Laboratoire de Génétique de l'Université Paris-Sud, Centre d'Orsay (laboratoire associé au CNRS No 86), Bâtiment 400, F 91405, Orsay, France.
Curr Genet. 1982 May;5(1):57-63. doi: 10.1007/BF00445742.
The hypersensitivity to paromomycin dis played by the su 1-60 suppressor, which was thought to be a ribosomal ambiguity mutation, was used to isolate a new antisuppressor, AS 71. This antisuppressor is not specific for ribosomal suppressors, since it is able to act on putative tRNA-type suppressors. Compared to the wild-type, the AS 7-1 mutation produces an increased resistance to paromomycin. In addition, it was found to stop the sporulation process. In the polyuridylic acid-dependant assay, the paromomycin induced misreading was shown to be higher on su 1-60 ribosomes and lower on ribosomes from AS 7-1 mutant and AS 7S-1-su 1-60 double mutant than on wild-type ribosomes. These data confirm that su 1-60 and AS 7-1 mutants are ribosomal mutants involved in the control of translational fidelity.
苏氨酸 1-60 抑制子所表现出的对巴龙霉素的超敏性被认为是一种核糖体模糊突变,利用这种超敏性分离到一种新的反抑制子 AS71。这种反抑制子并非特异性针对核糖体抑制子,因为它能够作用于假定的 tRNA 型抑制子。与野生型相比,AS7-1 突变使对巴龙霉素的抗性增加。此外,还发现它能够阻止孢子形成过程。在多聚尿嘧啶核苷酸依赖性测定中,巴龙霉素诱导的误读在 su1-60 核糖体上更高,在 AS7-1 突变体和 AS7S-1-su1-60 双突变体的核糖体上更低,而在野生型核糖体上则更低。这些数据证实 su1-60 和 AS7-1 突变体是参与控制翻译保真度的核糖体突变体。