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PubMed2005

The coevolution of insect muscle TpnT and TpnI gene isoforms.

In bilaterians, the main regulator of muscle contraction is the troponin (Tpn) complex, comprising three closely interacting subunits (C, T, and I). To understand how evolutionary forces drive molecular change in protein complexes, we have compared the gene structures and expression patterns of Tpn genes in insects. In this class, while TpnC is encoded by multiple genes, TpnT and TpnI are encoded by single genes. Their isoform expression pattern is highly conserved within the Drosophilidae, and single orthologous genes were identified in the sequenced genomes of Drosophila pseudoobscura, Anopheles gambiae, and Apis mellifera. Apis expression patterns also support the equivalence of their exon organization throughout holometabolous insects. All TpnT genes include a previously unidentified indirect flight muscle (IFM)-specific exon (10A) that has evolved an expression pattern similar to that of exon 9 in TpnI. Thus, expression patterns, sequence evolution trends, and structural data indicate that Tpn genes and their isoforms have coevolved, building species- and muscle-specific troponin complexes. Furthermore, a clear case can be made for independent evolution of the IFM-specific isoforms containing alanine/proline-rich sequences. Dipteran genomes contain one tropomyosin gene that encodes one or two high-molecular weight isoforms (TmH) incorporating APPAEGA-rich sequences, specifically expressed in IFM. Corresponding exons do not exist in the Apis tropomyosin gene, but equivalent sequences occur in a high-molecular weight Apis IFM-specific TpnI isoform (TnH). Overall, our approach to comparatively analyze supramolecular complexes reveals coevolutionary trends not only in gene families but in isoforms generated by alternative splicing.

Amino Acid Sequence↗
PubMed2002

Cleavage of hemoglobin by hookworm cathepsin D aspartic proteases and its potential contribution to host specificity.

Hookworms routinely reach the gut of nonpermissive hosts but fail to successfully feed, develop, and reproduce. To investigate the effects of host-parasite coevolution on the ability of hookworms to feed in nonpermissive hosts, we cloned and expressed aspartic proteases from canine and human hookworms. We show here that a cathepsin D-like protease from the canine hookworm Ancylosotoma caninum (Ac-APR-1) and the orthologous protease from the human hookworm Necator americanus (Na-APR-1) are expressed in the gut and probably exert their proteolytic activity extracellularly. Both proteases were detected immunologically and enzymatically in somatic extracts of adult worms. The two proteases were expressed in baculovirus, and both cleaved human and dog hemoglobin (Hb) in vitro. Each protease digested Hb from its permissive host between twofold (whole molecule) and sixfold (synthetic peptides) more efficiently than Hb from the nonpermissive host, despite the two proteases' having identical residues lining their active site clefts. Furthermore, both proteases cleaved Hb at numerous distinct sites and showed different substrate preferences. The findings suggest that the paradigm of matching the molecular structure of the food source within a host to the molecular structure of the catabolic proteases of the parasite is an important contributing factor for host-parasite compatibility and host species range.

Ancylostomatoidea↗
PubMed2007

Differential impact of simultaneous migration on coevolving hosts and parasites.

BACKGROUND: The dynamics of antagonistic host-parasite coevolution are believed to be crucially dependent on the rate of migration between populations. We addressed how the rate of simultaneous migration of host and parasite affected resistance and infectivity evolution of coevolving meta-populations of the bacterium Pseudomonas fluorescens and a viral parasite (bacteriophage). The increase in genetic variation resulting from small amounts of migration is expected to increase rates of adaptation of both host and parasite. However, previous studies suggest phages should benefit more from migration than bacteria; because in the absence of migration, phages are more genetically limited and have a lower evolutionary potential compared to the bacteria. RESULTS: The results supported the hypothesis: migration increased the resistance of bacteria to their local (sympatric) hosts. Moreover, migration benefited phages more than hosts with respect to 'global' (measured with respect to the whole range of migration regimes) patterns of resistance and infectivity, because of the differential evolutionary responses of bacteria and phage to different migration regimes. Specifically, we found bacterial global resistance peaked at intermediate rates of migration, whereas phage global infectivity plateaued when migration rates were greater than zero. CONCLUSION: These results suggest that simultaneous migration of hosts and parasites can dramatically affect the interaction of host and parasite. More specifically, the organism with the lower evolutionary potential may gain the greater evolutionary advantage from migration.

