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The evolution of the Armenian presence in mainland France from 1891 to 1990 is described on the basis of an inventory of more than 7000 family names of Armenian origin extracted from the INSEE surname database. Several surname samplings are proposed, and parameters such as the number of different Armenian names, the number of births with these names and their proportions are used as descriptors for each of the 320 French arrondissements and the four successive 25-year periods between 1891 and 1990. Before 1915, Armenian surnames and births with these names are infrequent and almost exclusively located in Paris and the arrondissements of Marseille. From 1915 onwards, subsequent to the genocide in Turkey, the number of births and the diversity of Armenian surnames rose sharply until 1940, before stabilizing thereafter. The diaspora remains essentially centred in Paris, Lyon, and Marseille, with little regional extension around these poles. [ABSTRACT FROM AUTHOR]

Known migration in The Netherlands between the periods 19501969 and 2007, for 4.5 million individuals, was used to estimate the origin of migration by means of a Bayesian method on the basis of surname distributions in these two periods. Results of the method depend on the geographic specificity of the surnames and tend to be positioned between population density and actual probability of migration origin. An optimum in the correlation between estimated and actual percentages of origin of migration, and their differentiation as expressed by the correlation between the estimated and actual entropy across 40 distinguished areas, was found after a few iterations. The optimal correlation was 0.806 (Spearman), which shows that the Bayesian method provides a reasonable proxy of the rank order of a migrant's origin. KEY WORDS: EVALUATION, BAYES, METHODOLOGY, MIGRATION, SURNAMES, NETHERLANDS., A Bayesian method can be used to infer the geographical origin of migrants, based on comparison of changes in surname distribution observed in successive periods of time. Initially published in [...]

Phylogenetic analysis of bacterial mismatch repair (MMR) genes from Escherichia coli reveal high sequence mosaicism reflecting their origin in diverse phylogenetic lineages suggesting a horizontal gene transfer. Data indicate that MMRs facilitate evolutionary adaptation by modulating the mutational and recombination processes.

From its very beginnings, this century has been under the sign of genetics. Indeed, it was in 1900 that the laws established by Mendel in the mid-nineteenth century were rediscovered. [...]

Abstract Background Genetically determined differences in N-acetylation capacity have proved to be important determinants of both the effectiveness of therapeutic response and the development of adverse drug reactions and toxicity during drug treatment. NAT2PRED is a web-server that allows a fast determination of NAT2 acetylation phenotype from genotype data without taking the extra step of reconstructing haplotypes for each individual (publicly available at http://nat2pred.rit.albany.edu). However, the classification accuracy of NAT2PRED needs to be assessed before its application can be advocated at a large scale. Methods The ability of NAT2PRED to classify individuals according to their acetylation status (slow, intermediate and rapid acetylators) was evaluated in a worldwide dataset composed of 56 population samples (8,489 individuals) from four continental regions. Results NAT2PRED correctly identified slow acetylators with a sensitivity above 99% for all populations outside sub-Saharan Africa. Nevertheless, NAT2PRED showed a poor ability to distinguish between intermediate and rapid acetylators, with a classification error rate reaching up to 10% in the non-African samples. Conclusion NAT2PRED is an excellent tool to infer the individual acetylation status from NAT2 genotype data when the main interest is to distinguish slow acetylators from the others. This should facilitate the determination of the individual acetylation status in routine clinical practice and lead to better monitoring of risks associated with cancer and adverse drug reactions.

