Memoirs: A Study of the Mitochondria of Trypanosomes

1940 ◽  
Vol s2-82 (326) ◽  
pp. 261-266
Author(s):  
ROBERT M. WOTTON

Mitochondria have been demonstrated in the adult forms of the following species of trypanosomes: Trypanosoma lewisi, Trypanosoma duttoni, Trypanosoma cruzi, and Trypanosoma equiperdum. They have been shown also in the crithidial forms of Trypanosoma cruzi from culture, and of Trypanosoma melophagium from the insect vector, Melophagus ovinus. No essential morphological variations in the mitochondria among the five species of trypanosomes studied, nor in those among the several growth stages, were observed.

1984 ◽  
Vol 79 (4) ◽  
pp. 513-515 ◽  
Author(s):  
Maria P. Deane ◽  
Henrique L. Lenzi ◽  
Ana Jansen

Epimastigotes multiplying extracellularly and metacyclic trypomastigotes, stages that correspond to the cycle of Trypanosoma cruzi in the intestinal lumen of its insect vector, were consistently found in the lumen of the anal glands of opossums Didelphis marsupialis inoculated subcutaneously with infective feces of triatomid bugs.


1993 ◽  
Vol 106 (4) ◽  
pp. 1023-1033 ◽  
Author(s):  
A.R. de Jesus ◽  
R. Cooper ◽  
M. Espinosa ◽  
J.E. Gomes ◽  
E.S. Garcia ◽  
...  

We have explored the biological function of a surface glycoprotein (GP72) of Trypanosoma cruzi by studying a null mutant parasite, generated by targeted gene deletion. GP72 deletion affected parasite morphology in several stages of the life cycle. Insect midgut (epimastigote) forms had a detached flagellum (apomastigote) in the null mutant. The abnormal flagellar phenotype persisted during development of the infective (metacyclic) forms but there was no impairment in the acquisition of complement resistance, sialidase expression or cell infectivity. The GP72 null mutant could efficiently infect and proliferate in mouse macrophages and non-phagocytic L6E9 cells. The mammalian stages of the life cycle also showed major morphological abnormalities. During early subcultures in L6E9 cells, few extracellular fully flagellated forms, expressing markers characteristic of trypomastigotes, were seen. The extracellular population consisted almost exclusively of rounded forms with short flagella (micromastigote), which expressed an amastigote-specific surface marker and no sialidase. The propagation of the parasite was not affected, despite the apparent lack of the trypomastigote forms, which are thought to be primarily responsible for cell invasion. After some subcultures, the extracellular population changed to about equal numbers of micromastigotes and a range of flagellated forms that still did not include true trypomastigotes. Instead, the kinetoplast remained close to the nucleus and the flagellum emerged from the middle of the cell (mesomastigote). Half of the flagellum adhered to the cell body and the remainder was free at the anterior end. In Triatoma infestans, the survival of the mutant was dramatically reduced, suggesting that either GP72 itself, or the altered properties of the flagellum, were critical for establishment in the insect vector.


Parasitology ◽  
2012 ◽  
Vol 139 (6) ◽  
pp. 735-743 ◽  
Author(s):  
F. O. R. OLIVEIRA ◽  
C. R. ALVES ◽  
F. SOUZA-SILVA ◽  
C. M. CALVET ◽  
L. M. C. CÔRTES ◽  
...  

