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    <title>Repositório Comunidade: Group activity: 2009-Present.</title>
    <link>http://hdl.handle.net/10400.7/300</link>
    <description>Group activity: 2009-Present.</description>
    <items>
      <rdf:Seq>
        <rdf:li rdf:resource="http://hdl.handle.net/10400.7/824" />
        <rdf:li rdf:resource="http://hdl.handle.net/10400.7/787" />
        <rdf:li rdf:resource="http://hdl.handle.net/10400.7/699" />
        <rdf:li rdf:resource="http://hdl.handle.net/10400.7/535" />
        <rdf:li rdf:resource="http://hdl.handle.net/10400.7/460" />
      </rdf:Seq>
    </items>
    <dc:date>2020-03-07T13:51:53Z</dc:date>
  </channel>
  <item rdf:about="http://hdl.handle.net/10400.7/824">
    <title>Within host selection for faster replicating bacterial symbionts</title>
    <link>http://hdl.handle.net/10400.7/824</link>
    <description>Título: Within host selection for faster replicating bacterial symbionts
Autor: Chrostek, Ewa; Teixeira, Luis
Resumo: Wolbachia is a widespread, intracellular symbiont of arthropods, able to induce reproductive distortions and antiviral protection in insects. Wolbachia can also be pathogenic, as is the case with wMelPop, a virulent variant of the endosymbiont of Drosophila melanogaster. An extensive genomic amplification of the 20kb region encompassing eight Wolbachia genes, called Octomom, is responsible for wMelPop virulence. The Octomom copy number in wMelPop can be highly variable between individual D. melanogaster flies, even when comparing siblings arising from a single female. Moreover, Octomom copy number can change rapidly between generations. These data suggest an intra-host variability in Octomom copy number between Wolbachia cells. Since wMelPop Wolbachia with different Octomom copy numbers grow at different rates, we hypothesized that selection could act on this intra-host variability. Here we tested if total Octomom copy number changes during the lifespan of individual Drosophila hosts, revealing selection for different Wolbachia populations. We performed a time course analysis of Octomom amplification in flies whose mothers were controlled for Octomom copy number. We show that despite the Octomom copy number being relatively stable it increases slightly throughout D. melanogaster adult life. This indicates that there is selection acting on the intra-host variation in the Octomom copy number over the lifespan of individual hosts. This within host selection for faster replicating bacterial symbionts may be in conflict with between host selection against highly pathogenic Wolbachia.
Descrição: This deposit is composed by the main article plus the supplementary materials of the publication.; The supplementary materials are present in the publisher's page in the following link:                                 http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0191530#sec010</description>
    <dc:date>2018-01-18T00:00:00Z</dc:date>
  </item>
  <item rdf:about="http://hdl.handle.net/10400.7/787">
    <title>Comment on Rohrscheib et al. 2016 "Intensity of mutualism breakdown is determined by temperature not amplification of Wolbachia genes"</title>
    <link>http://hdl.handle.net/10400.7/787</link>
    <description>Título: Comment on Rohrscheib et al. 2016 "Intensity of mutualism breakdown is determined by temperature not amplification of Wolbachia genes"
Autor: Chrostek, Ewa; Teixeira, Luis
Resumo: Rohrscheib et al. (PLOS Pathogens, 2016) discuss the interaction between the pathogenicity of the wMel variant wMelPop, temperature and Octomom copy number. The effect of temperature on wMelPop pathogenicity was already reported in the original work on wMelPop. The absence of pathogenicity at low temperatures was also shown before. We have recently demonstrated, in Chrostek and Teixeira 2015, that Octomom copy number determines wMelPop pathogenicity.
