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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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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Author(s):
Emilio Tavernelli, Luis [1] ; Motta, Maria Cristina M. [2] ; Silva Goncalves, Camila [2] ; da Silva, Marcelo Santos [3, 4] ; Elias, Maria Carolina [3, 4] ; Lucia Alonso, Victoria [5] ; Serra, Esteban [1, 5] ; Cribb, Pamela [1, 5]
Total Authors: 8
Affiliation:
[1] Consejo Nacl Invest Cient & Tecn, Inst Biol Mol & Celular Rosario IBR, Rosario - Argentina
[2] Univ Fed Rio de Janeiro, Inst Biofis Carlos Chagas Filho, Lab Ultraestrutura Celular Hertha Meyer, Rio De Janeiro - Brazil
[3] Inst Butantan, Lab Especial Ciclo Celular, BR-05503900 Sao Paulo, SP - Brazil
[4] Inst Butantan, Ctr Toxins Immune Response & Cell Signaling CeTIC, BR-05503900 Sao Paulo, SP - Brazil
[5] UNR, Fac Ciencias Bioquim & Farmaceut, Catedra Parasitol, Rosario - Argentina
Total Affiliations: 5
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 9, JAN 17 2019.
Web of Science Citations: 2
Abstract

Kinetoplastid 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. (AU)

FAPESP's process: 13/07467-1 - CeTICS - Center of Toxins, Immune-Response and Cell Signaling
Grantee:Hugo Aguirre Armelin
Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 14/24170-5 - DNA replication dynamics in Trypanosoma cruzi: licensing and replication rate characterization
Grantee:Marcelo Santos da Silva
Support Opportunities: Scholarships in Brazil - Post-Doctoral