Abstract Background Previous studies have established a correlation between electrophoretic polymorphism of esterase B, and virulence and phylogeny of Escherichia coli. Strains belonging to the phylogenetic group B2 are more frequently implicated in extraintestinal infections and include esterase B2 variants, whereas phylogenetic groups A, B1 and D contain less virulent strains and include esterase B1 variants. We investigated esterase B as a marker of phylogeny and/or virulence, in a thorough analysis of the esterase B-encoding gene. Results We identified the gene encoding esterase B as the acetyl-esterase gene (aes) using gene disruption. The analysis of aes nucleotide sequences in a panel of 78 reference strains, including the E. coli reference (ECOR) strains, demonstrated that the gene is under purifying selection. The phylogenetic tree reconstructed from aes sequences showed a strong correlation with the species phylogenetic history, based on multi-locus sequence typing using six housekeeping genes. The unambiguous distinction between variants B1 and B2 by electrophoresis was consistent with Aes amino-acid sequence analysis and protein modelling, which showed that substituted amino acids in the two esterase B variants occurred mostly at different sites on the protein surface. Studies in an experimental mouse model of septicaemia using mutant strains did not reveal a direct link between aes and extraintestinal virulence. Moreover, we did not find any genes in the chromosomal region of aes to be associated with virulence. Conclusion Our findings suggest that aes does not play a direct role in the virulence of E. coli extraintestinal infection. However, this gene acts as a powerful marker of phylogeny, illustrating the extensive divergence of B2 phylogenetic group strains from the rest of the species.

Abstract Background The N-acetyltransferase 2 (NAT2) gene plays a crucial role in the metabolism of many drugs and xenobiotics. As it represents a likely target of population-specific selection pressures, we fully sequenced the NAT2 coding region in 97 Mandenka individuals from Senegal, and compared these sequences to extant data on other African populations. The Mandenka data were further included in a worldwide dataset composed of 41 published population samples (6,727 individuals) from four continental regions that were adequately genotyped for all common NAT2 variants so as to provide further insights into the worldwide haplotype diversity and population structure at NAT2. Results The sequencing analysis of the NAT2 gene in the Mandenka sample revealed twelve polymorphic sites in the coding exon (two of which are newly identified mutations, C345T and C638T), defining 16 haplotypes. High diversity and no molecular signal of departure from neutrality were observed in this West African sample. On the basis of the worldwide genotyping survey dataset, we found a strong genetic structure differentiating East Asians from both Europeans and sub-Saharan Africans. This pattern could result from region- or population-specific selective pressures acting at this locus, as further suggested in the HapMap data by extremely high values of FST for a few SNPs positions in the NAT2 coding exon (T341C, C481T and A803G) in comparison to the empirical distribution of FST values accross the whole 400-kb region of the NAT gene family. Conclusion Patterns of sequence variation at NAT2 are consistent with selective neutrality in all sub-Saharan African populations investigated, whereas the high level of population differentiation between Europeans and East Asians inferred from SNPs could suggest population-specific selective pressures acting at this locus, probably caused by differences in diet or exposure to other environmental signals.

Abstract Background Numerous studies have attempted to relate genetic polymorphisms within the N-acetyltransferase 2 gene (NAT2) to interindividual differences in response to drugs or in disease susceptibility. However, genotyping of individuals single-nucleotide polymorphisms (SNPs) alone may not always provide enough information to reach these goals. It is important to link SNPs in terms of haplotypes which carry more information about the genotype-phenotype relationship. Special analytical techniques have been designed to unequivocally determine the allocation of mutations to either DNA strand. However, molecular haplotyping methods are labour-intensive and expensive and do not appear to be good candidates for routine clinical applications. A cheap and relatively straightforward alternative is the use of computational algorithms. The objective of this study was to assess the performance of the computational approach in NAT2 haplotype reconstruction from phase-unknown genotype data, for population samples of various ethnic origin. Results We empirically evaluated the effectiveness of four haplotyping algorithms in predicting haplotype phases at NAT2, by comparing the results with those directly obtained through molecular haplotyping. All computational methods provided remarkably accurate and reliable estimates for NAT2 haplotype frequencies and individual haplotype phases. The Bayesian algorithm implemented in the PHASE program performed the best. Conclusion This investigation provides a solid basis for the confident and rational use of computational methods which appear to be a good alternative to infer haplotype phases in the particular case of the NAT2 gene, where there is near complete linkage disequilibrium between polymorphic markers.

