INVESTIGADORES
PEREIRA Claudio Alejandro
congresos y reuniones científicas
Título:
Inhibition of Trypanosoma brucei arginine kinase gene expression by RNA interference.
Autor/es:
PEREIRA, CA; GINGER, MICHAEL; BOUVIER, LEON; TORRES, HECTOR; GULL, KEITH
Lugar:
Bariloche
Reunión:
Congreso; XXXIX Reunion anual Sociedad Argentina de Investigacion Bioquimica y Biologia Molecular.; 2003
Resumen:
Arginine kinase catalyzes the reversible transphosphorylation
between ADP and phosphoarginine, which is involved in temporal
and spatial ATP buffering. The molecular and biochemical
characterization of arginine kinase in Trypanosoma cruzi has been
reported by our laboratory. Here, we report that three distinct
arginine kinase genes are expressed by the African trypanosome
reported by our laboratory. Here, we report that three distinct
arginine kinase genes are expressed by the African trypanosome
Trypanosoma cruzi has been
reported by our laboratory. Here, we report that three distinct
arginine kinase genes are expressed by the African trypanosome
T. brucei. The three genes are clustered together in chromosome
IX and show a high degree of identity with one another, suggesting
that the family has evolved following a tandem duplication event.
The three proteins differ only in the nature of their N and C termini
raising the possibility that each gene is targeted to a different
cellular site or provide different cellular functions. Interestingly,
although the expression of all three genes in procyclic
trypanosomes can be efficiently silenced by RNAi, using a 400 bp
fragment common to all three genes, our initial phenotype studies
show there is no growth phenotype in the RNA knockdown mutants.
Nor do these mutants show an increased sensitivity towards sodium
azide, an inhibitor of the classical respiratory chain, or SHAM
which is an inhibitor of trypanosome alternative oxidase.
IX and show a high degree of identity with one another, suggesting
that the family has evolved following a tandem duplication event.
The three proteins differ only in the nature of their N and C termini
raising the possibility that each gene is targeted to a different
cellular site or provide different cellular functions. Interestingly,
although the expression of all three genes in procyclic
trypanosomes can be efficiently silenced by RNAi, using a 400 bp
fragment common to all three genes, our initial phenotype studies
show there is no growth phenotype in the RNA knockdown mutants.
Nor do these mutants show an increased sensitivity towards sodium
azide, an inhibitor of the classical respiratory chain, or SHAM
which is an inhibitor of trypanosome alternative oxidase.
. The three genes are clustered together in chromosome
IX and show a high degree of identity with one another, suggesting
that the family has evolved following a tandem duplication event.
The three proteins differ only in the nature of their N and C termini
raising the possibility that each gene is targeted to a different
cellular site or provide different cellular functions. Interestingly,
although the expression of all three genes in procyclic
trypanosomes can be efficiently silenced by RNAi, using a 400 bp
fragment common to all three genes, our initial phenotype studies
show there is no growth phenotype in the RNA knockdown mutants.
Nor do these mutants show an increased sensitivity towards sodium
azide, an inhibitor of the classical respiratory chain, or SHAM
which is an inhibitor of trypanosome alternative oxidase.