Biological Evolution↗
PubMed1990

Examination of protein sequence homologies. VII. The complementary molecular coevolution of ribosomal proteins equivalent to Escherichia coli L7/L12 and L10.

Recently reported P1, P2 and metabacteria line sequences of transposition-type 'A' proteins, equivalent to Escherichia coli ribosomal protein L7/L12, were examined using a correlation method which evaluates the sequence similarity quantitatively. As the sequences could be aligned along the alignment previously constructed for 25 various 'A' proteins, the inclusive alignment further supports the previous claims concerning the rule of "preservation units" and the transpositional regeneration for metabacterial and eukaryotic 'A' proteins. Yeasts contain multispecies of P1 and P2 line genes and their P1 line sequences show low correlation coefficient values compared to other P1 line sequences, indicating a great evolutionary distance between lower and higher eukaryotes. Five sequences of protein P0 from metabacteria, yeast, and human, of which about 20 residues at the C termini are homologous with those of their own transposition-type 'A' proteins, were similarly examined. The N-terminal three-quarters of the sequences align naturally and the first two-thirds of the alignment could involve the E. coli L10 (EL10) sequence. An alignment of the remaining sequences at the C termini was established, relying on the well-matching sequence similarities between the metabacteria 'A' protein and their P0 protein sequences. Finally, the C-terminal halves of P0 protein sequences corresponded with almost overall sequences of the transposition-type 'A' proteins. The gene fusion of a protein might have resulted in the formation of the P0 proteins. A coupling of this gene fusion and the transposition of prototype 'A' proteins may have given rise to the complementary molecular transformations required for the development toward higher organism cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1986

A stochastic model of gene-culture coevolution suggested by the "culture historical hypothesis" for the evolution of adult lactose absorption in humans.

A stochastic model of gene-culture coevolution, suggested by the "culture historical hypothesis" of Simoons and McCracken, is presented. According to this hypothesis, adult lactose absorption, believed to be an autosomal dominant trait, attained a high frequency in some human populations due to the positive selection pressure induced by culturally determined milk use in those populations. Two-dimensional Kolmogorov backward equations with appropriate boundary conditions are derived for the ultimate fixation probability of milk users, of the gene for adult lactose absorption, and of both jointly, and for the average time until fixation of the gene. These boundary value problems are solved numerically by the Gauss-Seidel method. I define a theoretical measure of the correlation between gene and culture in terms of the three ultimate fixation probabilities. Monte Carlo simulations are conducted to check and extend the numerical results and also to obtain the first arrival time at gene frequency 0.70, which is approximately the highest observed frequency in any population. Two results that pertain to the culture historical hypothesis are obtained. First, the incomplete correlation observed between adult lactose absorption and milk use does not necessarily constitute evidence against the hypothesis. Second, for the postulated genetic change to have occurred within the 6000-year period since the advent of dairying, either the effective population size was of the order of 100, or, if it was of larger order, the selection coefficient probably had to exceed 5%.

Animals↗
PubMed2005

Sex-ratio conflict between queens and workers in eusocial Hymenoptera: mechanisms, costs, and the evolution of split colony sex ratios.

Because workers in the eusocial Hymenoptera are more closely related to sisters than to brothers, theory predicts that natural selection should act on them to bias (change) sex allocation to favor reproductive females over males. However, selection should also act on queens to prevent worker bias. We use a simulation approach to analyze the coevolution of this conflict in colonies with single, once-mated queens. We assume that queens bias the primary (egg) sex ratio and workers bias the secondary (adult) sex ratio, both at some cost to colony productivity. Workers can bias either by eliminating males or by directly increasing female caste determination. Although variation among colonies in kin structure is absent, simulations often result in bimodal (split) colony sex ratios. This occurs because of the evolution of two alternative queen or two alternative worker biasing strategies, one that biases strongly and another that does not bias at all. Alternative strategies evolve because the mechanisms of biasing result in accelerating benefits per unit cost with increasing bias, resulting in greater fitness for strategies that bias more and bias less than the population equilibrium. Strategies biasing more gain from increased biasing efficiency whereas strategies biasing less gain from decreased biasing cost. Our study predicts that whether queens or workers evolve alternative strategies depends upon the mechanisms that workers use to bias the sex ratio, the relative cost of queen and worker biasing, and the rates at which queen and worker strategies evolve. Our study also predicts that population and colony level sex allocation, as well as colony productivity, will differ diagnostically according to whether queens or workers evolve alternative biasing strategies and according to what mechanism workers use to bias sex allocation.