Descrição: This deposit is composed by the main article plus the supplementary materials of the publication.</description>
    <dc:date>2017-09-11T00:00:00Z</dc:date>
  </item>
  <item rdf:about="http://hdl.handle.net/10400.7/699">
    <title>Drosophila Adaptation to Viral Infection through Defensive Symbiont Evolution</title>
    <link>http://hdl.handle.net/10400.7/699</link>
    <description>Título: Drosophila Adaptation to Viral Infection through Defensive Symbiont Evolution
Autor: Paulo, Tânia F.; Nolte, Viola; Schlötterer, Christian; Sucena, Élio; Teixeira, Luis
Resumo: Microbial symbionts can modulate host interactions with biotic and abiotic factors. Such interactions may affect the evolutionary trajectories of both host and symbiont. Wolbachia protects Drosophila melanogaster against several viral infections and the strength of the protection varies between variants of this endosymbiont. Since Wolbachia is maternally transmitted, its fitness depends on the fitness of its host. Therefore, Wolbachia populations may be under selection when Drosophila is subjected to viral infection. Here we show that in D. melanogaster populations selected for increased survival upon infection with Drosophila C virus there is a strong selection coefficient for specific Wolbachia variants, leading to their fixation. Flies carrying these selected Wolbachia variants have higher survival and fertility upon viral infection when compared to flies with the other variants. These findings demonstrate how the interaction of a host with pathogens shapes the genetic composition of symbiont populations. Furthermore, host adaptation can result from the evolution of its symbionts, with host and symbiont functioning as a single evolutionary unit.</description>
    <dc:date>2016-09-29T00:00:00Z</dc:date>
  </item>
  <item rdf:about="http://hdl.handle.net/10400.7/535">
    <title>Dynamics of Wolbachia pipientis gene expression across the Drosophila  melanogaster life cycle</title>
    <link>http://hdl.handle.net/10400.7/535</link>
    <description>Título: Dynamics of Wolbachia pipientis gene expression across the Drosophila  melanogaster life cycle
Autor: Florence Gutzwiller; Catarina R. Carmo; Danny E. Miller; Danny W. Rice; Irene L. Newton; R. Scott Hawley; Luis Teixeira; Casey M. Bergman
Resumo: Symbiotic interactions between microbes and their multicellular hosts have&#xD;
manifold impacts on molecular, cellular and organismal biology. To identify&#xD;
candidate bacterial genes involved in maintaining endosymbiotic associations&#xD;
with insect hosts, we analyzed genome-wide patterns of gene expression in the&#xD;
alpha-proteobacteria Wolbachia pipientis across the life cycle of Drosophila&#xD;
melanogaster using public data from the modENCODE project that was generated in&#xD;
a Wolbachia-infected version of the ISO1 reference strain. We find that the&#xD;
majority of Wolbachia genes are expressed at detectable levels in D.&#xD;
melanogaster across the entire life cycle, but that only 7.8% of 1195 Wolbachia&#xD;
genes exhibit robust stage- or sex-specific expression differences when studied&#xD;
in the "holo-organism" context. Wolbachia genes that are differentially&#xD;
expressed during development are typically up-regulated after D. melanogaster&#xD;
embryogenesis, and include many bacterial membrane, secretion system and&#xD;
ankyrin-repeat containing proteins. Sex-biased genes are often organised as&#xD;
small operons of uncharacterised genes and are mainly up-regulated in adult&#xD;
males D. melanogaster in an age-dependent manner suggesting a potential role in&#xD;
cytoplasmic incompatibility. Our results indicate that large changes in&#xD;
Wolbachia gene expression across the Drosophila life-cycle are relatively rare&#xD;
when assayed across all host tissues, but that candidate genes to understand&#xD;
host-microbe interaction in facultative endosymbionts can be successfully&#xD;
identified using holo-organism expression profiling. Our work also shows that&#xD;
mining public gene expression data in D. melanogaster provides a rich set of&#xD;
resources to probe the functional basis of the Wolbachia-Drosophila symbiosis&#xD;
and annotate the transcriptional outputs of the Wolbachia genome.</description>
    <dc:date>2015-10-23T00:00:00Z</dc:date>
  </item>
  <item rdf:about="http://hdl.handle.net/10400.7/460">
    <title>Host Adaptation Is Contingent upon the Infection Route Taken by Pathogens</title>
    <link>http://hdl.handle.net/10400.7/460</link>
    <description>Título: Host Adaptation Is Contingent upon the Infection Route Taken by Pathogens
Autor: Martins, Nelson E.; Faria, Vitor G.; Teixeira, Luis; Magalhães, Sara; Sucena, Élio
Resumo: Evolution of pathogen virulence is affected by the route of infection. Also, alternate infection routes trigger different physiological responses on hosts, impinging on host adaptation and on its interaction with pathogens. Yet, how route of infection may shape adaptation to pathogens has not received much attention at the experimental level. We addressed this question through the experimental evolution of an outbred Drosophila melanogaster population infected by two different routes (oral and systemic) with Pseudomonas entomophila. The two selection regimes led to markedly different evolutionary trajectories. Adaptation to infection through one route did not protect from infection through the alternate route, indicating distinct genetic bases. Finally, relatively to the control population, evolved flies were not more resistant to bacteria other than Pseudomonas and showed higher susceptibility to viral infections. These specificities and trade-offs may contribute to the maintenance of genetic variation for resistance in natural populations. Our data shows that the infection route affects host adaptation and thus, must be considered in studies of host-pathogen interaction.</description>
    <dc:date>2013-09-26T00:00:00Z</dc:date>
  </item>
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