integrates a suite of different tools selected among the most popular stand-alone programs in phylogenetic and evolutionary analysis. It has been conceived as a natural response to the increasing demand of data analysis of many experimental scientists wishing to add a molecular evolution and phylogenetics insight into their research. Tools included in Phylemon cover a wide yet selected range of programs: from the most basic for multiple sequence alignment to elaborate statistical methods of phylogenetic reconstruction including methods for evolutionary rates analyses and molecular adaptation. Phylemon has several features that differentiates it from other resources: (i) It offers an integrated environment that enables the direct concatenation of evolutionary analyses, the storage of results and handles required data format conversions, (ii) Once an outfile is produced, Phylemon suggests the next possible analyses, thus guiding the user and facilitating the integration of multi-step analyses, and (iii) users can define and save complete pipelines for specific phylogenetic analysis to be automatically used on many genes in subsequent sessions or multiple genes in a single session (phylogenomics). The Phylemon web server is available at http://phylemon.bioinfo.cipf.es.</style></abstract><notes><style face="normal" font="default" size="100%">Tarraga, Joaquin Medina, Ignacio Arbiza, Leonardo Huerta-Cepas, Jaime Gabaldon, Toni Dopazo, Joaquin Dopazo, Hernan Research Support, Non-U.S. Gov’t England Nucleic acids research Nucleic Acids Res. 2007 Jul;35(Web Server issue):W38-42. Epub 2007 Apr 22.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>5</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">La clasificación de los organismos</style></title><secondary-title><style face="normal" font="default" size="100%">Invitación a la Biología</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2006</style></year></dates><publisher><style face="normal" font="default" size="100%">Curtis, Barnes, Schnek &amp; Flores. 2da, Editorial Medica Panamericana</style></publisher><pub-location><style face="normal" font="default" size="100%">Buenos Aires</style></pub-location><language><style face="normal" font="default" size="100%">eng</style></language><section><style face="normal" font="default" size="100%">22</style></section></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Arbiza, L.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Positive selection, relaxation, and acceleration in the evolution of the human and chimp genome</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS Comput Biol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adaptation</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological/genetics Animals *Evolution</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Genome/*genetics Humans Pan troglodytes/*genetics *Selection (Genetics)</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=16683019</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">4</style></number><volume><style face="normal" font="default" size="100%">2</style></volume><pages><style face="normal" font="default" size="100%">e38</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">For years evolutionary biologists have been interested in searching for the genetic bases underlying humanness. Recent efforts at a large or a complete genomic scale have been conducted to search for positively selected genes in human and in chimp. However, recently developed methods allowing for a more sensitive and controlled approach in the detection of positive selection can be employed. Here, using 13,198 genes, we have deduced the sets of genes involved in rate acceleration, positive selection, and relaxation of selective constraints in human, in chimp, and in their ancestral lineage since the divergence from murids. Significant deviations from the strict molecular clock were observed in 469 human and in 651 chimp genes. The more stringent branch-site test of positive selection detected 108 human and 577 chimp positively selected genes. An important proportion of the positively selected genes did not show a significant acceleration in rates, and similarly, many of the accelerated genes did not show significant signals of positive selection. Functional differentiation of genes under rate acceleration, positive selection, and relaxation was not statistically significant between human and chimp with the exception of terms related to G-protein coupled receptors and sensory perception. Both of these were over-represented under relaxation in human in relation to chimp. Comparing differences between derived and ancestral lineages, a more conspicuous change in trends seems to have favored positive selection in the human lineage. Since most of the positively selected genes are different under the same functional categories between these species, we suggest that the individual roles of the alternative positively selected genes may be an important factor underlying biological differences between these species.</style></abstract><notes><style face="normal" font="default" size="100%">Arbiza, Leonardo Dopazo, Joaquin Dopazo, Hernan Research Support, Non-U.S. Gov’t United States PLoS computational biology PLoS Comput Biol. 2006 Apr;2(4):e38. Epub 2006 Apr 28.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">L. Conde</style></author><author><style face="normal" font="default" size="100%">Vaquerizas, J. M.