ABSTRACT
In a previous study, the Schistosoma mansoni Rho1 protein was able to complement Rho1 null mutant Saccharomyces cerevisiae cells at restrictive temperatures and under osmotic stress (low calcium concentration) better than the human homologue (RhoA). It is known that under osmotic stress, the S. cerevisiae Rho1 triggers two distinct pathways: activation of the membrane 1,3-beta-glucan synthase enzymatic complex and activation of the protein kinase C1 signal transduction pathway, promoting the transcription of response genes. In the present work the SmRho1 protein and its mutants smrho1E97P, smrho1L101T, and smrho1E97P, L101T were used to try to clarify the basis for the differential complementation of Rho1 knockout yeast strain by the human and S. mansoni genes. Experiments of functional complementation in the presence of caffeine and in the presence of the osmotic regulator sorbitol were conducted. SmRho1 and its mutants showed a differential complementation of the yeast cells in the presence of caffeine, since smrho1E97P and smrho1E97P, L101T mutants showed a delay in the growth when compared to the yeast complemented with the wild type SmRho1. However, in the presence of sorbitol and caffeine the wild type SmRho1 and mutants showed a similar complementation phenotype, as they allowed yeast growth in all caffeine concentrations tested.
Subject(s)
Animals , Humans , Caffeine/pharmacology , Protein Kinase C/genetics , Saccharomyces cerevisiae Proteins/genetics , Saccharomyces cerevisiae/genetics , Schistosoma mansoni/genetics , rho GTP-Binding Proteins/genetics , Genes, Helminth , Mutation , Saccharomyces cerevisiae Proteins/metabolism , Saccharomyces cerevisiae/drug effects , Saccharomyces cerevisiae/metabolism , Schistosoma mansoni/metabolism , Signal Transduction/genetics , rho GTP-Binding Proteins/metabolismABSTRACT
Chagas disease, caused by the protozoan Trypanosoma cruzi, has a variable clinical course, ranging from symptomless infection to severe chronic disease with cardiovascular or gastrointestinal involvement or, occasionally, overwhelming acute episodes. The factors influencing this clinical variability have not been elucidated, but it is likely that the genetic variability of both the host and the parasite are of importance. In this work we review the the genetic structure of T. cruzi populations and analyze the importance of genetic variation of the parasite in the pathogenesis of the disease under the light of the histotropic-clonal model.
Subject(s)
Animals , Humans , Chagas Disease , Trypanosoma cruzi , Chagas Disease , Genetic Variation , Host-Parasite Interactions , Trypanosoma cruziABSTRACT
Se presenta una serie de seis casos operados por angiomas cavernosos del tronco cerebral. Todos ellos habían sangrado por lo menos una vez y tenían compromiso neurológico moderado y severo. El diagnóstico en todos los casos fue por resonancia magnética y confirmado con el estudio anatomopatológico de la lesión. La presentación clínica, los hallazgos quirúrgicos y la evolución son similares a los ya establecidos. La evaluación fue favorable en cinco casos. Hubo una muerte por complicaciones propias de la gravedad, pero sin haber sufrido agravacion posoperatoria. Se hace hincapié en los beneficios de la cirugía a pesar de la gravedad que pueden presentar los episodios hemorrágicos de los angiomas