Abstract Background The cladistic approach proposed by Templeton has been presented as promising for the study of the genetic factors involved in common diseases. This approach allows the joint study of multiple markers within a gene by considering haplotypes and grouping them in nested clades. The idea is to search for clades with an excess of cases as compared to the whole sample and to identify the mutations defining these clades as potential candidate disease susceptibility sites. However, the performance of this approach for the study of the genetic factors involved in complex diseases has never been studied. Results In this paper, we propose a new method to perform such a cladistic analysis and we estimate its power through simulations. We show that under models where the susceptibility to the disease is caused by a single genetic variant, the cladistic test is neither really more powerful to detect an association nor really more efficient to localize the susceptibility site than an individual SNP testing. However, when two interacting sites are responsible for the disease, the cladistic analysis greatly improves the probability to find the two susceptibility sites. The impact of the linkage disequilibrium and of the tree characteristics on the efficiency of the cladistic analysis are also discussed. An application on a real data set concerning the CARD15 gene and Crohn disease shows that the method can successfully identify the three variant sites that are involved in the disease susceptibility. Conclusion The use of phylogenies to group haplotypes is especially interesting to pinpoint the sites that are likely to be involved in disease susceptibility among the different markers identified within a gene.

This paper compares and categorizes historical ideas about trees showing relationships among biological entities. The hierarchical structure of a tree is used to test the global consistency of similarities among these ideas; in other words we assess the "treeness" of the tree of historical trees. The collected data are figures and ideas about trees showing relationships among biological entities published or drawn by naturalists from 1555 to 2012. They are coded into a matrix of 235 historical trees and 141 descriptive attributes. From the most parsimonious "tree" of historical trees, treeness is measured by consistency index, retention index and homoplasy excess ratio. This tree is used to create sets or categories of trees, or to study the circulation of ideas. From an unrooted network of historical trees, treeness is measured by the delta-score. This unrooted network is used to measure and visualize treeness. The two approaches show a rather good treeness of the data, with respectively a retention idex of 0.83 and homoplasy excess ratio of 0.74, on one hand, and a delta-score of 0.26 on the other hand. It is interpreted as due to vertical transmission, i.e. an inheritance of shared ideas about biological trees among authors. This tree of trees is then used to test categories previously made. For instance, cladists and gradists are « paraphyletic ». The branches of this tree of trees suggest new categories of tree-thinkers that could have been overlooked by historians or systematists. [ABSTRACT FROM AUTHOR]

A study reports on red cell blood group variation in samples from Algerian populations, geographical patterns of gene frequency distributions used to characterize the genetic structure of Algeria, and tests of the isolation-by-distance model through an examination of genetic diversity in the Maghrib regions. Results indicate the predominance of genetic homogeneity due to the gene flow between regions, and a combination of gene flow, ecology and history best explains the genetic structure of the Algerian population.

Studies of how a mammal's daily energy expenditure scales with its body mass suggest that humans, whether Westerners, agro-pastoralists, or hunter–gatherers, all have much lower energy expenditures for their body mass than other mammals. However, non-human primates also differ from other mammals in several life history traits suggestive of low energy use. Judging by field metabolic rates of free-ranging strepsirhine and haplorhine primates with different lifestyle and body mass, estimated using doubly labeled water, primates have lower energy expenditure than other similar-sized eutherian mammals. Daily energy expenditure in humans fell along the regression line of non-human primates. The results suggest that thrifty energy use could be an ancient strategy of primates. Although physical activity is a major component of energy balance, our results suggest a need to revise the basis for establishing norms of energy expenditure in modern humans. [ABSTRACT FROM AUTHOR]

