We propose a general theory of clonal reproduction for parasitic protozoa, which has important medical and biological consequences. Many parasitic protozoa have been assumed to reproduce sexually, because of diploidy and occasional sexuality in the laboratory. However, a population genetic analysis of extensive data on biochemical polymorphisms indicates that the two fundamental consequences of sexual reproduction (i.e., segregation and recombination) are apparently rare or absent in natural populations of the parasitic protozoa. Moreover, the clones recorded appear to be stable over large geographical areas and long periods of time.
Simple phylogenetic tests were applied to a large data set of nucleotide sequences from two nuclear genes and a region of the mitochondrial genome of Trypanosoma cruzi, the agent of Chagas' disease. Incongruent gene genealogies manifest genetic exchange among distantly related lineages of T. cruzi. Two widely distributed isoenzyme types of T. cruzi are hybrids, their genetic composition being the likely result of genetic exchange between two distantly related lineages. The data show that the reference strain for the T. cruzi genome project (CL Brener) is a hybrid. Well-supported gene genealogies show that mitochondrial and nuclear gene sequences from T. cruzi cluster, respectively, in three or four distinct clades that do not fully correspond to the two previously defined major lineages of T. cruzi. There is clear genetic differentiation among the major groups of sequences, but genetic diversity within each major group is low. We estimate that the major extant lineages of T. cruzi have diverged during the Miocene or early Pliocene (3-16 million years ago).
Leishmaniasis is a geographically widespread severe disease, with an increasing incidence of two million cases per year and 350 million people from 88 countries at risk. The causative agents are species of Leishmania, a protozoan flagellate. Visceral leishmaniasis, the most severe form of the disease, lethal if untreated, is caused by species of the Leishmania donovani complex. These species are morphologically indistinguishable but have been identified by molecular methods, predominantly multilocus enzyme electrophoresis. We have conducted a multifactorial genetic analysis that includes DNA sequences of protein-coding genes as well as noncoding segments, microsatellites, restriction-fragment length polymorphisms, and randomly amplified polymorphic DNAs, for a total of Ϸ18,000 characters for each of 25 geographically representative strains. Genotype is strongly correlated with geographical (continental) origin, but not with current taxonomy or clinical outcome. We propose a new taxonomy, in which Leishmania infantum and L. donovani are the only recognized species of the L. donovani complex, and we present an evolutionary hypothesis for the origin and dispersal of the species. The genus Leishmania may have originated in South America, but diversified after migration into Asia. L. donovani and L. infantum diverged Ϸ1 Mya, with further divergence of infraspecific genetic groups between 0.4 and 0.8 Mya. The prevailing mode of reproduction is clonal, but there is evidence of genetic exchange between strains, particularly in Africa.Leishmania infantum ͉ Leishmaniasis ͉ parasitic protozoa ͉ phylogeny ͉ population genetics
Pseudogenes have been defined as nonfunctional sequences of genomic DNA originally derived from functional genes. It is therefore assumed that all pseudogene mutations are selectively neutral and have equal probability to become fixed in the population. Rather, pseudogenes that have been suitably investigated often exhibit functional roles, such as gene expression, gene regulation, generation of genetic (antibody, antigenic, and other) diversity. Pseudogenes are involved in gene conversion or recombination with functional genes. Pseudogenes exhibit evolutionary conservation of gene sequence, reduced nucleotide variability, excess synonymous over nonsynonymous nucleotide polymorphism, and other features that are expected in genes or DNA sequences that have functional roles. We first review the Drosophila literature and then extend the discussion to the various functional features identified in the pseudogenes of other organisms. A pseudogene that has arisen by duplication or retroposition may, at first, not be subject to natural selection if the source gene remains functional. Mutant alleles that incorporate new functions may, nevertheless, be favored by natural selection and will have enhanced probability of becoming fixed in the population. We agree with the proposal that pseudogenes be considered as potogenes, i.e., DNA sequences with a potentiality for becoming new genes.
Chromosome rearrangements (such as inversions, fusions, and fissions) may play significant roles in the speciation between parapatric (contiguous) or partly sympatric (geographically overlapping) populations. According to the ''hybrid-dysfunction'' model, speciation occurs because hybrids with heterozygous chromosome rearrangements produce dysfunctional gametes and thus have low reproductive fitness. Natural selection will, therefore, promote mutations that reduce the probability of intercrossing between populations carrying different rearrangements and thus promote their reproductive isolation. This model encounters a disabling difficulty: namely, how to account for the spread in a population of a chromosome rearrangement after it first arises as a mutation in a single individual. The ''suppressed-recombination'' model of speciation points out that chromosome rearrangements act as a genetic filter between populations. Mutations associated with the rearranged chromosomes cannot flow from one to another population, whereas genetic exchange will freely occur between colinear chromosomes. Mutations adaptive to local conditions will, therefore, accumulate differentially in the protected chromosome regions so that parapatric or partially sympatric populations will genetically differentiate, eventually evolving into different species. The speciation model of suppressed recombination has recently been tested by gene and DNA sequence comparisons between humans and chimpanzees, between Drosophila species, and between species related to Anopheles gambiae, the vector of malignant malaria in Africa.genetic divergence ͉ chromosomal rearrangements ͉ human speciation ͉ Drosophila speciation ͉ Anopheles speciation
