14 results on '"Lindsey J. Plenderleith"'
Search Results
2. Ape Origins of Human Malaria
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Beatrice H. Hahn, Lindsey J. Plenderleith, and Paul M. Sharp
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Plasmodium ,Pan troglodytes ,Plasmodium falciparum ,030231 tropical medicine ,Plasmodium vivax ,Population ,Cross-species transmission ,Gorilla ,Plasmodium malariae ,Microbiology ,Article ,Evolution, Molecular ,03 medical and health sciences ,0302 clinical medicine ,Zoonoses ,biology.animal ,parasitic diseases ,medicine ,Animals ,Humans ,education ,Phylogeny ,030304 developmental biology ,0303 health sciences ,education.field_of_study ,Gorilla gorilla ,biology ,Genetic Variation ,Hominidae ,DNA, Protozoan ,biology.organism_classification ,medicine.disease ,Malaria ,Evolutionary biology - Abstract
African apes harbor at least twelve Plasmodium species, some of which have been a source of human infection. It is now well established that Plasmodium falciparum emerged following the transmission of a gorilla parasite, perhaps within the last 10,000 years, while Plasmodium vivax emerged earlier from a parasite lineage that infected humans and apes in Africa before the Duffy-negative mutation eliminated the parasite from humans there. Compared to their ape relatives, both human parasites have greatly reduced genetic diversity and an excess of nonsynonymous mutations, consistent with severe genetic bottlenecks followed by rapid population expansion. A putative new Plasmodium species widespread in chimpanzees, gorillas, and bonobos places the origin of Plasmodium malariae in Africa. Here, we review what is known about the origins and evolutionary history of all human-infective Plasmodium species, the time and circumstances of their emergence, and the diversity, host specificity, and zoonotic potential of their ape counterparts.
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- 2020
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3. Zoonotic origin of the human malaria parasite Plasmodium malariae from African apes
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Lindsey J, Plenderleith, Weimin, Liu, Yingying, Li, Dorothy E, Loy, Ewan, Mollison, Jesse, Connell, Ahidjo, Ayouba, Amandine, Esteban, Martine, Peeters, Crickette M, Sanz, David B, Morgan, Nathan D, Wolfe, Markus, Ulrich, Andreas, Sachse, Sébastien, Calvignac-Spencer, Fabian H, Leendertz, George M, Shaw, Beatrice H, Hahn, and Paul M, Sharp
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Plasmodium ,Plasmodium malariae ,Animals ,Humans ,Hominidae ,Malaria, Falciparum ,Phylogeny ,Malaria - Abstract
The human parasite Plasmodium malariae has relatives infecting African apes (Plasmodium rodhaini) and New World monkeys (Plasmodium brasilianum), but its origins remain unknown. Using a novel approach to characterise P. malariae-related sequences in wild and captive African apes, we found that this group comprises three distinct lineages, one of which represents a previously unknown, highly divergent species infecting chimpanzees, bonobos and gorillas across central Africa. A second ape-derived lineage is much more closely related to the third, human-infective lineage P. malariae, but exhibits little evidence of genetic exchange with it, and so likely represents a separate species. Moreover, the levels and nature of genetic polymorphisms in P. malariae indicate that it resulted from the zoonotic transmission of an African ape parasite, reminiscent of the origin of P. falciparum. In contrast, P. brasilianum falls within the radiation of human P. malariae, and thus reflects a recent anthroponosis.
