RESUMO
Deinococcus radiodurans is extraordinarily resistant to DNA damage, because of its unusually efficient DNA repair processes. The mtcA+ and mtcB+ genes of D. radiodurans, both implicated in excision repair, have been cloned and sequenced, showing that they are a single gene, highly homologous to the uvrA+ genes of other bacteria. The Escherichia coli uvrA+ gene was expressed in mtcA and mtcB strains, and it produced a high degree of complementation of the repair defect in these strains, suggesting that the UvrA protein of D. radiodurans is necessary but not sufficient to produce extreme DNA damage resistance. Upstream of the uvrA+ gene are two large open reading frames, both of which are directionally divergent from the uvrA+ gene. Evidence is presented that the proximal of these open reading frames may be irrB+.
Assuntos
Adenosina Trifosfatases/genética , Proteínas de Bactérias/genética , Reparo do DNA/genética , Proteínas de Ligação a DNA/genética , Proteínas de Escherichia coli , Escherichia coli/genética , Genes Bacterianos , Cocos Gram-Positivos/genética , Adenosina Trifosfatases/química , Sequência de Aminoácidos , Proteínas de Bactérias/química , Sequência de Bases , Proteínas de Ligação a DNA/química , Vetores Genéticos , Cocos Gram-Positivos/fisiologia , Immunoblotting , Micrococcus/genética , Micrococcus/fisiologia , Dados de Sequência Molecular , Fases de Leitura Aberta , Alinhamento de Sequência , Transformação BacterianaRESUMO
Interferon (IFN) can either prevent or exacerbate the pathogenic effects of the diabetogenic variant of encephalomyocarditis (EMC-D) virus. The effect seen is dependent upon the mouse strain and the time of IFN administration. For example, IFN-alpha beta protects SWR/J but not ICR Swiss male mice against the diabetogenic effects of the virus. Administration of either IFN-alpha beta or the IFN-inducer poly(I):poly(C) 4 days post infection, results in an exacerbation of the infection in ICR Swiss and C57BL/6 male mice. Studies have been initiated to investigate the role of the IFN system in the pathogenesis of this virus infection. In this study IFNs or poly(I):poly(C) were administered to several mouse strains at 24 h before or 4 days after infection with EMC-D virus. The results of such treatment ranged from complete protection of the animals from the diabetogenic effects of the virus to exacerbation of the infection as reflected by the virus content in selected organs. The effect was dependent upon the mouse strain, the type of IFN, and the time of its administration in relation to virus infection.
