The differentiation of epimastigotes into metacyclic trypomastigotes (metacyclogenesis) involves the transformation of a replicative non-infective form of Trypanosoma cruzi into a non-replicative infective stage. The study of genes with stage-specific expression may provide insight into the mechanisms involved in the regulation of gene expression in this parasite. We cloned and characterized two genes whose expression is up-regulated in metacyclic trypomastigote, those encoding metacyclin-II (Met-II) and metacyclin-III (Met-III). Nucleotide sequence analysis identified no sequence similarity with sequences available from genetic databases. The deduced amino acid sequences of the genes indicated that Met-III encodes a basic polypeptide whereas Met-II encodes an acidic polypeptide. Northern and Western blot analyses showed that Met-II and Met-III were expressed by metacyclic trypomastigotes, but not by epimastigotes. Antisera directed against the recombinant Met-II and Met-III proteins recognized two polypeptides on Western blots: a 16-kDa and a 24-kDa polypeptide. Immunocytochemistry analysis using electron microscopy showed that metacyclin-II is localized mainly at the kinetoplast whereas metacyclin-III is localized at the nucleus of the parasite. Southern blot analysis, using genomic DNA and T. cruzi chromosomes separated by pulsed-field gel electrophoresis, indicated that these genes were present as single copies on different chromosomes of T. cruzi Dm28c.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.actatropica.2003.10.018 | DOI Listing |
J Extracell Vesicles
November 2024
School of Human Sciences, Cell Communication in Disease Pathology, London Metropolitan University, London, UK.
During cell invasion, large Extracellular Vesicle (lEV) release from host cells was dose-dependently triggered by Trypanosoma cruzi metacyclic trypomastigotes (Mtr). This lEV release was inhibited when IP-mediated Ca exit from the ER and further Ca entry from plasma membrane channels was blocked, but whilst any store-independent Ca entry (SICE) could continue unabated. That lEV release was equally inhibited if all entry from external sources was blocked by chelation of external Ca points to the major contributor to Mtr-triggered host cell lEV release being IP/store-mediated Ca release, SICE playing a minor role.
View Article and Find Full Text PDFMem Inst Oswaldo Cruz
November 2024
Fundação Oswaldo Cruz-Fiocruz, Instituto René Rachou, Grupo de Comportamento de Vetores e Interação com Patógenos, Belo Horizonte, MG, Brasil.
Background: Trypanosoma rangeli is a haemoflagellate parasite that infects triatomine bugs and mammals in South and Central America. Trypanosoma cruzi, the etiological agent of Chagas disease, has a partially overlapping geographical distribution with T. rangeli, that leads to mixed human infections and cross-reactivity in immunodiagnosis.
View Article and Find Full Text PDFPLoS Negl Trop Dis
October 2024
Laboratory of Biochemistry of Tryps - LaBTryps - Department of Parasitology, Instituto de Ciências Biomédicas II, Universidade de São Paulo, São Paulo, Brazil.
Trypanosoma cruzi, the causative agent of Chagas disease, has a complex life cycle that involves triatomine insects as vectors and mammals as hosts. The differentiation of epimastigote forms into metacyclic trypomastigotes within the insect vector is crucial for the parasite's life cycle progression. Factors influencing this process, including temperature, pH, and nutritional stress, along with specific metabolite availability, play a pivotal role.
View Article and Find Full Text PDFExp Parasitol
October 2024
Postgraduate Program in Health Sciences, Health Sciences Center, State University of Maringá, Maringá, 87.020.900, Brazil; Postgraduate Program in Biological Sciences, Biological Sciences Center, State University of Maringá, Maringá, 87.020.900, Brazil; Department of Basic Health Sciences, Health Sciences Center, State University of Maringá, Maringá, 87.020.900, Brazil. Electronic address:
In Brazil, where Chagas disease is endemic, the most frequent form of transmission of the parasite is the oral route, associated with greater severity and worse response to benznidazole (BZ), the drug used in its treatment. This study aimed to evaluate the impact of gastrointestinal infection (GI) and BZ treatment on the parasitological and histopathological parameters in mice inoculated with a strain of T. cruzi II.
View Article and Find Full Text PDFFront Cell Infect Microbiol
July 2024
Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Uberlândia, Minas Gerais, Brazil.
P21 is a protein secreted by all forms of () with recognized biological activities determined in studies using the recombinant form of the protein. In our recent study, we found that the ablation of P21 gene decreased Y strain axenic epimastigotes multiplication and increased intracellular replication of amastigotes in HeLa cells infected with metacyclic trypomastigotes. In the present study, we investigated the effect of P21 using C2C12 cell lines infected with tissue culture-derived trypomastigotes (TCT) of wild-type and P21 knockout (TcP21) Y strain, and using an experimental model of infection in BALB/c mice.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!