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- 2021
4. CD4 receptor diversity represents an ancient protection mechanism against primate lentiviruses
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Preston A. Marx, William J. Kohler, Sandrine François-Souquiere, Alexander V. Georgiev, Weimin Liu, Ronnie M. Russell, Stephanie Trimboli, Scott Sherrill-Mix, Ronald G. Collman, Beatrice H. Hahn, Paul M. Sharp, Alex K. Piel, Paco Bertolani, Martine Peeters, Dorothy E. Loy, Marcos V. P. Gondim, Ahidjo Ayouba, Amandine Esteban, George M. Shaw, Lindsey J. Plenderleith, Volker Sommer, Frederic Bibollet-Ruche, Jesse Connell, Terese B. Hart, Fiona A. Stewart, Andrew G. Smith, Vanessa M. Hirsch, William M. Switzer, John Hart, Alexa N. Avitto, Katherine S. Wetzel, Yingying Li, and Richard A. Miller
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parallel evolution ,balancing selection ,viruses ,Simian Acquired Immunodeficiency Syndrome ,Simian ,Balancing selection ,Microbiology ,Evolution, Molecular ,03 medical and health sciences ,QH301 ,0302 clinical medicine ,Immune system ,Viral envelope ,Protein Domains ,Polymorphism (computer science) ,biology.animal ,Catarrhini ,Animals ,Humans ,Primate ,Alleles ,030304 developmental biology ,chemistry.chemical_classification ,Genetics ,QR355 ,0303 health sciences ,QL ,Acquired Immunodeficiency Syndrome ,Multidisciplinary ,biology ,virus diseases ,Gene Products, env ,Genetic Variation ,HIV ,Biological Sciences ,biology.organism_classification ,CD4 ,trans-specific polymorphism ,chemistry ,CD4 Antigens ,Simian Immunodeficiency Virus ,primate lentiviruses ,Glycoprotein ,030217 neurology & neurosurgery ,Binding domain ,Protein Binding - Abstract
Significance The CD4 protein of primates has undergone rapid diversification, but the reasons for this remain unknown. Here we show that within-species diversity of the HIV/simian immunodeficiency virus (SIV) envelope (Env) binding (D1) domain is common among African primate species, and that these polymorphisms can inhibit SIV Env-mediated cell entry. Amino acid replacements in the D1 domain changed putative Env contact residues as well as potential N-linked glycosylation sites in many species, with evidence for parallel evolution and trans-specific polymorphism. These data suggest that the primate CD4 receptor is under long-term balancing selection and that this diversification has been the result of a coevolutionary arms race between primate lentiviruses and their hosts., Infection with human and simian immunodeficiency viruses (HIV/SIV) requires binding of the viral envelope glycoprotein (Env) to the host protein CD4 on the surface of immune cells. Although invariant in humans, the Env binding domain of the chimpanzee CD4 is highly polymorphic, with nine coding variants circulating in wild populations. Here, we show that within-species CD4 diversity is not unique to chimpanzees but found in many African primate species. Characterizing the outermost (D1) domain of the CD4 protein in over 500 monkeys and apes, we found polymorphic residues in 24 of 29 primate species, with as many as 11 different coding variants identified within a single species. D1 domain amino acid replacements affected SIV Env-mediated cell entry in a single-round infection assay, restricting infection in a strain- and allele-specific fashion. Several identical CD4 polymorphisms, including the addition of N-linked glycosylation sites, were found in primate species from different genera, providing striking examples of parallel evolution. Moreover, seven different guenons (Cercopithecus spp.) shared multiple distinct D1 domain variants, pointing to long-term trans-specific polymorphism. These data indicate that the HIV/SIV Env binding region of the primate CD4 protein is highly variable, both within and between species, and suggest that this diversity has been maintained by balancing selection for millions of years, at least in part to confer protection against primate lentiviruses. Although long-term SIV-infected species have evolved specific mechanisms to avoid disease progression, primate lentiviruses are intrinsically pathogenic and have left their mark on the host genome.
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- 2021
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5. Ancient introgression between two ape malaria parasite species
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David Morgan, Paco Bertolani, Terese B. Hart, Weimin Liu, Beatrice H. Hahn, Crickette M. Sanz, Dorothy E. Loy, Lindsey J. Plenderleith, Gerald H. Learn, Paul M. Sharp, Sheri Speede, and John Hart
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0106 biological sciences ,Plasmodium ,Letter ,Pan troglodytes ,exported proteins ,Introgression ,Laverania ,Biology ,Genetic Introgression ,010603 evolutionary biology ,01 natural sciences ,Genome ,Evolution, Molecular ,03 medical and health sciences ,chimpanzee ,Genetics ,Animals ,Humans ,Parasite hosting ,Clade ,Gene ,Phylogeny ,Ecology, Evolution, Behavior and Systematics ,030304 developmental biology ,0303 health sciences ,Virulence ,Plasmodium falciparum ,biology.organism_classification ,Malaria ,Evolutionary biology - Abstract
The Laverania clade comprises the human malaria parasite Plasmodium falciparum as well as at least seven additional parasite species that infect wild African apes. A recent analysis of Laverania genome sequences (Otto TD, et al. 2018. Genomes of all known members of a Plasmodium subgenus reveal paths to virulent human malaria. Nat Microbiol. 3:687-697) reported three instances of inter-species gene transfer, one of which had previously been described. Generating gene sequences from additional ape parasites and re-examining sequencing reads generated in the Otto et al. study, we identified one of the newly described gene transfers as an assembly artefact of sequences derived from a sample co-infected by two parasite species. The second gene transfer between ancestors of two divergent chimpanzee parasite lineages was confirmed, but involved a much larger number of genes than originally described, many of which encode exported proteins that remodel, or bind to, erythrocytes. Because successful hybridisation between Laverania species is very rare, it will be important to determine to what extent these gene transfers have shaped their host interactions.