SUMMARYHeparin-binding proteins (HBPs) have been demonstrated in both infective forms of Trypanosoma cruzi and are involved in the recognition and invasion of mammalian cells. In this study, we evaluated the potential biological function of these proteins during the parasite-vector interaction. HBPs, with molecular masses of 65·8 kDa and 59 kDa, were isolated from epimastigotes by heparin affinity chromatography and identified by biotin-conjugated sulfated glycosaminoglycans (GAGs). Surface plasmon resonance biosensor analysis demonstrated stable receptor-ligand binding based on the association and dissociation values. Pre-incubation of epimastigotes with GAGs led to an inhibition of parasite binding to immobilized heparin. Competition assays were performed to evaluate the role of the HBP-GAG interaction in the recognition and adhesion of epimastigotes to midgut epithelial cells of Rhodnius prolixus. Epithelial cells pre-incubated with HBPs yielded a 3·8-fold inhibition in the adhesion of epimastigotes. The pre-treatment of epimastigotes with heparin, heparan sulfate and chondroitin sulfate significantly inhibited parasite adhesion to midgut epithelial cells, which was confirmed by scanning electron microscopy. We provide evidence that heparin-binding proteins are found on the surface of T. cruzi epimastigotes and demonstrate their key role in the recognition of sulfated GAGs on the surface of midgut epithelial cells of the insect vector.


1995 ◽  
Vol 81 (3) ◽  
pp. 255-261 ◽  
Author(s):  
E.S. Garcia ◽  
M.S. Gonzalez ◽  
P. Deazambuja ◽  
F.E. Baralle ◽  
D. Fraidenraich ◽  
...  

Glycobiology ◽  
1995 ◽  
Vol 5 (6) ◽  
pp. 625-631 ◽  
Author(s):  
Rogerio Amino ◽  
Alvaro Acosta Serrano ◽  
Olga M. Morita ◽  
Vera Lucia Pereira-Chioccola ◽  
Sergio Schenkman

2021 ◽  
Author(s):  
Brian S Mantilla ◽  
Lisvane Paes-Vieira ◽  
Felipe Almeida Dias ◽  
Simone G. Caldeirano ◽  
Maria Carolina Elias ◽  
...  

The pathogenic protist Trypanosoma cruzi uses kissing bugs as intermediate hosts that vectorize the infection among mammals. This parasite oxidizes proline to glutamate through two enzymatic steps and one nonenzymatic step. In insect vectors, T. cruzi differentiates from a noninfective replicating form to nonproliferative infective forms. Proline sustains this differentiation, but to date, a link between proline metabolism and differentiation has not been established. In T. cruzi, the enzymatic steps of the proline-glutamate oxidation pathway are catalysed exclusively by the mitochondrial enzymes proline dehydrogenase [TcPRODH, EC: 1.5.5.2] and D1-pyrroline-5-carboxylate dehydrogenase [TcP5CDH, EC: 1.2.1.88]. Both enzymatic steps produce reducing equivalents that are able to directly feed the mitochondrial electron transport chain (ETC) and thus produce ATP. In this study, we demonstrate the contribution of each enzyme of the proline-glutamate pathway to ATP production. In addition, we show that parasites overexpressing these enzymes produce increased levels of H2O2, but only those overexpressing TcP5CDH produce increased levels of superoxide anion. We show that parasites overexpressing TcPRODH, but not parasites overexpressing TcP5CDH, exhibit a higher rate of differentiation into metacyclic trypomastigotes in vitro. Finally, insect hosts infected with parasites overexpressing TcPRODH showed a diminished parasitic load but a higher percent of metacyclic trypomastigotes, when compared with controls. Our data show that parasites overexpressing both, PRODH and P5CDH had increased mitochondrial functions that orchestrated different oxygen signalling, resulting in different outcomes in relation to the efficiency of parasitic differentiation in the invertebrate host.


2017 ◽  
Vol 70 ◽  
pp. 320
Author(s):  
J.N. Furlong ◽  
J. Vereijssen ◽  
A.R. Pitman ◽  
R.C. Butler