Animals↗
PubMed2006

One day is enough: rapid and specific host-parasite interactions in a stickleback-trematode system.

Red Queen models of host-parasite coevolution are based on genotype by genotype host-parasite interactions. Such interactions require a genotype specific host defence and, simultaneously, a genotype specific parasite infectivity. Specificity is defined here as defence or infection ability successful against only a subset of genotypes of the same species. A specific defence depends on detectable genotypic variation on the parasite side and on a host defence mechanism that differentiates between parasite genotypes. In vertebrates, the MHC-based adaptive immune system can provide such a defence mechanism, but it needs at least several days to get fully mounted. In contrast, the innate immune system is immediately ready. The trematode parasite species used here reaches the immunologically protected eye lens of its three-spined stickleback (Gasterosteus aculeatus) host within 24 h. Thus, it disappears too fast for the fully mounted MHC-based adaptive immune system. In a complete cross-infection experiment using five fish-families and five parasite-clones, we found for the first time fish-family by parasite-clone interactions in vertebrates, although the parasite was only exposed to the immune system for maximally one day. Such interactions require a fast genotype specific defence, suggesting the importance of other defence mechanisms than the too slow, fully mounted adaptive immune system in vertebrates.

Adaptation, Physiological↗
PubMed2005

Reduced genetic variation occurs among genes of the highly clonal plant pathogen Xanthomonas axonopodis pv. vesicatoria, including the effector gene avrBs2.

The bacterial plant pathogen Xanthomonas axonopodis pv. vesicatoria, also known as Xanthomonas campestris pv. vesicatoria group A, is the causal agent of bacterial spot in pepper and tomato. In order to test different models that may explain the coevolution of avrBs2 with its host plants, we sequenced avrBs2 and six chromosomal loci (total of 5.5 kb per strain) from a global sample of 55 X. axonopodis pv. vesicatoria strains collected from diseased peppers. We found an extreme lack of genetic variation among all X. axonopodis pv. vesicatoria genomic loci (average nucleotide diversity, pi = 9.1 x 10(-5)), including avrBs2. This lack of diversity is consistent with X. axonopodis pv. vesicatoria having undergone a recent population bottleneck and/or selective sweep followed by population expansion. Coalescent analysis determined that approximately 1.4 x 10(4) to 7.16 x 10(4) bacterial generations have passed since the most recent common ancestor (MRCA) of the current X. axonopodis pv. vesicatoria population. Assuming a range of 50 to 500 bacterial generations per year, only 28 to 1,432 years have passed since the MRCA. This time frame coincides with human intervention with the pathogen's host plants, from domestication to modern agricultural practices. Examination of 19 mutated (loss-of-function) avrBs2 alleles detected nine classes of mutations. All mutations affected protein coding, while no synonymous changes were found. The nature of at least one of the avrBs2 mutations suggests that it may be possible to observe one stage of an evolutionary arms race as X. axonopodis pv. vesicatoria responds to selection pressure to alter avrBs2 to escape host plant resistance.

Alleles↗
PubMed1993

Evolution of human papillomavirus type 18: an ancient phylogenetic root in Africa and intratype diversity reflect coevolution with human ethnic groups.