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Arbiza, L.</style></author><author><style face="normal" font="default" size="100%">Reumers, J.</style></author><author><style face="normal" font="default" size="100%">Rousseau, F.</style></author><author><style face="normal" font="default" size="100%">Schymkowitz, J.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">PupaSuite: finding functional single nucleotide polymorphisms for large-scale genotyping purposes</style></title><secondary-title><style face="normal" font="default" size="100%">Nucleic Acids Res</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Algorithms Computer Graphics Databases</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Genotype Haplotypes Internet Linkage Disequilibrium *Polymorphism</style></keyword><keyword><style  face="normal" font="default" size="100%">Nucleic Acid Evolution</style></keyword><keyword><style  face="normal" font="default" size="100%">Single Nucleotide *Software User-Computer Interface</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://nar.oxfordjournals.org/cgi/content/full/34/suppl_2/W621</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">Web Server issue</style></number><volume><style face="normal" font="default" size="100%">34</style></volume><pages><style face="normal" font="default" size="100%">W621-5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We have developed a web tool, PupaSuite, for the selection of single nucleotide polymorphisms (SNPs) with potential phenotypic effect, specifically oriented to help in the design of large-scale genotyping projects. PupaSuite uses a collection of data on SNPs from heterogeneous sources and a large number of pre-calculated predictions to offer a flexible and intuitive interface for selecting an optimal set of SNPs. It improves the functionality of PupaSNP and PupasView programs and implements new facilities such as the analysis of user’s data to derive haplotypes with functional information. A new estimator of putative effect of polymorphisms has been included that uses evolutionary information. Also SNPeffect database predictions have been included. The PupaSuite web interface is accessible through http://pupasuite.bioinfo.cipf.es and through http://www.pupasnp.org.&lt;/p&gt;</style></abstract><notes><style face="normal" font="default" size="100%">&lt;p&gt;Conde, Lucia Vaquerizas, Juan M Dopazo, Hernan Arbiza, Leonardo Reumers, Joke Rousseau, Frederic Schymkowitz, Joost Dopazo, Joaquin Research Support, Non-U.S. Gov’t England Nucleic acids research Nucleic Acids Res. 2006 Jul 1;34(Web Server issue):W621-5.&lt;/p&gt;</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Arbiza, L.</style></author><author><style face="normal" font="default" size="100%">Duchi, S.</style></author><author><style face="normal" font="default" size="100%">Montaner, D.</style></author><author><style face="normal" font="default" size="100%">Burguet, J.</style></author><author><style face="normal" font="default" size="100%">Pantoja-Uceda, D.</style></author><author><style face="normal" font="default" size="100%">Pineda-Lucena, A.</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author><author><style face="normal" font="default" size="100%">H. Dopazo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Selective pressures at a codon-level predict deleterious mutations in human disease genes</style></title><secondary-title><style face="normal" font="default" size="100%">J Mol Biol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Amino Acid Sequence Amino Acid Substitution Codon/*genetics Databases</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Evolution</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Human Humans Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Inborn/*genetics Genome</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Genes</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Molecular Sequence Data *Mutation Neoplasms/genetics Proteins/genetics *Selection (Genetics) Tumor Suppressor Protein p53/chemistry/genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">p53 Genetic Diseases</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=16584746</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">5</style></number><volume><style face="normal" font="default" size="100%">358</style></volume><pages><style face="normal" font="default" size="100%">1390-404</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Deleterious mutations affecting biological function of proteins are constantly being rejected by purifying selection from the gene pool. The non-synonymous/synonymous substitution rate ratio (omega) is a measure of selective pressure on amino acid replacement mutations for protein-coding genes. Different methods have been developed in order to predict non-synonymous changes affecting gene function. However, none has considered the estimation of selective constraints acting on protein residues. Here, we have used codon-based maximum likelihood models in order to estimate the selective pressures on the individual amino acid residues of a well-known model protein: p53. We demonstrate that the number of residues under strong purifying selection in p53 is much higher than those that are strictly conserved during the evolution of the species. In agreement with theoretical expectations, residues that have been noted to be of structural relevance, or in direct association with DNA, were among those showing the highest signals of purifying selection. Conversely, those changing according to a neutral, or nearly neutral mode of evolution, were observed to be irrelevant for protein function. Finally, using more than 40 human disease genes, we demonstrate that residues evolving under strong selective pressures (omega&lt;0.1) are significantly associated (p&lt;0.01) with human disease. We hypothesize that non-synonymous change on amino acids showing omega&lt;0.1 will most likely affect protein function. The application of this evolutionary prediction at a genomic scale will provide an a priori hypothesis of the phenotypic effect of non-synonymous coding single nucleotide polymorphisms (SNPs) in the human genome.