Trypanosoma cruzi: High ribosomal resistance to trichosanthin inactivation

Trypanosoma cruzi is the parasite causing Chagas Disease. Several results already published suggest that T. cruzi ribosomes have remarkable differences with their mammalian counterparts. In the present work, we showed that trypanosomatid (T. cruzi and Crithidia fasciculata) ribosomes are highly resi...

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Detalles Bibliográficos
Autores: Juri Ayub, Maximiliano, Ma, Kit-Wan, Shaw, Pang-Chui, Wong, Kam-Bo
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2008
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/125061
Acceso en línea:http://hdl.handle.net/11336/125061
Access Level:acceso abierto
Palabra clave:CHAGAS DISEASE
PROTEIN SYNTHESIS
RIBOSOME-INACTIVATING PROTEIN (RIP)
TRICHOSANTHIN
TRYPANOSOMA
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
Descripción
Sumario:Trypanosoma cruzi is the parasite causing Chagas Disease. Several results already published suggest that T. cruzi ribosomes have remarkable differences with their mammalian counterparts. In the present work, we showed that trypanosomatid (T. cruzi and Crithidia fasciculata) ribosomes are highly resistant to inactivation by trichosanthin (TCS), which is active against mammalian ribosomes. Differential resistance is an intrinsic feature of the ribosomal particles, as demonstrated by using assays where the only variable was the ribosomes source. Because we have recently described that TCS interacts with the acidic C-terminal end of mammalian ribosomal P proteins, we assayed the effect of a TCS variant, which is unable to interact with P proteins, on trypanosomatid ribosomes. This mutant showed similar shifting of IC50 values on rat, T. cruzi and C. fasciculata ribosomes, suggesting that the resistance mechanism might involve other ribosomal components rather than the C-terminal end of P proteins.