Background: The arylamine N-acetyltransferases (NATs) are a unique family of enzymes widely distributed in nature that play a crucial role in the detoxification of aromatic amine xenobiotics. Considering the temporal changes in the levels and toxicity of environmentally available chemicals, the metabolic function of NATs is likely to be under adaptive evolution to broaden or change substrate specificity over time, making NATs a promising subject for evolutionary analyses. In this study, we trace the molecular evolutionary history of the NAT gene family during the last ~450 million years of vertebrate evolution and define the likely role of gene duplication, gene conversion and positive selection in the evolutionary dynamics of this family. Results: A phylogenetic analysis of 77 NAT sequences from 38 vertebrate species retrieved from public genomic databases shows that NATs are phylogenetically unstable genes, characterized by frequent gene duplications and losses even among closely related species, and that concerted evolution only played a minor role in the patterns of sequence divergence. Local signals of positive selection are detected in several lineages, probably reflecting response to changes in xenobiotic exposure. We then put a special emphasis on the study of the last ~85 million years of primate NAT evolution by determining the NAT homologous sequences in 13 additional primate species. Our phylogenetic analysis supports the view that the three human NAT genes emerged from a first duplication event in the common ancestor of Simiiformes, yielding NAT1 and an ancestral NAT gene which in turn, duplicated in the common ancestor of Catarrhini, giving rise to NAT2 and the NATP pseudogene. Our analysis suggests a main role of purifying selection in NAT1 protein evolution, whereas NAT2 was predicted to mostly evolve under positive selection to change its amino acid sequence over time. These findings are consistent with a differential role of the two human isoenzymes and support the involvement of NAT1 in endogenous metabolic pathways. Conclusions: This study provides unequivocal evidence that the NAT gene family has evolved under a dynamic process of birth-and-death evolution in vertebrates, consistent with previous observations made in fungi. [ABSTRACT FROM AUTHOR]

Arylamine N-acetyltransferase 2 (NAT2) is involved in human physiological responses to a variety of xenobiotic compounds, including common therapeutic drugs and exogenous chemicals present in the diet and the environment. Many questions remain about the evolutionary mechanisms that have led to the high prevalence of slow acetylators in the human species. Evidence from recent surveys of NAT2 gene variation suggests that NAT2 slow-causing variants might have become targets of positive selection as a consequence of the shift in modes of subsistence and lifestyle in human populations in the last 10,000 years. We aimed to test more extensively the hypothesis that slow acetylation prevalence in humans is related to the subsistence strategy adopted by the past populations. To this end, published frequency data on the most relevant genetic variants of NAT2 were collected from 128 population samples (14,679 individuals) representing different subsistence modes and dietary habits, allowing a thorough analysis at both a worldwide and continent scale. A significantly higher prevalence of the slow acetylation phenotype was observed in populations practicing farming (45.4%) and herding (48.2%) as compared to populations mostly relying on hunting and gathering (22.4%) (P = 0.0007). This was closely mirrored by the frequency of the slow 590A variant that was found to occur at a three-fold higher frequency in food producers (25%) as compared to hunter-gatherers (8%). These findings are consistent with the hypothesis that the Neolithic transition to subsistence economies based on agricultural and pastoral resources modified the selective regime affecting the NAT2 acetylation pathway. Furthermore, the vast amount of data collected enabled us to provide a comprehensive and up-todate description of NAT2 worldwide genetic diversity, thus building up a useful resource of frequency data for further studies interested in epidemiological or anthropological research questions involving NAT2. [ABSTRACT FROM AUTHOR]