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- 2019
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6. Multigenomic Delineation ofPlasmodiumSpecies of theLaveraniaSubgenus Infecting Wild-Living Chimpanzees and Gorillas
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Jean-Bosco N. Ndjango, George M. Shaw, Martine Peeters, Julian C. Rayner, Rebeca Atencia, Debby Cox, Gerald H. Learn, Sesh A. Sundararaman, Dorothy E. Loy, Beatrice H. Hahn, Lindsey J. Plenderleith, Weimin Liu, Yingying Li, Sheri Speede, Ahidjo Ayouba, and Paul M. Sharp
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0301 basic medicine ,Mitochondrial DNA ,Letter ,Plasmodium parasites infecting chimpanzees and gorillas ,Pan troglodytes ,Plasmodium falciparum ,030231 tropical medicine ,Laverania ,Gorilla ,P. falciparum ,DNA, Mitochondrial ,Plasmodium ,Evolution, Molecular ,Feces ,03 medical and health sciences ,0302 clinical medicine ,Phylogenetics ,biology.animal ,parasitic diseases ,Genetics ,Animals ,Humans ,Malaria, Falciparum ,Phylogeny ,Ecology, Evolution, Behavior and Systematics ,Apicoplast ,Gorilla gorilla ,biology ,Phylogenetic tree ,Sequence Analysis, DNA ,cryptic Plasmodium species ,biology.organism_classification ,3. Good health ,single genome sequencing ,030104 developmental biology ,Evolutionary biology ,Africa - Abstract
Plasmodium falciparum, the major cause of malaria morbidity and mortality worldwide, is only distantly related to other human malaria parasites and has thus been placed in a separate subgenus, termed Laverania. Parasites morphologically similar to P. falciparum have been identified in African apes, but only one other Laverania species, Plasmodium reichenowi from chimpanzees, has been formally described. Although recent studies have pointed to the existence of additional Laverania species, their precise number and host associations remain uncertain, primarily because of limited sampling and a paucity of parasite sequences other than from mitochondrial DNA. To address this, we used limiting dilution polymerase chain reaction to amplify additional parasite sequences from a large number of chimpanzee and gorilla blood and fecal samples collected at two sanctuaries and 30 field sites across equatorial Africa. Phylogenetic analyses of more than 2,000 new sequences derived from the mitochondrial, nuclear, and apicoplast genomes revealed six divergent and well-supported clades within the Laverania parasite group. Although two of these clades exhibited deep subdivisions in phylogenies estimated from organelle gene sequences, these sublineages were geographically defined and not present in trees from four unlinked nuclear loci. This greatly expanded sequence data set thus confirms six, and not seven or more, ape Laverania species, of which P. reichenowi, Plasmodium gaboni, and Plasmodium billcollinsi only infect chimpanzees, whereas Plasmodium praefalciparum, Plasmodium adleri, and Pladmodium blacklocki only infect gorillas. The new sequence data also confirm the P. praefalciparum origin of human P. falciparum.
