Seiberg M, Aloni Y, Levine A J
Department of Genetics, Weizmann Institute of Science, Rehovot, Israel.
J Virol. 1989 Mar;63(3):1134-41. doi: 10.1128/JVI.63.3.1134-1141.1989.
The adenovirus 72-kilodalton DNA-binding protein (DBP) binds to the attenuated RNA derived from the viral major late promoter. Protection from T1 RNase digestion can be observed when DBP is incubated with attenuated RNA. By using attenuated RNA labeled at one end, the T1 RNase digestion pattern can be mapped to residues located at specific sites in this RNA. Heterologous competitor RNAs do not alter the pattern of DBP protection of a labeled attenuated RNA, as does the identical attenuated RNA. These data indicate some specificity of the interaction between DBP and attenuated RNA. Adenovirus infection of monkey cells results in a more efficient attenuation of RNA initiated at the major late promoter and a reduced level of infectious virus. Adenovirus mutations in DBP relieve this restriction. These DBP mutant proteins do not change their binding properties to the attenuated RNA but suggest a mechanism by which DBP plays a role in the adenovirus host range restriction in monkey cells.
腺病毒72千道尔顿DNA结合蛋白(DBP)与源自病毒主要晚期启动子的弱化RNA结合。当DBP与弱化RNA一起孵育时,可以观察到对T1核糖核酸酶消化的保护作用。通过使用一端标记的弱化RNA,可以将T1核糖核酸酶消化模式映射到该RNA中特定位点的残基上。异源竞争RNA不会像相同的弱化RNA那样改变DBP对标记的弱化RNA的保护模式。这些数据表明DBP与弱化RNA之间的相互作用具有一定的特异性。腺病毒感染猴细胞会导致在主要晚期启动子起始的RNA更有效地弱化,以及感染性病毒水平降低。DBP中的腺病毒突变可缓解这种限制。这些DBP突变蛋白对弱化RNA的结合特性没有改变,但提示了一种DBP在猴细胞腺病毒宿主范围限制中发挥作用的机制。