Papillomaviruses are an ideal model system for the study of DNA virus evolution. On several levels, phylogenetic trees of papillomaviruses reflect the relationship of their hosts. Papillomaviruses isolated from remotely related vertebrates form major branches. One branch of human papillomaviruses (HPVs) includes an ape and two monkey papillomaviruses, possibly because the diversification of the viruses predated the separation of the infected-primate taxa. This hypothesis predicts that the root of the evolution of some if not all HPV types should point to Africa, since humans evolved from nonhuman primates in this continent. We tested this hypothesis and compared the genomic sequences of HPV type 18 (HPV-18) isolates from four continents. Diversity within HPV-18 correlates with patterns of the evolution and spread of Homo sapiens: HPV-18 variants, just like HPV-16 variants, are specific for the major human races, with maximal diversity in Africa. Outgroup rooting of the HPV-18 tree against HPV-45, which is closely related to HPV-18, identifies African HPV-18 variants at the root of the tree. The identification of an African HPV-45 isolate further reduces the evolutionary distance between HPV-18 and HPV-45. HPV-18 variants from Amazonian Indians are the closest relatives to those from Japanese and Chinese patients and suggest that a single point mutation in the phylogenetically evaluated genomic segment represents at least 12,000 years of evolution. We estimate that diversity within HPV-18 and probably within other HPV types evolved over a period of more than 200,000 years and that diversity between HPV types evolved over several million years.

Africa↗
PubMed2002

Reconciling genetic expectations from host specificity with historical population dynamics in an avian brood parasite, Horsfield's Bronze-Cuckoo Chalcites basalis of Australia.

Mitochondrial DNA (mtDNA) is being used increasingly to explore the evolution of host specificity in avian brood parasites. A stable coevolutionary equilibrium between multiple phylogenetically unrelated hosts and a brood parasitic species predicts that mtDNA diversity in the parasite should be relatively deep and phylogenetically structured. Also, the different intraspecific clades resulting from parasitism to multiple sympatric hosts should themselves occur sympatrically. However, mtDNA diversity in brood parasites is as susceptible to effects of historical population dynamics as in any species. We demonstrate the relevance of these dynamics to the use of mtDNA in understanding coevolution between an Australian brood-parasite, Horsfield's Bronze-Cuckoo Chalcites basalis and its hosts, Malurus fairy-wrens and Acanthiza thornbills. Previous ecological and behavioural analyses argue that Malurus- and Acanthiza-specific host races exist in C. basalis. Yet mtDNA diversity in C. basalis is low and phylogenetically unstructured (mean sequence divergence 0.15 +/- 0.07%, range 0.00%-0.31%) and tests of mtDNA neutrality and range expansion vs. population stability (Tajima's D, Fu & Li's F* and D*, Fu's F(S), mismatch analyses) all indicate that C. basalis has expanded its range very recently, probably within the last few tens of thousands of years following climatic amelioration after a peak of aridity in the late Pleistocene. The low mtDNA diversity and its lack of phylogenetic structure in C. basalis deny the existence of evolutionarily long-term stable host races in C. basalis but not the possibility of recently evolved ones. They highlight the need for renewed behavioural and ecological study of the relationship between C. basalis and its hosts. Our findings illustrate the need to understand the evolutionary context in which a brood parasite and its hosts have evolved if mtDNA data are to be used in testing hypotheses concerning the origin and maintenance of host specificity. They also add to the growing body of work illustrating the use of mismatch analyses and Fu's F(S) in detecting range expansions.

Animals↗
PubMed2005

Coevolution between nonhomologous but functionally similar proteins and their conserved partners in the Legionella pathogenesis system.

Legionella pneumophila, the causative agent of Legionnaires' disease, and other pathogenic Legionella species multiply inside protozoa and human macrophages by using the intracellular multiplication (Icm)/defect in organelle trafficking (Dot) type-IV secretion system. The IcmQ protein, which possesses pore-forming activity, and IcmR, which regulates the IcmQ activity, are two essential components of this system. Analysis of the region expected to contain these two genes from 29 Legionella species revealed the presence of a conserved icmQ gene and a large hypervariable gene family [functional homologues of icmR (fir) genes], located at the icmR genomic position. Although hypervariable in their sequence, the fir genes from all 29 Legionella species were found, together with their corresponding icmQ genes, to function similarly during infection. In addition, all FIR proteins we examined were found to interact with their corresponding IcmQ proteins. Detailed bioinformatic, biochemical, and genetic analysis of the interaction between the variable FIR proteins and conserved IcmQ proteins revealed that their interaction depends on a variable region located between two conserved domains of IcmQ. This variable region was also found to be critical for IcmQ self-interaction, and the region probably coevolved with the corresponding FIR protein. A FIR-IcmQ pair was also found in Coxiella burnetii, the only known non-Legionella bacterium that contains an Icm/Dot system, indicating the significance of this protein pair for the function of this type-IV secretion system. We hypothesize that this gene variation, which is probably mediated by positive selection, plays an important role in the evolutionary arms race between the protozoan host cell and the pathogen.