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- 2016
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7. Reply to Forni et al., 'Multiple Selected Changes May Modulate the Molecular Interaction between Laverania RH5 and Primate Basigin'
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Frederic Bibollet-Ruche, Dorothy E. Loy, Oscar A. MacLean, Gerald H. Learn, Beatrice H. Hahn, Paul M. Sharp, Lindsey J. Plenderleith, Weimin Liu, Yingying Li, and Sesh A. Sundararaman
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Primates ,0301 basic medicine ,Plasmodium ,plasmodium falciparum ,Plasmodium falciparum ,Laverania ,Gorilla ,Microbiology ,Biophysical Phenomena ,03 medical and health sciences ,chimpanzee ,Virology ,biology.animal ,Animals ,Primate ,Author Reply ,biology ,gorilla ,biology.organism_classification ,QR1-502 ,basigin ,RH5 ,030104 developmental biology ,Evolutionary biology ,Basigin ,laverania - Published
- 2018
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8. Wild bonobos host geographically restricted malaria parasites including a putative new Laverania species
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Lindsey J. Plenderleith, Steve Ahuka-Mundeke, Martine Peeters, Abigail Lauder, Paul M. Sharp, Weimin Liu, Scott Sherrill-Mix, Terese B. Hart, Beatrice H. Hahn, Gerald H. Learn, George M. Shaw, Jef Dupain, Cintia Garai, Paco Bertolani, Alexander V. Georgiev, Jean Bosco N. Ndjango, Yingying Li, Sesh A. Sundararaman, Dorothy E. Loy, Erik J. Scully, John Hart, and Alexa N. Avitto
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0301 basic medicine ,Plasmodium ,Range (biology) ,Science ,General Physics and Astronomy ,Zoology ,Animals, Wild ,Gorilla ,Article ,General Biochemistry, Genetics and Molecular Biology ,Laverania ,Feces ,03 medical and health sciences ,Phylogenetics ,biology.animal ,parasitic diseases ,medicine ,Animals ,lcsh:Science ,Phylogeny ,Ecological epidemiology ,Multidisciplinary ,biology ,Ecology ,Bonobo ,Parasite genomics ,Primate Diseases ,General Chemistry ,Pan paniscus ,biology.organism_classification ,medicine.disease ,Malaria ,3. Good health ,030104 developmental biology ,Congo ,Parasite evolution ,lcsh:Q - Abstract
Malaria parasites, though widespread among wild chimpanzees and gorillas, have not been detected in bonobos. Here, we show that wild-living bonobos are endemically Plasmodium infected in the eastern-most part of their range. Testing 1556 faecal samples from 11 field sites, we identify high prevalence Laverania infections in the Tshuapa-Lomami-Lualaba (TL2) area, but not at other locations across the Congo. TL2 bonobos harbour P. gaboni, formerly only found in chimpanzees, as well as a potential new species, Plasmodium lomamiensis sp. nov. Rare co-infections with non-Laverania parasites were also observed. Phylogenetic relationships among Laverania species are consistent with co-divergence with their gorilla, chimpanzee and bonobo hosts, suggesting a timescale for their evolution. The absence of Plasmodium from most field sites could not be explained by parasite seasonality, nor by bonobo population structure, diet or gut microbiota. Thus, the geographic restriction of bonobo Plasmodium reflects still unidentified factors that likely influence parasite transmission., Unlike chimpanzees and gorillas, bonobos have not been found infected by malaria parasites in the wild. Here, Liu et al. report more thorough survey and sequencing results showing that bonobos host malaria parasites, including a yet-unknown species, but only in the eastern-most part of their range.
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- 2017
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9. Resistance to type 1 interferons is a major determinant of HIV-1 transmission fitness
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Ronnie M. Russell, Shilpa S. Iyer, Timothy Decker, Persephone Borrow, Gerald H. Learn, Marcos V. P. Gondim, Lindsey J. Plenderleith, Hannah J. Barbian, Yingying Li, Paul M. Sharp, Scott Sherrill-Mix, Beatrice H. Hahn, Christiana M. Shaw, Frederic Bibollet-Ruche, Barton F. Haynes, George M. Shaw, Catherine Y. Bahari, and Andrew G. Smith
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Male ,type 1 interferons ,0301 basic medicine ,Sexual transmission ,HIV Infections ,Mucosal HIV-1 transmission ,Viral quasispecies ,Biology ,Virus Replication ,Virus ,03 medical and health sciences ,Semen ,medicine ,Humans ,innate immunity ,chemistry.chemical_classification ,Multidisciplinary ,Innate immune system ,Virion ,transmission fitness ,Virology ,Titer ,030104 developmental biology ,PNAS Plus ,Viral replication ,chemistry ,Host-Pathogen Interactions ,Interferon Type I ,HIV-1 ,Vaginal Douching ,Female ,transmission pairs ,Glycoprotein ,Interferon type I ,medicine.drug - Abstract