Horizontal gene transfer is a key step in the evolution of bacterial pathogens. Besides phages and plasmids, pathogenicity islands (PAIs) are subjected to horizontal transfer. The transfer mechanisms of PAIs within a certain bacterial species or between different species are still not well understood. This study is focused on the High-Pathogenicity Island (HPI), which is a PAI widely spread among extraintestinal pathogenic Escherichia coli and serves as a model for horizontal transfer of PAIs in general. We applied a phylogenetic approach using multilocus sequence typing on HPI-positive and -negative natural E. coli isolates representative of the species diversity to infer the mechanism of horizontal HPI transfer within the E. coli species. In each strain, the partial nucleotide sequences of 6 HPI-encoded genes and 6 housekeeping genes of the genomic backbone, as well as DNA fragments immediately upstream and downstream of the HPI were compared. This revealed that the HPI is not solely vertically transmitted, but that recombination of large DNA fragments beyond the HPI plays a major role in the spread of the HPI within E. coli species. In support of the results of the phylogenetic analyses, we experimentally demonstrated that HPI can be transferred between different E. coli strains by F-plasmid mediated mobilization. Sequencing of the chromosomal DNA regions immediately upstream and downstream of the HPI in the recipient strain indicated that the HPI was transferred and integrated together with HPI-flanking DNA regions of the donor strain. The results of this study demonstrate for the first time that conjugative transfer and homologous DNA recombination play a major role in horizontal transfer of a pathogenicity island within the species E. coli. [ABSTRACT FROM AUTHOR]

The article focuses on a study of patronymic lineages in the rural society of Savoie, France, in order to define their frequency, permanence and mobility, from the early 18th century to the middle of the 20th century. Geographic mobility is analyzed in relation to land property. The region of Savoie is examined as a departure place and the study is based on the baptismal and birth certificates issued during this period. The authors' purpose is to show if the last names of the main land owners of the beginning of the 18th century evolved in a same or different way than other names.

Background: The N-acetyltransferase 2 (NAT2) gene plays a crucial role in the metabolism of many drugs and xenobiotics. As it represents a likely target of population-specific selection pressures, we fully sequenced the NAT2 coding region in 97 Mandenka individuals from Senegal, and compared these sequences to extant data on other African populations. The Mandenka data were further included in a worldwide dataset composed of 41 published population samples (6,727 individuals) from four continental regions that were adequately genotyped for all common NAT2 variants so as to provide further insights into the worldwide haplotype diversity and population structure at NAT2. Results: The sequencing analysis of the NAT2 gene in the Mandenka sample revealed twelve polymorphic sites in the coding exon (two of which are newly identified mutations, C345T and C638T), defining 16 haplotypes. High diversity and no molecular signal of departure from neutrality were observed in this West African sample. On the basis of the worldwide genotyping survey dataset, we found a strong genetic structure differentiating East Asians from both Europeans and sub-Saharan Africans. This pattern could result from region- or population-specific selective pressures acting at this locus, as further suggested in the HapMap data by extremely high values of FST for a few SNPs positions in the NAT2 coding exon (T341C, C481T and A803G) in comparison to the empirical distribution of FST values accross the whole 400-kb region of the NAT gene family. Conclusion: Patterns of sequence variation at NAT2 are consistent with selective neutrality in all sub-Saharan African populations investigated, whereas the high level of population differentiation between Europeans and East Asians inferred from SNPs could suggest population-specific selective pressures acting at this locus, probably caused by differences in diet or exposure to other environmental signals. [ABSTRACT FROM AUTHOR]

Haplotypes are now widely used in association studies between markers and disease susceptibility locus. However, when a large number of markers are considered, the number of possible haplotypes increases leading to two problems: an increased number of degrees of freedom that may result in a lack of power and the existence of rare haplotypes that may be difficult to take into account in the statistical analysis. In a recent paper, Durrant et al proposed a method, CLADHC, to group haplotypes based on distance matrices and showed that this could considerably increase the power of the association test as compared to either single-locus analysis or haplotype analysis without prior grouping. Although the authors considered different one-disease-locus susceptibility models in their simulations, they did not study the impact of the linkage disequilibrium (LD) pattern and of the susceptibility allele frequency on their conclusions. Here, we show, using haplotype data from five regions of the genome of different lengths and with different LD patterns, that, when a single disease susceptibility locus is simulated, the prior grouping of haplotypes based on the algorithm of Durrant et al does not increase the power of association testing except in very particular situations of LD patterns and allele frequencies.European Journal of Human Genetics (2006) 14, 202–206. doi:10.1038/sj.ejhg.5201501; published online 23 November 2005 [ABSTRACT FROM AUTHOR]

