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Forward genetics in Wolbachia: Regulation of Wolbachia proliferation by the amplification and deletion of an addictive genomic island

2021-06-18Journal article Open access
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dc.contributor.authorHeleno Duarte, Elves
dc.contributor.authorCarvalho, Ana
dc.contributor.authorLópez-Madrigal, Sergio
dc.contributor.authorCosta, João
dc.contributor.authorTeixeira, Luís
dc.date.accessioned2021-07-01T11:06:34Z
dc.date.available2021-07-01T11:06:34Z
dc.date.issued2021-06-18
dc.description.abstractWolbachia is one of the most prevalent bacterial endosymbionts, infecting approximately 40% of terrestrial arthropod species. Wolbachia is often a reproductive parasite but can also provide fitness benefits to its host, as, for example, protection against viral pathogens. This protective effect is currently being applied to fight arboviruses transmission by releasing Wolbachia-transinfected mosquitoes. Titre regulation is a crucial aspect of Wolbachia biology. Higher titres can lead to stronger phenotypes and fidelity of transmission but can have a higher cost to the host. Since Wolbachia is maternally transmitted, its fitness depends on host fitness, and, therefore, its cost to the host may be under selection. Understanding how Wolbachia titres are regulated and other aspects of Wolbachia biology has been hampered by the lack of genetic tools. Here we developed a forward genetic screen to identify new Wolbachia over-proliferative mutant variants. We characterized in detail two new mutants, wMelPop2 and wMelOctoless, and show that the amplification or loss of the Octomom genomic region lead to over-proliferation. These results confirm previous data and expand on the complex role of this genomic region in the control of Wolbachia proliferation. Both new mutants shorten the host lifespan and increase antiviral protection. Moreover, we show that Wolbachia proliferation rate in Drosophila melanogaster depends on the interaction between Octomom copy number, the host developmental stage, and temperature. Our analysis also suggests that the life shortening and antiviral protection phenotypes of Wolbachia are dependent on different, but related, properties of the endosymbiont; the rate of proliferation and the titres near the time of infection, respectively. We also demonstrate the feasibility of a novel and unbiased experimental approach to study Wolbachia biology, which could be further adapted to characterize other genetically intractable bacterial endosymbionts.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationDuarte EH, Carvalho A, López-Madrigal S, Costa J, Teixeira L (2021) Forward genetics in Wolbachia: Regulation of Wolbachia proliferation by the amplification and deletion of an addictive genomic island. PLoS Genet 17(6): e1009612.pt_PT
dc.identifier.doi10.1371/journal.pgen.1009612pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/969
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationFCT - IF/00839/2015pt_PT
dc.relationFunctional genetics of Wolbachia proliferation and protection to viruses
dc.relation.publisherversionhttps://doi.org/10.1371/journal.pgen.1009612pt_PT
dc.subjectWolbachiapt_PT
dc.subjectDrosophilapt_PT
dc.subjectOctomompt_PT
dc.subjectTiter regulationpt_PT
dc.subjectForward geneticspt_PT
dc.subjectSymbiosispt_PT
dc.titleForward genetics in Wolbachia: Regulation of Wolbachia proliferation by the amplification and deletion of an addictive genomic islandpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleFunctional genetics of Wolbachia proliferation and protection to viruses
oaire.awardURIinfo:eu-repo/grantAgreement/EC/H2020/773260/EU
oaire.citation.issue6pt_PT
oaire.citation.titlePLOS Geneticspt_PT
oaire.citation.volume17pt_PT
oaire.fundingStreamH2020
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.nameEuropean Commission
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublicationf0166b3d-5466-4e50-8bf4-2bc13a460949
relation.isProjectOfPublication.latestForDiscoveryf0166b3d-5466-4e50-8bf4-2bc13a460949

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