Acanthamoeba castellanii↗
PubMed1991

Coevolution of self-fertilization and inbreeding depression. I. Mutation-selection balance at one and two loci.

Simple theories for the evolution of breeding systems suggest that the fate of an allele that modifies the rate of self-fertilization hinges only on the degree to which selfing reduces opportunities for outcrossing ("pollen discounting") and the extent of inbreeding depression. These theories predict that outcrossing evolves whenever deleterious mutations have a more severe effect in combination than expected from their individual effects. We study the evolutionary dynamics of a modifier of the rate of self-fertilization in populations subject to complete pollen discounting and recurrent mutations which impair viability at a single locus in diploids and at two loci in haploids. Our analysis indicates that genetic associations arising immediately upon the introduction of a rare modifier allele generate substantial quantitative and qualitative departures from expectation. Higher rates of segregation under selfing in our one-locus diploid model generate positive associations between enhancers of selfing and wild-type viability alleles, which in turn favor the evolution of selfing under a wider range of conditions than expected. Greater opportunities for recombination under outcrossing in our two-locus haploid model generate positive associations between enhancers of outcrossing and wild-type viability alleles. These associations favor the evolution of outcrossing under a wider range of conditions, and introduce the possibility of stable mixed mating systems involving both selfing and outcrossing. Our explicit analysis of genetic associations between loci affecting viability and the rate of self-fertilization indicates that modifiers that enhance the production of offspring with very high (and very low) viability by promoting segregation or recombination develop positive associations with high viability. This advantage of producing extremes can compensate for an initial disadvantage in offspring number.

Alleles↗
PubMed2004

Parasite biodiversity and host defenses: chewing lice and immune response of their avian hosts.

Antagonistic host-parasite interactions lead to coevolution of host defenses and parasite virulence. Such adaptation by parasites to host defenses may occur to the detriment of the ability of parasites to exploit alternative hosts, causing parasite specialization and speciation. We investigated the relationship between level of anti-parasite defense in hosts and taxonomic richness of two chewing louse suborders (Phthiraptera: Amblycera, Ischnocera) on birds. While Amblyceran lice tend to occur in contact with host skin, feed on host skin and chew emerging tips of developing feathers to obtain blood, Ischnoceran lice live on feathers and feed on the non-living keratin of feather barbules. We hypothesized that Amblyceran abundance and richness would have evolved in response to interaction with the immune system of the host, while Ischnoceran taxonomic richness would have evolved independently of immunological constraints. In an interspecific comparison, the abundance of Ischnocerans was positively related to host body size, while host body mass and Ischnoceran taxonomic richness accounted for the abundance of Amblycerans. Amblyceran taxonomic richness was predicted by the intensity of T-cell mediated immune response of nestling hosts, while the T-cell response of adults had no significant effect. In contrast, Ischnoceran taxonomic richness was not predicted by host T-cell responses. These results suggest that the taxonomic richness of different parasite taxa is influenced by different host defenses, and they are consistent with the hypothesis that increasing host allocation to immune defense increases Amblyceran biodiversity.

Animals↗
PubMed1993

Phylogenetic analysis of the outer-membrane-protein genes of Chlamydiae, and its implication for vaccine development.