Evolutionary biology and historical linguistics both aim at inferring historical relationships between objects: their genetic affiliation and/or their convergence or mutual borrowing of traits. The similarity of the methodologies developed in each field – cladistics in biology and comparatism in linguistics – is striking. However, the comparative method is specifically applied to lexical data and so fails to analyze language relationships directly through another material, phonological data for instance. The cladistic approach appears then as a good alternative to overcome this particular limitation, since it is not specific to a particular type of data. This study focuses on vowel systems to reconstruct evolutionary linguistic trees. It is based on typologies of the vowel space structure (Vallée, 1994). The phonological data used are those of the UCLA Phonological Segment Inventory Database (UPSID) developed by Maddieson (1984). We suggest a cladistics coding based on the Dispersion-Focalization Theory (Schwartz et al., 1997) and in agreement with computer models for vowel systems emergence by self-organization (De Boer, 2000). The trees inferred by this procedure are compared to those obtained with the classical comparative method of historical linguistics. Factors possibly responsible for the topologies of these trees are investigated and the efficiency of the suggested coding is discussed. [ABSTRACT FROM AUTHOR]

To explore the role of transcriptome polymorphism in adaptation of organisms to their environment, we evaluated this parameter for the Escherichia coli/Shigella bacterial species, which is composed of well-characterized phylogenetic groups that exhibit characteristic life styles ranging from commensalism to intracellular pathogenicity. Both the genomic content and the transcriptome of 10 strains representative of the major E. coli/Shigella phylogenetic groups were evaluated using macroarrays displaying the 4290 K12-MG1655 open reading frames (ORFs). Although Shigella and enteroinvasive E. coli (EIEC) are not monophyletic, phylogenetic analysis of the binary coded (presence/absence) gene content data showed that these organisms group together due to similar patterns of undetectable K12-MG1655 genes. The variation in transcript abundance was then analyzed using a core genome of 2880 genes present in all strains, after adjusting RNA hybridization signals for DNA hybridization signals. Nonrandom changes in gene expression during the evolution of the E. coli/Shigella species were evidenced. Phylogenetic analysis of transcriptome data again showed that Shigella and EIEC strains group together in terms of gene expression, and this convergence involved groups of genes displaying biologically coherent patterns of functional divergence. Unlike the other E. coli strains evaluated, Shigella and EIEC are intracellular pathogens, and therefore face similar selective pressures. Thus, within the E. coli/Shigella species, strains exhibiting a particular life style have converged toward a specific gene expression pattern in a subset of genes common to the species, revealing the role of selection in shaping transcriptome polymorphism. [ABSTRACT FROM AUTHOR]

Background: The cladistic approach proposed by Templeton has been presented as promising for the study of the genetic factors involved in common diseases. This approach allows the joint study of multiple markers within a gene by considering haplotypes and grouping them in nested clades. The idea is to search for clades with an excess of cases as compared to the whole sample and to identify the mutations defining these clades as potential candidate disease susceptibility sites. However, the performance of this approach for the study of the genetic factors involved in complex diseases has never been studied. Results: In this paper, we propose a new method to perform such a cladistic analysis and we estimate its power through simulations. We show that under models where the susceptibility to the disease is caused by a single genetic variant, the cladistic test is neither really more powerful to detect an association nor really more efficient to localize the susceptibility site than an individual SNP testing. However, when two interacting sites are responsible for the disease, the cladistic analysis greatly improves the probability to find the two susceptibility sites. The impact of the linkage disequilibrium and of the tree characteristics on the efficiency of the cladistic analysis are also discussed. An application on a real data set concerning the CARD15 gene and Crohn disease shows that the method can successfully identify the three variant sites that are involved in the disease susceptibility. Conclusion: The use of phylogenies to group haplotypes is especially interesting to pinpoint the sites that are likely to be involved in disease susceptibility among the different markers identified within a gene. [ABSTRACT FROM AUTHOR]

