Overexpression of Trypanosoma cruzi high mobility group B protein (TcHMGB) alters the nuclear structure, impairs cytokinesis and reduces the parasite infectivity

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dc.citation.titleScientific Reports
dc.citation.volume9
dc.contributor.otherDr. De Gaudenzi, Javier: provide the pTcINDEX-eGFP strain
dc.creatorTavernelli, Luis Emilio
dc.creatorMotta, María Cristina M.
dc.creatorSilva Gonçalves, Camila
dc.creatorSantos da Silva, Marcelo
dc.creatorElías, María Carolina
dc.creatorAlonso, Victoria Lucía
dc.creatorSerra, Esteban Carlos
dc.creatorCribb, Pamela
dc.date.accessioned2024-08-02T14:41:20Z
dc.date.available2024-08-02T14:41:20Z
dc.date.issued2019-01-17
dc.description.abstractKinetoplastid parasites, included Trypanosoma cruzi, the causal agent of Chagas disease, present a unique genome organization and gene expression. Although they control gene expression mainly post-transcriptionally, chromatin accessibility plays a fundamental role in transcription initiation control. We have previously shown that High Mobility Group B protein from Trypanosoma cruzi (TcHMGB) can bind DNA in vitro. Here, we show that TcHMGB also acts as an architectural protein in vivo, since the overexpression of this protein induces changes in the nuclear structure, mainly the reduction of the nucleolus and a decrease in the heterochromatin:euchromatin ratio. Epimastigote replication rate was markedly reduced presumably due to a delayed cell cycle progression with accumulation of parasites in G2/M phase and impaired cytokinesis. Some functions involved in pathogenesis were also altered in TcHMGB-overexpressing parasites, like the decreased efficiency of trypomastigotes to infect cells in vitro, the reduction of intracellular amastigotes replication and the number of released trypomastigotes. Taken together, our results suggest that the TcHMGB protein is a pleiotropic player that controls cell phenotype and it is involved in key cellular processes.
dc.description.filFil: Tavernelli, Luis Emilio. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET); Argentina.
dc.description.filFil: Motta, Maria Cristina M. Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Laboratório de Ultraestrutura Celular Hertha Meyer; Brasil.
dc.description.filFil: Silva Gonçalves, Camila. Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Laboratório de Ultraestrutura Celular Hertha Meyer; Brasil.
dc.description.filFil: Santos da Silva, Marcelo. Instituto Butantan. Laboratório Especial de Ciclo Celular; Brasil.
dc.description.filFil: Santos da Silva, Marcelo. Instituto Butantan. Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS); Brasil.
dc.description.filFil: Elías, María Carolina. Instituto Butantan. Laboratório Especial de Ciclo Celular; Brasil.
dc.description.filFil: Elías, María Carolina. Instituto Butantan. Centro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS); Brasil.
dc.description.filFil: Alonso, Victoria Lucía. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Cátedra de Parasitología; Argentina.
dc.description.filFil: Serra, Esteban Carlos. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET); Argentina.
dc.description.filFil: Serra, Esteban Carlos. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Cátedra de Parasitología; Argentina.
dc.description.filFil: Cribb, Pamela. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET); Argentina.
dc.description.filFil: Cribb, Pamela. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Cátedra de Parasitología; Argentina.
dc.description.sponsorshipAgencia Nacional de Promoción de la Investigación, el Desarrollo Tecnológico y la Innovación (Agencia I+D+i): PICT 2008–1871
dc.description.sponsorshipConsejo Nacional de Investigaciones Científicas y Técnicas (CONICET): PIP 114-201101-00372
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipCentro de Toxinas, Resposta-imune e Sinalização Celular (CeTICS): grants 2014/24170-5, 2013/07467-1
dc.description.versionpeerreviewed
dc.format.extent1-16
dc.identifier.e-issn2045-2322
dc.identifier.urihttps://hdl.handle.net/2133/27504
dc.language.isoen
dc.publisherSpringer Nature
dc.relation.publisherversionhttps://doi.org/10.1038/s41598-018-36718-0
dc.relation.publisherversionhttps://www.nature.com/articles/s41598-018-36718-0
dc.rightsopenAccess
dc.rights.holderTavernelli, Luis Emilio
dc.rights.holderMotta, María Cristina M.
dc.rights.holderSilva Gonçalves, Camila
dc.rights.holderSantos da Silva, Marcelo
dc.rights.holderElías, María Carolina
dc.rights.holderAlonso, Victoria Lucía
dc.rights.holderSerra, Esteban Carlos
dc.rights.holderCribb, Pamela
dc.rights.holderUniversidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas
dc.rights.textAttribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectTrypanosoma cruzi
dc.subjectTcHMGB
dc.subjectGroup B protein
dc.subjectCytokinesis
dc.subjectCell nucleus structures
dc.subjectParasite infectivity
dc.subjectGene expression
dc.titleOverexpression of Trypanosoma cruzi high mobility group B protein (TcHMGB) alters the nuclear structure, impairs cytokinesis and reduces the parasite infectivity
dc.typearticulo
dc.type.versionpublishedVersion

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