Examination of 18 complete and 6 partial sequences of the major outer-membrane protein from 24 chlamydiae isolates was used to reconstruct their evolutionary relationships. From this analysis, assuming that the clades with 100% bootstrap support are correct, come the following conclusions: (1) The tree of these sequences is not congruent with the phylogeny of the hosts, and thus host switching would seem to have occurred, thereby limiting the extent to which there has been coevolution of parasite and host. (2) The tree is also noncongruent with clustering by type of cell infected, thereby limiting the extent to which there has been coevolution of parasite and the cell type that it infects. (3) The tree is also noncongruent with clustering by the organ infected (eyes or genitalia), thereby limiting the extent to which there has been coevolution of parasite and the organ that it infects. (4) The tree is also noncongruent with genital strains arising from lymphogranuloma venereum strains. (5) The tree is also noncongruent with the geographic site at which the isolates were obtained, thereby limiting the extent of divergence explained by geographic separation. (6) There are estimated to be 185 amino acid positions that are invariable (as opposed to unvaried) in the major outer-membrane protein. There are 10 unvaried positions in the variable domains, of which 9 appear to be invariable, giving some reason to hope that development of a vaccine might be possible. (7) The rate of change of this protein is too small to see increased divergence over the time span of isolation of these genes, giving hope to any vaccine having longevity. Bootstrapping supports those portions of the tree on which the first five conclusions above depend. The picture that these results provide is more one of pathogen versatility than one of coevolutionary constraints. In addition, we examined 10 60-KDa, outer-membrane protein-2 genes, all but one of which were from these same strains. The tree was not, among the trachomatis strains, congruent with the major-outer-membrane protein tree, suggesting that gene exchange could be occurring among strains. Moreover, there is an apparent slowdown in divergence in this gene, among the trachomatis strains.

Amino Acid Sequence↗
PubMed1998

The origin and evolution of viruses (a review).

Viroids and prions might have existed early at the border of inanimate and living worlds. Most extant viruses can be characterized as derivatives of ancestors originating from episomal elements of prokaryotes (DNA phages) and later from eukaryotes. Retroviruses very likely originated from cellular retrotransposons. Retrograde evolution of some large viruses from obligatory intracellular bacteria is possible but the ontogenesis of extant bacteria does not include a viral form of existence (the filterable L forms are not viruses) and well-defined viruses do not regenerate back into vegetative bacterial forms. Biologists experimenting with the evolution of prokaryotic and eukaryotic ancient cells cannot ignore the earliest appearance of viruses within or outside the living matter. Viruses participated in and gave direction to the evolution and natural selection by coexisting with uni- and multicellular organisms for billions of years. The coevolution of viruses and their host cells is characterized by incessant attacks and counterattacks through gene rearrangements and mutations (induced in the virus by an immunological counterattack of the host or by transgression of species barriers by the virus) and recombinations. Recombinations occurred between viral and viral or viral and host genes. Acts of "molecular piracy" as practiced by ancient viruses endowed the virus with the expression of several host genes for the advantage of the virus in its replicative cycle and host-to-host spread. Probably the first immortalized and malignantly transformed cells were induced by viruses as viruses evolved anti-apoptotic measures. While infected cells resort to apoptotic death before the assembly of a new viral progeny, prominent are the anti-apoptotic measures viruses evolved in order to assure the completion of their full replicative cycle. Further, viruses may escape neutralization by host antibodies and may survive a counterattack by the host's T cells directed at virally infected cells of its own. Viruses may induce a form of tolerance and coexist with their host without inducing disease. Persistent and apparently or deceivingly apathogenic or even attenuated viral "quasi-species" populations may contain individual particles that regain virulence due to recombinations and/or gene rearrangements, especially when transgressing species barriers. Xenotropic viruses of animals may replicate in human cells and vice versa confounding experiments with xenotransplants or with use of veterinary viral vaccines for the treatment of human diseases.

Animals↗
PubMed1993

Coevolution of persistently infecting small DNA viruses and their hosts linked to host-interactive regulatory domains.

