Host mutant (tabD)-induced inhibition of bacteriophage T4 late transcription

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Abstract In this paper we show that the tab D mutants, selected with ts 553 or ts CB53, and described in the accompanying paper (Coppo et al. , 1975): (a) are recessive to tab + ; (b) fail to complement each other, and thus map in the same cistron; (c) by their linkage to rif and their dominance relationships with well characterized amber mutations in the Escherichia coli RNA polymerase operon, probably all map in the gene controlling the synthesis of the β′ subunit of the enzyme. We also describe the isolation of a ts + , k D mutant in phage T4 gene 55, used in the selection of a new tab D mutant ( tab D k292 ). This tab mutant: (a) generates a defective phenotype which differs somewhat from that of the other tab D mutants; (b) complements the other tab D mutants; (c) by its dominance relationship to amber mutants in the RNA polymerase operon, can be assigned to the structural gene coding for the β subunit of the enzyme. A new type of interaction between T4 genes 55 and 45 is also described. The k D properties of ts 553 (gene 55) are suppressed at 30 °C, by a temperature-sensitive mutation in gene 45. This type of interaction between missense mutations in genes 45 and 55 apparently occurs even in tab + strains, since temperature-sensitive mutations in gene 45 accumulate in lysates of two gene 55 mutants ( ts 553 and ts A81).

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