</style></abstract><notes><style face="normal" font="default" size="100%">Arbiza, Leonardo Duchi, Serena Montaner, David Burguet, Jordi Pantoja-Uceda, David Pineda-Lucena, Antonio Dopazo, Joaquin Dopazo, Hernan Research Support, Non-U.S. Gov’t England Journal of molecular biology J Mol Biol. 2006 May 19;358(5):1390-404. Epub 2006 Mar 15.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Genome-scale evidence of the nematode-arthropod clade</style></title><secondary-title><style face="normal" font="default" size="100%">Genome Biol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals Arthropods/*classification/genetics Caenorhabditis elegans/classification/genetics Evolution</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular *Genome Genomics Nematoda/*classification/genetics *Phylogeny</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15892869</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">5</style></number><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">R41</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">BACKGROUND: The issue of whether coelomates form a single clade, the Coelomata, or whether all animals that moult an exoskeleton (such as the coelomate arthropods and the pseudocoelomate nematodes) form a distinct clade, the Ecdysozoa, is the most puzzling issue in animal systematics and a major open-ended subject in evolutionary biology. Previous single-gene and genome-scale analyses designed to resolve the issue have produced contradictory results. Here we present the first genome-scale phylogenetic evidence that strongly supports the Ecdysozoa hypothesis. RESULTS: Through the most extensive phylogenetic analysis carried out to date, the complete genomes of 11 eukaryotic species have been analyzed in order to find homologous sequences derived from 18 human chromosomes. Phylogenetic analysis of datasets showing an increased adjustment to equal evolutionary rates between nematode and arthropod sequences produced a gradual change from support for Coelomata to support for Ecdysozoa. Transition between topologies occurred when fast-evolving sequences of Caenorhabditis elegans were removed. When chordate, nematode and arthropod sequences were constrained to fit equal evolutionary rates, the Ecdysozoa topology was statistically accepted whereas Coelomata was rejected. CONCLUSIONS: The reliability of a monophyletic group clustering arthropods and nematodes was unequivocally accepted in datasets where traces of the long-branch attraction effect were removed. This is the first phylogenomic evidence to strongly support the ’moulting clade’ hypothesis.</style></abstract><notes><style face="normal" font="default" size="100%">Dopazo, Hernan Dopazo, Joaquin Research Support, Non-U.S. Gov’t England Genome biology Genome Biol. 2005;6(5):R41. Epub 2005 Apr 28.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">J. Santoyo</style></author><author><style face="normal" font="default" size="100%">Dopazo, J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Phylogenomics and the number of characters required for obtaining an accurate phylogeny of eukaryote model species</style></title><secondary-title><style face="normal" font="default" size="100%">Bioinformatics</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2004</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15262789</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">20 Suppl 1</style></volume><pages><style face="normal" font="default" size="100%">i116-21</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;MOTIVATION: Through the most extensive phylogenomic analysis carried out to date, complete genomes of 11 eukaryotic species have been examined in order to find the homologous of more than 25,000 amino acid sequences. These sequences correspond to the exons of more than 3000 genes and were used as presence/absence characters to test one of the most controversial hypotheses concerning animal evolution, namely the Ecdysozoa hypothesis. Distance, maximum parsimony and Bayesian methods of phylogenetic reconstruction were used to test the hypothesis. RESULTS: The reliability of the ecdysozoa, grouping arthropods and nematodes in a single clade was unequivocally rejected in all the consensus trees. The Coelomata clade, grouping arthropods and chordates, was supported by the highest statistical confidence in all the reconstructions. The study of the dependence of the genomes’ tree accuracy on the number of exons used, demonstrated that an unexpectedly larger number of characters are necessary to obtain robust phylogenies. Previous studies supporting ecdysozoa, could not guarantee an accurate phylogeny because the number of characters used was clearly below the minimum required.