Sexual transmission of HIV-1 is an inefficient process, with only one or few variants of the donor quasispecies establishing the new infection. A critical, and as yet unresolved, question is whether the mucosal bottleneck selects for viruses with increased transmission fitness. Here, we characterized 300 limiting dilution-derived virus isolates from the plasma, and in some instances genital secretions, of eight HIV-1 donor and recipient pairs. Although there were no differences in the amount of virion-associated envelope glycoprotein, recipient isolates were on average 3-fold more infectious (P = 0.0001), replicated to 1.4-fold higher titers (P = 0.004), were released from infected cells 4.2-fold more efficiently (P < 0.00001), and were significantly more resistant to type I interferons (IFNs) than the corresponding donor isolates. Remarkably, transmitted viruses exhibited 7.8-fold higher IFNα2 (P < 0.00001) and 39-fold higher IFNβ (P < 0.00001) half-maximal inhibitory concentrations (IC50) than did donor isolates, and their odds of replicating in CD4+ T cells at the highest IFNα2 and IFNβ doses were 35-fold (P < 0.00001) and 250-fold (P < 0.00001) greater, respectively. Interestingly, pretreatment of CD4+ T cells with IFNβ, but not IFNα2, selected donor plasma isolates that exhibited a transmitted virus-like phenotype, and such viruses were also detected in the donor genital tract. These data indicate that transmitted viruses are phenotypically distinct, and that increased IFN resistance represents their most distinguishing property. Thus, the mucosal bottleneck selects for viruses that are able to replicate and spread efficiently in the face of a potent innate immune response.
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- 2017
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10. Genomes of cryptic chimpanzee Plasmodium species reveal key evolutionary events leading to human malaria
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Gerald H. Learn, George M. Shaw, Ahidjo Ayouba, Dustin Brisson, Weimin Liu, Dorothy E. Loy, Julian C. Rayner, Frederic D. Bushman, Katharina S. Shaw, Sesh A. Sundararaman, Yingying Li, Beatrice H. Hahn, Lindsey J. Plenderleith, Martine Peeters, Paul M. Sharp, and Sheri Speede
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0301 basic medicine ,Plasmodium ,Chemistry(all) ,Pan troglodytes ,Science ,Plasmodium falciparum ,General Physics and Astronomy ,Physics and Astronomy(all) ,Real-Time Polymerase Chain Reaction ,Genome ,General Biochemistry, Genetics and Molecular Biology ,Laverania ,Article ,Evolution, Molecular ,03 medical and health sciences ,Phylogenetics ,parasitic diseases ,Parasite hosting ,Animals ,Humans ,Malaria, Falciparum ,Gene ,Phylogeny ,Genetics ,Multidisciplinary ,biology ,Biochemistry, Genetics and Molecular Biology(all) ,Genetic Variation ,General Chemistry ,biology.organism_classification ,Biological Evolution ,3. Good health ,030104 developmental biology ,Multigene Family ,Human parasite ,Genome, Protozoan - Abstract
African apes harbour at least six Plasmodium species of the subgenus Laverania, one of which gave rise to human Plasmodium falciparum. Here we use a selective amplification strategy to sequence the genome of chimpanzee parasites classified as Plasmodium reichenowi and Plasmodium gaboni based on the subgenomic fragments. Genome-wide analyses show that these parasites indeed represent distinct species, with no evidence of cross-species mating. Both P. reichenowi and P. gaboni are 10-fold more diverse than P. falciparum, indicating a very recent origin of the human parasite. We also find a remarkable Laverania-specific expansion of a multigene family involved in erythrocyte remodelling, and show that a short region on chromosome 4, which encodes two essential invasion genes, was horizontally transferred into a recent P. falciparum ancestor. Our results validate the selective amplification strategy for characterizing cryptic pathogen species, and reveal evolutionary events that likely predisposed the precursor of P. falciparum to colonize humans., African apes harbour six Plasmodium species, one of which gave rise to the human malaria parasite. Here, Sundaraman et al. use selective whole-genome amplification to determine genome sequences from two chimpanzee Plasmodium species, shedding light on the evolutionary origin of the human parasite.