Since its 2006 detection in New Zealand, the tomato potato psyllid (TPP), Bactericera cockerelli, has been responsible for yield and quality-reducing damage to potatoes as well as to other solanaceous crops. TPP is best known as the insect vector for the zebra chip disease-associated bacterium Candidatus Liberibacter solanacearum (CLso), but feeding by CLso-negative TPP on potatoes is also linked to damaging effects. An improved understanding of which potato plant physiological stages are most affected by feeding of CLso-negative TPP will allow for more directed integrated pest management (IPM) plans. As part of a two-year repeated eld study to assess the effect of TPP feeding timing on potatoes, CLso-negative TPP were released into mesh cages over outdoor potato (‘Moonlight’) plantings at ve different growth stages: post-emergence, owering, post- owering, late-season, and pre-harvest. Tubers were grouped by plant at harvest. (Un)marketable numbers and weights, marketable dry matter and zebra chip severity were determined. Results from this trial and other shadehouse trials conducted previously are still being analysed but have the potential to better target IPM plans and reduce costly, labour-intensive, and environmentally impactful pesticide spray use, which is currently relied on heavily throughout growing seasons.


Pathogens ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 661
Author(s):  
Juana P. Correa ◽  
Antonella Bacigalupo ◽  
Esteban Yefi-Quinteros ◽  
Gemma Rojo ◽  
Aldo Solari ◽  
...  

We present a review on the natural infection by trypanosomatids of nonhuman vertebrates in Chile, aiming to synthesize and update the knowledge on the diversity of trypanosomatids infecting native and alien vertebrate species. To this end, we conducted a systematic review of literature records published from 1900 to April 2020 on four databases, focusing on the 21 genera of trypanosomatids and Chile. The methods and findings of our review have been based on the preferred reporting items for systematic reviews and meta-analysis (prisma) checklist. We found 29,756 records but only 71 presented relevant information for this review. Overall, there are only two reported trypanosomatid genera infecting vertebrate species in Chile, the genera Trypanosoma and Leishmania. The former is mostly represented by Trypanosoma cruzi (90% of the total records) and to a much lesser extent by Trypanosoma avium, Trypanosoma humboldti, Trypanosoma lewisi, and a couple of unidentified trypanosomatids. A total of 25 mammals have been reported as being infected by T. cruzi, including 14 native and 11 alien species from Orders Artiodactyla, Carnivora, Chiroptera, Didelphimorphia, Lagomorpha, Perissodactyla, and Rodentia. Extensive screening studies using new analytical tools are necessary to grasp the whole potential diversity of trypanosomatid species infecting vertebrates in Chile.


2007 ◽  
Vol 76 (1) ◽  
pp. 443-451 ◽  
Author(s):  
M. Paola Zago ◽  
Alejandra B. Barrio ◽  
Rubén M. Cardozo ◽  
Tomás Duffy ◽  
Alejandro G. Schijman ◽  
...  

ABSTRACT Trypanosoma cruzi infection of host cells is a complex process in which many proteins participate but only a few of these proteins have been identified experimentally. One parasite factor likely to be involved is the protein product of LYT1, a single-copy gene cloned, sequenced, and characterized by Manning-Cela et al. (Infect. Immun. 69:3916-3923, 2001). This gene was potentially associated with infectivity, since the deletion of both LYT1 alleles in the CL Brenner strain (the wild type [WT]) resulted in a null mutant T. cruzi clone (L16) that shows an attenuated phenotype in cell culture models. The aim of this work was to characterize the infective behavior of L16 in the insect vector and murine models. The infection of adult Swiss mice with 103 trypomastigotes of both clones revealed a significant reduction in infective behavior of L16, as shown by direct parasitemia, spleen index, and quantitation of tissue parasite burden, suggesting the loss of virulence in the null mutant clone. Although L16 blood counts were almost undetectable, blood-based PCRs indicated the presence of latent and persistent infection during all of the study period and epimastigotes were reisolated from hemocultures until 12 months postinfection. Nevertheless, virulence was not restored in L16 by serial passages in mice, and reisolated parasites lacking the LYT1 gene and bearing the antibiotic resistance genes revealed the stability of the genetic manipulation. Histopathological studies showed a strong diminution in the muscle inflammatory response triggered by L16 compared to that triggered by the WT group, consistent with a lower tissue parasite load. A strong protection against a virulent challenge in both L16- and WT-infected mice was observed; however, the immunizing infection by the genetically modified parasite was highly attenuated.


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