A RIBOSOMAL AMBIGUITY MUTATION
A RIBOSOMAL AMBIGUITY MUTATION
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DOI:
10.1016/0022-2836(69)90336-2
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发表时间:
1969-01-01
影响因子:
5.6
通讯作者:
GORINI, L
中科院分区:
文献类型:
--
作者:
ROSSET, R;GORINI, L
The existence of a genetic determinantram‡for a 30 s ribosomal component controlling translation ambiguity has been demonstrated. It is located in thestrA(streptomycin sensitivity) region and is 99% cotransducible with thespc(spectinomycin sensitivity) gene.In vitro, rammutant ribosomes misread extensively and by interchanging the subunits oframandram+ribosomes it is shown that misreading is a property of the 30 s subunit.In vivo, therammutation confers on the cell the ability to suppress all three nonsense codons. Streptomycin induces a similar generalized ambiguity phenotypically bothin vitroandin vivo. The effects oframand of streptomycin are additive.Ambiguity caused byram, by streptomycin and by their combination is antagonizedin vivoandin vitroby additional mutations at thestrAlocus. Thus thestrA40(resistant competent) andstrA1(resistant incompetent) alleles increasingly restrict ribosomal (as well as tRNA) suppression and return to normal the reduced growth rate produced byrammutation in a wild-typestrA+strain. Growth is inhibited completely in aram1,strA+strain by sublethal doses of streptomycin and inram1,strA40strains by higher doses, while strainram1,strA1is indifferent to streptomycin. The bactericidal action of the drug is unrelated to these effects.