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- 2015
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11. Ape parasite origins of human malaria virulence genes
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Lindsey J. Plenderleith, Weimin Liu, Daniel B. Larremore, Sheri Speede, Julian C. Rayner, Sesh A. Sundararaman, Dorothy E. Loy, William R. Proto, Beatrice H. Hahn, Caroline O. Buckee, Paul M. Sharp, and Aaron Clauset
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Plasmodium ,Pan troglodytes ,Molecular Sequence Data ,Protozoan Proteins ,General Physics and Astronomy ,Virulence ,Synteny ,General Biochemistry, Genetics and Molecular Biology ,Laverania ,Article ,Host-Parasite Interactions ,Evolution, Molecular ,parasitic diseases ,Gene family ,Animals ,Gene ,Genetics ,Multidisciplinary ,Gorilla gorilla ,biology ,Plasmodium falciparum ,General Chemistry ,Sequence Analysis, DNA ,biology.organism_classification ,3. Good health ,Subgenus - Abstract
Antigens encoded by the var gene family are major virulence factors of the human malaria parasite Plasmodium falciparum, exhibiting enormous intra- and interstrain diversity. Here we use network analysis to show that var architecture and mosaicism are conserved at multiple levels across the Laverania subgenus, based on var-like sequences from eight single-species and three multi-species Plasmodium infections of wild-living or sanctuary African apes. Using select whole-genome amplification, we also find evidence of multi-domain var structure and synteny in Plasmodium gaboni, one of the ape Laverania species most distantly related to P. falciparum, as well as a new class of Duffy-binding-like domains. These findings indicate that the modular genetic architecture and sequence diversity underlying var-mediated host-parasite interactions evolved before the radiation of the Laverania subgenus, long before the emergence of P. falciparum., Antigens encoded by var genes are major virulence factors of the human malaria parasite Plasmodium falciparum. Here, Larremore et al. identify var-like genes in distantly related Plasmodium species infecting African apes, indicating that these genes already existed in an ancestral ape parasite many millions of years ago.
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- 2015
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12. Withstanding the Challenges of Host Immunity: Antigenic Variation and the Trypanosome Surface Coat
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James P. J. Hall and Lindsey J. Plenderleith
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Genetics ,Mutation ,Effector ,Pseudogene ,Biology ,Subtelomere ,medicine.disease_cause ,Virology ,Phenotype ,Immune system ,parasitic diseases ,Antigenic variation ,medicine ,Gene - Abstract
Prolonged survival in the face of host immunity has been a major force shaping the biology and evolution of the African trypanosomes, and nowhere are the effects of this force more apparent than in the antigenic variation of the trypanosome variant surface glycoprotein (VSG) coat. The coat protects the trypanosome within it from immune effectors, and spontaneous and stochastic events occurring at the molecular level cause individual trypanosomes to change the VSG variant they are expressing. The consequence of this switching at the population level is a diverse population that can pre-empt the specific immune responses that arise against VSG. The template for changes to VSG is an extensive archive of silent VSG genes and pseudogenes. VSG from the archive are activated not only as full-length genes but also through the combination of segments to form mosaic VSG genes, a process that augments the potential for antigenic variation by introducing combinatorial variation and allowing VSG pseudogenes to be used. The main part of the archive occupies subtelomeres and so is itself prone to mutation and rapid evolution, which are important features when superinfection or reinfection of partially immune hosts is necessary. The antigenic variation ‘diversity phenotype’ is thus a multifaceted one, enlisting and coordinating fundamental mechanisms of cell biology to bring about a process that unfolds across populations, thereby facilitating the success of the African trypanosomes.