Although most RNA viral genomes (and related cellular retroposons) can evolve at rates a millionfold greater than that of their host genomes, some of the small DNA viruses (polyomaviruses and papillomaviruses) appear to evolve at much slower rates. These DNA viruses generally cause host species-specific inapparent primary infections followed by life-long, benign persistent infections. Using global progressive sequence alignments for kidney-specific Polyomaviridae (mouse, hamster, primate, human), we have constructed parsimonious evolutionary trees for the viral capsid proteins (VP1, VP2/VP3) and the large tumor (T) antigen. We show that these three coding sequences can yield phylogenetic trees similar to each other and to that of their host species. Such virus-host "co-speciation" appears incongruent with some prevailing views of viral evolution, and we suggest that inapparent persistent infections may link virus and most host evolution. Similarity analysis identified three specific regions of polyoma regulatory gene products (T antigens) as highly conserved, and two of these regions correspond to binding sites for host regulatory proteins (p53, the retinoblastoma gene product p105, and the related protein p107). The p53 site overlaps with a conserved ATPase domain and the retinoblastoma site corresponds to conserved region 1 of E1A protein of adenovirus type 5. We examined the local conservation of these binding sequences and show that the conserved retinoblastoma binding domain is characteristic and inclusive of the entire polyomavirus family, but the conserved p53-like binding domain is characteristic and inclusive of three entire families of small DNA viruses: polyomaviruses, papillomaviruses, and parvoviruses. The evolution of small-DNA-virus families may thus be tightly linked to host evolution and speciation by interaction with a subset of host regulatory proteins.

Amino Acid Sequence↗
PubMed1999

Coevolution of PERB11 (MIC) and HLA class I genes with HERV-16 and retroelements by extended genomic duplication.

The recent availability of genomic sequence information for the class I region of the MHC has provided an opportunity to examine the genomic organization of HLA class I (HLAcI) and PERB11/MIC genes with a view to explaining their evolution from the perspective of extended genomic duplications rather than by simple gene duplications and/or gene conversion events. Analysis of genomic sequence from two regions of the MHC (the alpha- and beta-blocks) revealed that at least 6 PERB11 and 14 HLAcI genes, pseudogenes, and gene fragments are contained within extended duplicated segments. Each segment was searched for the presence of shared (paralogous) retroelements by RepeatMasker in order to use them as markers of evolution, genetic rearrangements, and evidence of segmental duplications. Shared Alu elements and other retroelements allowed the duplicated segments to be classified into five distinct groups (A to E) that could be further distilled down to an ancient preduplication segment containing a HLA and PERB11 gene, an endogenous retrovirus (HERV-16), and distinctive retroelements. The breakpoints within and between the different HLAcI segments were found mainly within the PERB11 and HLA genes, HERV-16, and other retroelements, suggesting that the latter have played a major role in duplication and indel events leading to the present organization of PERB11 and HLAcI genes. On the basis of the features contained within the segments, a coevolutionary model premised on tandem duplication of single and multipartite genomic segments is proposed. The model is used to explain the origins and genomic organization of retroelements, HERV-16, DNA transposons, PERB11, and HLAcI genes as distinct segmental combinations within the alpha- and beta-blocks of the human MHC.

Alu Elements↗
PubMed1997

[Coevolutive mechanisms between retroviruses and their hosts. The murine mammary tumor model].

Mouse mammary tumor virus (MMTV) is a type B retrovirus that is transmitted as an infectious milk-borne particle and that causes mammary carcinomas by insertional activation of cellular protooncogenes. Germ line infections result in endogenous Mtv proviruses integrated in the genome of most mouse strains. These endogenous proviruses have been integrated into the genomes of mice for only the past 3-5 million years. The open reading frame present in the 3' long terminal repeat (LTR) of the provirus encodes a superantigen (SAg) which is able to stimulate a large proportion of T cells sharing a common T-cell receptor beta chain variable domain (v beta). Expression of this SAg is critical to the MMTV life cycle. After expression of the SAg in B cells a significant number of T cells are recruited to respond to these MMTV infected cells. As a consequence both the T cells expressing the relevant TCR V beta domain and the infected B cells become activated and start dividing. This would facilitate integration of MMTV and amplify the number of virus infected lymphocytes. Most likely during lactation the mammary glands become receptive to viral infection. The presence of endogenous Mtvs induces an early clonal deletion of reactive T cells. For this reason it has been argued that the presence of these proviruses confers a selective advantage to the mouse population by protecting the host from infection with an exogenous MMTV coding for a cross-reactive SAg. However, recent results discussed herein suggest that Mtv proviruses may also be detrimental to the mouse population by participating in recombinations with exogenous MMTVs, giving rise to highly tumorigenic recombinant particles. These results are discussed in the light of recent reports suggesting the involvement of viral sequences with a high homology to MMTV in human mammary tumorigenesis.

Animals↗