Very precise data on the dynamics of a competitive system of two species of Drosophila have been obtained. By a curvilinear regression approach, analytical models of competition have been fitted. By statistical and biological criteria of simplicity, reality, generality, and accuracy, the best of these models has been chosen. This model represents an extension of the Lotka-Volterra model of competition; it adds a fourth parameter that controls the degree of nonlinearity in intraspecific growth regulation. It represents a similar extension of the logistic model of population growth.Population ecology is at a Keplerian stage of development. Much of the present theory is based on idealized linear interactions (which are valid first-order approximations of more general interaction), somewhat as preKeplerian astronomy was based on idealized circular motions (which approximate ellipses). For interspecies competition, the present need is to obtain precise data that disclose the global dynamics of real competition systems, that is, the rates of population growth at any combination of population densities. Simple but general analytical models may then be sought to represent such systems. Only if this attempt achieves success should the Newton-like effort of producing a law for the repulsive "forces" of intraspecies and interspecies competition be undertaken, though the obviously pluralistic nature of biological mechanisms could make this effort profitless.In the 1920s, the linear model of competition was proposed independently by Lotka (1) and Volterra (2); it isN1 is the population density of the ith species; ri is the exponential rate of growth of the ith species when both the ith and jth population densities are low; Ki is the carrying capacity of the ith species in the absence of its competitor, the jth species; and aij is the linear reduction (in terms of K1) of the ith species' rate of growth by its competitor, the jth species. This model and other analytical models of competition ignore time lags, thresholds, and stochastic effects; but this is necessary if the mathematics are to be kept tractable and should lead to no difficulties if not forgotten.Volterra, in the absence of any competition data whatsoever, felt that the above model could be globally valid. Lotka indicated that the correct competition model was likely to be nonlinear; but by making a Taylor's series expansion about the point of equilibrium and dropping the higher order terms, he was able to arrive at the same model of competition as an approximation valid in a "neighborhood" of the equilibrium point. Levins (3) and MacArthur (4) have added to the importance of this linear model by basing their niche theory on it, and they have provided independent formulas to calculate the K and a parameters. Vandermeer (5) has used the as of the Lotka-Volterra competition equations to determine the "community matrix" of a competition ecosystem. But such epitheory does nothing to validate the linear model.In 1934, Gause (9) determined the dynamics of yeast...
We have studied genetic variation at 27 loci in 42 samples from natural populations of a neotropical species, Drosophila equinoxialis, using standard techniques of starch-gel electrophoresis to detect allelic variation in genes coding for enzymes. There is considerable genetic variability in D. equinoxialis. We have found allelic variation in each of the 27 loci, although not in every population. On the average, 71 % of the loci are polymorphic -that is, the most common allele has a frequency no greater than 0-95 -in a given population. An individual is heterozygous on the average at 21-8% of its loci.The amount of genetic variation fluctuates widely from locus to locus. At the Mdh-2 locus about 1 % of the individuals are heterozygotes; at the other extreme more than 56 % of the individuals are heterozygous at the Est-3. At any given locus the configuration of allelic frequencies is strikingly similar from locality to locality. At each and every locus the same allele is generally the most common throughout the distribution of the species. Yet differences in gene frequencies occur between localities. The pattern of genetic variation is incompatible with the hypothesis that the variation is adaptively neutral. Genetic variation in D. equinoxialis is maintained by balancing natural selection.The amount and pattern of genetic variation is similar in D. equinoxialis and its sibling species, D. willistoni. Yet the two species are genetically very different. Different sets of alleles occur at nearly 40 % of the loci.
We propose that clonal evolution in micropathogens be defined as restrained recombination on an evolutionary scale, with genetic exchange scarce enough to not break the prevalent pattern of clonal population structure, a definition already widely used for all kinds of pathogens, although not clearly formulated by many scientists and rejected by others. The two main manifestations of clonal evolution are strong linkage disequilibrium (LD) and widespread genetic clustering ("near-clading"). We hypothesize that this pattern is not mainly due to natural selection, but originates chiefly from in-built genetic properties of pathogens, which could be ancestral and could function as alternative allelic systems to recombination genes ("clonality/sexuality machinery") to escape recombinational load. The clonal framework of species of pathogens should be ascertained before any analysis of biomedical phenotypes (phylogenetic character mapping). In our opinion, this model provides a conceptual framework for the population genetics of any micropathogen. molecular epidemiology | infectious disease | selfing I n the last two decades, the population genetics and evolution of pathogens have received much deserved attention. Impressive progress has been achieved through the development of wholegenome sequencing (WGS), bioinformatics, and other powerful molecular technologies. This progress has made it possible to explore, in depth, the central question of genetic exchange in pathogens, the issue of clonality vs. sexuality, which emerged in the 1980s, both in parasitic protozoa (the "clonal theory of parasitic protozoa") (1-3) and in bacteria (4-6). We seek to update the terms and interpretations of the controversy. Compartmentalization among researchers working on different pathogens has resulted in misinterpretations, semantic confusion, and different methods of analysis that often reflect idiosyncratic practices among different scientific communities, rather than distinctive evolutionary features.We analyze population genetic data for bacteria (48 species) (4-82), fungi and yeasts (9 species) (83-93), parasitic protozoa (21 species) (1-3, 94-162), and viruses (11 species or categories) (163-188) (Table S1). There are striking evolutionary similarities among different kinds of pathogens, which are obscured by compartmentalization. We propose ways of consolidating the different approaches and of exploring whether similar evolutionary strategies represent ancestral characters or convergent evolution. We summarize the implications for applied research (including taxonomy, molecular epidemiology, medical characters, and experimental evolution). Definition of Clonal Evolution: Restricted Genetic RecombinationIn our early papers dealing with the clonality/sexuality issue in parasitic protozoa and fungi (1-3), we advanced an unambiguous definition of clonality/clonal evolution. It did not refer to the cytological mechanism of reproduction, but rather to the population structure that results from an absence or restriction of genetic reco...
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