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- 2013
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13. Polyuridylylation and processing of transcripts from multiple gene minicircles in chloroplasts of the dinoflagellate Amphidinium carterae
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Christopher J. Howe, Lindsey J. Plenderleith, Adrian C. Barbrook, Jennifer Burrows, R. Ellen R. Nisbet, Richard G. Dorrell, Barbrook, Adrian C, Dorrell, Richard G, Burrows, Jennifer, Plenderleith, Lindsey J, Nisbet, R Ellen R, and Howe, Christopher J
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Poly U ,Chloroplasts ,ved/biology.organism_classification_rank.species ,Genes, Protozoan ,Plant Science ,Biology ,Minicircle ,Genome ,Models, Biological ,chloroplast ,Transcription (biology) ,Amphidinium carterae ,Genes, Chloroplast ,Genetics ,RNA Processing, Post-Transcriptional ,Gene ,minicircles ,Messenger RNA ,ved/biology ,food and beverages ,RNA ,General Medicine ,DNA, Protozoan ,polyU ,Molecular biology ,transcript processing ,Rolling circle replication ,Dinoflagellida ,DNA, Circular ,protist ,Agronomy and Crop Science ,RNA, Protozoan - Abstract
Although transcription and transcript processing in the chloroplasts of plants have been extensively characterised, the RNA metabolism of other chloroplast lineages across the eukaryotes remains poorly understood. In this paper, we use RT-PCR to study transcription and transcript processing in the chloroplasts of Amphidinium carterae, a model peridinin-containing dinoflagellate. These organisms have a highly unusual chloroplast genome, with genes located on multiple small 'minicircle' elements, and a number of idiosyncratic features of RNA metabolism including transcription via a rolling circle mechanism, and 3' terminal polyuridylylation of transcripts. We demonstrate that transcription occurs in A. carterae via a rolling circle mechanism, as previously shown in the dinoflagellate Heterocapsa, and present evidence for the production of both polycistronic and monocistronic transcripts from A. carterae minicircles, including several regions containing ORFs previously not known to be expressed. We demonstrate the presence of both polyuridylylated and non-polyuridylylated transcripts in A. carterae, and show that polycistronic transcripts can be terminally polyuridylylated. We present a model for RNA metabolism in dinoflagellate chloroplasts where long polycistronic precursors are processed to form mature transcripts. Terminal polyuridylylation may mark transcripts with the correct 3' end. Refereed/Peer-reviewed
- Published
- 2012
14. Comparative analysis of dinoflagellate chloroplast genomes reveals rRNA and tRNA genes
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Christopher J. Howe, Nicole Santucci, Roger G. Hiller, Lindsey J. Plenderleith, Adrian C. Barbrook, Barbrook, Adrian [0000-0002-6209-7413], Howe, Christopher [0000-0002-6975-8640], and Apollo - University of Cambridge Repository
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Nuclear gene ,Chloroplasts ,lcsh:QH426-470 ,lcsh:Biotechnology ,Molecular Sequence Data ,Biology ,Minicircle ,Genome ,Polymerase Chain Reaction ,REGION ,RNA, Transfer ,MINICIRCLES ,AMPHIDINIUM-OPERCULATUM ,lcsh:TP248.13-248.65 ,evolution ,Genetics ,Animals ,subunit ,NUCLEUS ,Gene ,Base Sequence ,Dinoflagellate ,COMPARATIVE SEQUENCE ,food and beverages ,PLASTID GENOME ,Genome project ,Ribosomal RNA ,biology.organism_classification ,Chloroplast ,lcsh:Genetics ,TANDEM ,RNA, Ribosomal ,Dinoflagellida ,protein ,Genome, Protozoan ,Sequence Alignment ,RNA, Protozoan ,Biotechnology ,Research Article - Abstract
Background Peridinin-containing dinoflagellates have a highly reduced chloroplast genome, which is unlike that found in other chloroplast containing organisms. Genome reduction appears to be the result of extensive transfer of genes to the nuclear genome. Unusually the genes believed to be remaining in the chloroplast genome are found on small DNA 'minicircles'. In this study we present a comparison of sets of minicircle sequences from three dinoflagellate species. Results PCR was used to amplify several minicircles from Amphidinium carterae so that a homologous set of gene-containing minicircles was available for Amphidinium carterae and Amphidinium operculatum, two apparently closely related peridinin-containing dinoflagellates. We compared the sequences of these minicircles to determine the content and characteristics of their chloroplast genomes. We also made comparisons with minicircles which had been obtained from Heterocapsa triquetra, another peridinin-containing dinoflagellate. These in silico comparisons have revealed several genetic features which were not apparent in single species analyses. The features include further protein coding genes, unusual rRNA genes, which we show are transcribed, and the first examples of tRNA genes from peridinin-containing dinoflagellate chloroplast genomes. Conclusion Comparative analysis of minicircle sequences has allowed us to identify previously unrecognised features of dinoflagellate chloroplast genomes, including additional protein and RNA genes. The chloroplast rRNA gene sequences are radically different from those in other organisms, and in many ways resemble the rRNA genes found in some highly reduced mitochondrial genomes. The retention of certain tRNA genes in the dinoflagellate chloroplast genome has important implications for models of chloroplast-mitochondrion interaction.
- Published
- 2006
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