[Progress in medical virology. I. Virus-cell interactions as the basis for the pathogenesis of virus diseases].
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Biomedical subjects
Publications and source records attributed to W Presber.
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The closely related phages T3 and T7 exhibit different growth patterns on Escherichia coli W hosts cells (E. coli K12 derivatives). T7 grows normally while T3 does not adsorb. T3hw mutants displaying a T7-like host range were isolated and described.
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When passaging phage T7 and SAMase-negative T3 mutants between E. coli strains with identical (EcoB) or without (EcoO) DNA host specificity, phenotypically a host-controlled modification and restriction is observed. This phenomenon is not due to "classical" modification and restriction of the bacteriophage DNA but depends on the reversibly altered adsorption capacity of the phages on the different host strains.
The intracellular growth of the phages T3 and T7 is restricted in the presence of the Escherichia coli prophage P1. Phage T3 has a higher ability to express its genome and to damage the host cell than T7. This partial protection of T3 against P1 restriction is due to the T3-coded SAMase, an enzyme which degrades S-adenosylmethionine, the cofactor of the P1 restriction endonuclease. Since we did not observe DNA cleavage in vivo, we conclude that the in vivo action of the P1 nuclease is limited to a SAM-dependent repressor-like binding to T3 and T7 DNA, while further reactions with the DNA (modification vs cleavage) are blocked.
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Certain differences between phage T3 on the one hand and T3sam- and T7 on the other hand indicate that the T3-coded SAMase function is responsible (i) for the development of the pseudolysogenic state by preventing T3 DNA methylation, and (ii) for the partial protection of the phage DNA against restriction by the P system.
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