The first statistical analysis of the French National Registry of volunteer bone marrow donors estimated the probabilities of haplotype frequencies separately for each of the 20 administrative regions of France. Here we propose to use donors' surnames to increase the accuracy of location of the donor's geographical origin. This approach allows us to estimate haplotype frequencies for administrative entities (90 departments) smaller than regions and to correct for bias resulting from recent mobility. We analysed 30?777 donors typed for HLA-A,B and 17?745 donors typed for HLA-A,B,DR,DQ. By using the donors' surnames, we identified common and rare haplotypes (those found in only one department) and estimated the degree of HLA polymorphism at the department level. We also identified departments with a distinctive genetic structure (for example, Paris, Corsica, Pyrenees and Meurthe-et- Moselle). By providing a more accurate geographical distribution of HLA polymorphisms in France, this study will enable us to optimise policies for recruiting bone marrow donors and to improve the fit between the donor file and patients' needs.European Journal of Human Genetics (2003) 11, 794-801. doi:10.1038/sj.ejhg.5201038 [ABSTRACT FROM AUTHOR]

This paper examines the efficiency of the incongruence length difference test (ILD) proposed by Farris et al. (1994)<$REFLINK> for assessing the incongruence between sets of characters. DNA sequences were simulated under various evolutionary conditions: (1) following symmetric or asymmetric trees, (2) with various mutation rates, (3) with constant or variable evolutionary rates along the branches, and (4) with different among-site substitution rates. We first compared two sets of sequences generated along the same tree and under the same evolutionary conditions. The probability of a Type-I error (wrongly rejecting the true hypothesis of congruence) was substantially below the standard 5% level of significance given by the ILD test; this finding indicates that the choice of the 5% level is rather conservative in this case. We then compared two data sets, still generated along the same tree, but under different evolutionary conditions (constant vs. variable evolutionary rate, homogeneity vs. heterogeneity rate of substitution). Under these conditions, the probability of rejecting the true hypothesis of congruence was greater than the 5% given by the ILD test and increased with the number of sites and the degree to which the tree was asymmetric. Finally, the comparison of the two data sets, simulated under contrasting tree structures (symmetric vs. asymmetric) but under the same evolutionary conditions, led us to reject the hypothesis of congruence, albeit weakly, particularly when the number of informative sites was low and among-site substitution rate heterogeneous. We conclude that the ILD test has only limited power to detect incongruence caused by differences in the evolutionary conditions or in the tree topology, except when numerous characters are present and the substitution rate is homogeneous from site to site. [ABSTRACT FROM PUBLISHER]

The remarkable conservation of protein structure, compared with that of sequences, suggests that in the course of evolution, residue substitutions which tend to destabilize a particular structure must be compensated by other substitutions that confer greater stability on that structure. Several approaches have been designed to detect correlated changes in a set of homologous sequences. However, most of them do not take into account the phylogeny of the sequences, and it has been shown that their detection power is weak. It remains unclear whether coevolution could be a general process at the level of amino acids of proteins. In the present study, we analyze the phylogenetic reconstruction of 15 sets of homologous proteins to assess, under different conditions, whether a significant amount of coevolving sites can be detected. Two criteria are used to detect significantly cosubstituting sites. One criterion corresponds to that of Shindyalov, Kolchanov, and Sander. The second one is based on intensive simulations of evolution of protein sequences along a phylogeny to estimate the significance of the number of observed cosubstitutions for pairs of sites. Our results show an important sensitivity of the detection of cosubstituting sites to the model used for the phylogenetic reconstruction. Not considering the uncertainty associated with the reconstructed data might lead to detecting numerous false-positive pairs of sites. Finally, significant amounts of coevolving pairs could be found only when substitutions affecting the physicochemical properties of the amino acids were considered. Such results suggest evidence of a cosubstitution mechanism in protein evolution. However, the identification of nonambiguous coevolving sites is still unresolved. [ABSTRACT FROM PUBLISHER]

The article presents an obituary for anthropologist Hélène Pagezy is presented.