&lt;/p&gt;</style></abstract><notes><style face="normal" font="default" size="100%">&lt;p&gt;Dopazo, Hernan Santoyo, Javier Dopazo, Joaquin Research Support, Non-U.S. Gov’t England Bioinformatics (Oxford, England) Bioinformatics. 2004 Aug 4;20 Suppl 1:i116-21.&lt;/p&gt;</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Gordon, M. B.</style></author><author><style face="normal" font="default" size="100%">Perazzo, R.</style></author><author><style face="normal" font="default" size="100%">Risau-Gusman, S.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A model for the emergence of adaptive subsystems</style></title><secondary-title><style face="normal" font="default" size="100%">Bull Math Biol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">*Adaptation</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Algorithms Alleles Animals Evolution Genotype Humans *Learning *Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Statistical Neural Networks (Computer) Phenotype Synapses/genetics</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2003</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=12597115</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">1</style></number><volume><style face="normal" font="default" size="100%">65</style></volume><pages><style face="normal" font="default" size="100%">27-56</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We investigate the interaction of learning and evolution in a changing environment. A stable learning capability is regarded as an emergent adaptive system evolved by natural selection of genetic variants. We consider the evolution of an asexual population. Each genotype can have ’fixed’ and ’flexible’ alleles. The former express themselves as synaptic connections that remain unchanged during ontogeny and the latter as synapses that can be adjusted through a learning algorithm. Evolution is modelled using genetic algorithms and the changing environment is represented by two optimal synaptic patterns that alternate a fixed number of times during the ’life’ of the individuals. The amplitude of the change is related to the Hamming distance between the two optimal patterns and the rate of change to the frequency with which both exchange roles. This model is an extension of that of Hinton and Nowlan in which the fitness is given by a probabilistic measure of the Hamming distance to the optimum. We find that two types of evolutionary pathways are possible depending upon how difficult (costly) it is to cope with the changes of the environment. In one case the population loses the learning ability, and the individuals inherit fixed synapses that are optimal in only one of the environmental states. In the other case a flexible subsystem emerges that allows the individuals to adapt to the changes of the environment. The model helps us to understand how an adaptive subsystem can emerge as the result of the tradeoff between the exploitation of a congenital structure and the exploration of the adaptive capabilities practised by learning.</style></abstract><notes><style face="normal" font="default" size="100%">Dopazo, H Gordon, M B Perazzo, R Risau-Gusman, S Research Support, Non-U.S. Gov’t United States Bulletin of mathematical biology Bull Math Biol. 2003 Jan;65(1):27-56.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">H. Dopazo</style></author><author><style face="normal" font="default" size="100%">Gordon, M. B.</style></author><author><style face="normal" font="default" size="100%">Perazzo, R.</style></author><author><style face="normal" font="default" size="100%">Risau-Gusman, S.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A model for the interaction of learning and evolution</style></title><secondary-title><style face="normal" font="default" size="100%">Bull Math Biol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Algorithms Alleles Animals *Evolution Genotype Humans *Learning *Neural Networks (Computer) Numerical Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Computer-Assisted Phenotype Synapses/genetics</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2001</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11146879</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">1</style></number><volume><style face="normal" font="default" size="100%">63</style></volume><pages><style face="normal" font="default" size="100%">117-34</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We present a simple model in order to discuss the interaction of the genetic and behavioral systems throughout evolution. This considers a set of adaptive perceptrons in which some of their synapses can be updated through a learning process. This framework provides an extension of the well-known Hinton and Nowlan model by blending together some learning capability and other (rigid) genetic effects that contribute to the fitness. We find a halting effect in the evolutionary dynamics, in which the transcription of environmental data into genetic information is hindered by learning, instead of stimulated as is usually understood by the so-called Baldwin effect. The present results are discussed and compared with those reported in the literature. An interpretation is provided of the halting effect.</style></abstract><notes><style face="normal" font="default" size="100%">Dopazo, H Gordon, M B Perazzo, R Risau-Gusman, S Comparative Study Research Support, Non-U.S. Gov’t United States Bulletin of mathematical biology Bull Math Biol. 2001 Jan;63(1):117-34.</style></notes></record></records></xml>