The trans -sialidase from the african trypanosome Trypanosoma brucei

2002 ◽  
Vol 269 (12) ◽  
pp. 2941-2950 ◽  
Author(s):  
Georgina Montagna ◽  
M. Laura Cremona ◽  
Gastón Paris ◽  
M. Fernanda Amaya ◽  
Alejandro Buschiazzo ◽  
...  
eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Harriet Lane-Serff ◽  
Paula MacGregor ◽  
Lori Peacock ◽  
Olivia JS Macleod ◽  
Christopher Kay ◽  
...  

The haptoglobin-haemoglobin receptor of the African trypanosome species, Trypanosoma brucei, is expressed when the parasite is in the bloodstream of the mammalian host, allowing it to acquire haem through the uptake of haptoglobin-haemoglobin complexes. Here we show that in Trypanosoma congolense this receptor is instead expressed in the epimastigote developmental stage that occurs in the tsetse fly, where it acts as a haemoglobin receptor. We also present the structure of the T. congolense receptor in complex with haemoglobin. This allows us to propose an evolutionary history for this receptor, charting the structural and cellular changes that took place as it adapted from a role in the insect to a new role in the mammalian host.


2000 ◽  
Vol 28 (5) ◽  
pp. 531-536 ◽  
Author(s):  
E. Hendriks ◽  
F. J. van Deursen ◽  
J. Wilson ◽  
M. Sarkar ◽  
M. Timms ◽  
...  

Differentiation between bloodstream and tsetse midgut procyclic forms during the life cycle of the African trypanosome is an attractive model for the analysis of stage-regulated events. In particular, this transformation occurs synchronously, there are well-defined markers for stage-regulated processes and cell lines with specific defects in differentiation have been identified. This combination of tools, combined with the developing Trypanosoma brucei genome database is allowing its underlying controls to be investigated at the molecular and cytological levels. This paper examines some recent discoveries that illuminate some of the key events during trypanosome life-cycle progression.


2012 ◽  
Vol 22 (5) ◽  
pp. 2151-2162 ◽  
Author(s):  
Houssou Raymond Fatondji ◽  
Salomé Kpoviessi ◽  
Fernand Gbaguidi ◽  
Joanne Bero ◽  
Veronique Hannaert ◽  
...  

1983 ◽  
Vol 209 (2) ◽  
pp. 481-487 ◽  
Author(s):  
G Allen ◽  
L P Gurnett

The locations of the six disulphide bonds and the single free cysteine residue in a variant surface glycoprotein, VSG 117, from the African trypanosome Trypanosoma brucei have been determined to be Cys-14-Cys-140, Cys-121-Cys-182, Cys-389-Cys-404, Cys-398-417, Cys-447-Cys-461 and Cys-455-Cys-468. Cys-244 bears the single thiol group, which is unreactive towards 2-nitro-5-thiocyanobenzoate in the native molecule and is probably buried. Biosynthetically incorporated [35S]cysteine aided the location of the disulphide bonds. Two proteinase-resistant glycosylated domains, each containing two disulphide bonds, were identified in the C-terminal region of the glycoprotein. Details of purification of [35S]cysteine-containing peptides, and Tables of amino acid analyses, are presented in Supplementary Publication SUP 50119 (32 pages), which has been deposited with the British Library Lending Division, Boston Spa, Wetherby, West Yorkshire LS23 7BQ, U.K., from whom copies can be obtained on the terms indicated in Biochem. J. (1981) 193,5.


2018 ◽  
Vol 24 (1) ◽  
pp. 125-148 ◽  
Author(s):  
Stephen John Bentley ◽  
Miebaka Jamabo ◽  
Aileen Boshoff

1999 ◽  
Vol 43 (4) ◽  
pp. 985-987 ◽  
Author(s):  
John M. Kelly ◽  
Michael A. Miles ◽  
Anita C. Skinner

ABSTRACT We report here that bloodstream forms of the African trypanosome,Trypanosoma brucei, are sensitive to the anti-influenza virus drug rimantadine (50% inhibitory concentration of 1.26 μg ml−1 at pH 7.4). The activity is pH dependent and is consistent with a mechanism involving inhibition of the ability to regulate internal pH. Rimantadine is also toxic to the trypanosomatid parasites Trypanosoma cruzi and Leishmania major.


2004 ◽  
Vol 199 (10) ◽  
pp. 1445-1450 ◽  
Author(s):  
Kisaburo Nagamune ◽  
Alvaro Acosta-Serrano ◽  
Haruki Uemura ◽  
Reto Brun ◽  
Christina Kunz-Renggli ◽  
...  

The African trypanosome Trypanosoma brucei, which causes sleeping sickness in humans and Nagana disease in livestock, is spread via blood-sucking Tsetse flies. In the fly's intestine, the trypanosomes survive digestive and trypanocidal environments, proliferate, and translocate into the salivary gland, where they become infectious to the next mammalian host. Here, we show that for successful survival in Tsetse flies, the trypanosomes use trans-sialidase to transfer sialic acids that they cannot synthesize from host's glycoconjugates to the glycosylphosphatidylinositols (GPIs), which are abundantly expressed on their surface. Trypanosomes lacking sialic acids due to a defective generation of GPI-anchored trans-sialidase could not survive in the intestine, but regained the ability to survive when sialylated by means of soluble trans-sialidase. Thus, surface sialic acids appear to protect the parasites from the digestive and trypanocidal environments in the midgut of Tsetse flies.


2000 ◽  
Vol 28 (5) ◽  
pp. 536-540 ◽  
Author(s):  
G. Rudenko

African trypanosomes have plastic genomes with extensive variability at the chromosome ends. The genes encoding the expressed major surface protein of the infective bloodstream form stages of Trypanosoma brucei and are located at telomeres. These telomeric expression-site transcription units are turning out to be surprisingly polymorphic in structure and sequence.


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