Subtelomeric I-Scel-Mediated Double-Strand Breaks Are Repaired by Homologous Recombination in Trypanosoma cruzi

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dc.citation.volume7
dc.contributor.authorChiurillo, Miguel A.
dc.contributor.authorMoraes Barros, Roberto R.
dc.contributor.authorSouza, Renata Torres [UNIFESP]
dc.contributor.authorMarini, Marjorie Mendes [UNIFESP]
dc.contributor.authorAntonio, Cristiane Regina [UNIFESP]
dc.contributor.authorCortez, Danielle Rodrigues [UNIFESP]
dc.contributor.authorCurto, Maria A.
dc.contributor.authorLorenz, Hernan A.
dc.contributor.authorSchijman, Alejandro G.
dc.contributor.authorRamirez, Jose L.
dc.contributor.authorSilveira, Jose Franco da [UNIFESP]
dc.coverageLausanne
dc.date.accessioned2020-07-31T12:47:02Z
dc.date.available2020-07-31T12:47:02Z
dc.date.issued2016
dc.description.abstractTrypanosoma cruzi chromosome ends are enriched in surface protein genes and pseudogenes (e.g., trans-sialidases) surrounded by repetitive sequences. It has been proposed that the extensive sequence variability among members of these protein families could play a role in parasite infectivity and evasion of host immune response. In previous reports we showed evidence suggesting that sequences located in these regions are subjected to recombination. To support this hypothesis we introduced a double-strand break (DSB) at a specific target site in a I cruzi subtelomeric region cloned into an artificial chromosome (pTAC). This construct was used to transfect T. cruzi epimastigotes expressing the I-Scel meganuclease. Examination of the repaired sequences showed that DNA repair occurred only through homologous recombination (HR) with endogenous subtelomeric sequences. Our findings suggest that DSBs in subtelomeric repetitive sequences followed by HR between them may contribute to increased variability in T. cruzi multigene families.en
dc.description.affiliationUniv Centroccidental Lisandro Alvarado, Lab Genet Mol Dr Yunis Turbay, Ciencias Salud, Barquisimeto, Venezuela
dc.description.affiliationNIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, Sao Paulo, Brazil
dc.description.affiliationConsejo Nacl Invest Cient & Tecn, Inst Invest Ingn Genet & Biol Mol, Lab Biol Mol Enfermedad Chagas, Buenos Aires, DF, Argentina
dc.description.affiliationJ Craig Venter Inst, Dept Infect Dis, Rockville, MD USA
dc.description.affiliationFdn Inst Estudios Avanzados, Ctr Biotecnol, Caracas, Venezuela
dc.description.affiliationUniv Estadual Campinas, Fac Ciencias Med, Dept Patol Clin, Campinas, SP, Brazil
dc.description.affiliationUnifespDepartamento de Microbiologia, Imunologia e Parasitologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIDFAPESP: 11/51693-0
dc.description.sponsorshipIDFAPESP: 11/51475-3
dc.description.sponsorshipIDCNPq: 306591/2015-4
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.3389/fmicb.2016.02041
dc.identifier.citationFrontiers In Microbiology. Lausanne, v. 7, p. -, 2016.
dc.identifier.doi10.3389/fmicb.2016.02041
dc.identifier.fileWOS000390654600001.pdf
dc.identifier.issn1664-302X
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/56538
dc.identifier.wosWOS:000390654600001
dc.language.isoeng
dc.publisherFrontiers Media Sa
dc.relation.ispartofFrontiers In Microbiology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectT. cruzien
dc.subjecttelomereen
dc.subjectI-Scel meganucleaseen
dc.subjectdouble-strand breaken
dc.subjecthomologous recombinationen
dc.subjectDNA repairen
dc.subjectartificial chromosomesen
dc.titleSubtelomeric I-Scel-Mediated Double-Strand Breaks Are Repaired by Homologous Recombination in Trypanosoma cruzien
dc.typeinfo:eu-repo/semantics/article
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