Clinton G M, Little S P, Hagen F S, Huang A S
Cell. 1978 Dec;15(4):1455-62. doi: 10.1016/0092-8674(78)90069-7.
Temperature-sensitive mutants of vesicular stomatitis virus (VSV) belonging to complementation group III contain a lesion in the matrix (M) protein. This results in a 2--5 fold increase in transcription at the nonpermissive temperature. Co-infection of cells with one of these mutants and wild-type virus reverses this mutant phenotype. Separation of the transcriptional and translational products from mutant-infected cells reveals an overall increase in each of the viral mRNA species concomitant with degradation of the M protein at the nonpermissive temperature. The increase in mRNA, however, does not lead to increased synthesis of viral proteins. Quantitation of individual mRNA species indicates that M protein acts as a direct inhibitor of transcription as well as an attenuator of sequential transcription.
属于互补组III的水泡性口炎病毒(VSV)温度敏感突变体在基质(M)蛋白中存在损伤。这导致在非允许温度下转录增加2至5倍。用这些突变体之一与野生型病毒共同感染细胞可逆转这种突变体表型。从突变体感染的细胞中分离转录和翻译产物发现,在非允许温度下,每种病毒mRNA种类总体增加,同时M蛋白降解。然而,mRNA的增加并未导致病毒蛋白合成增加。对单个mRNA种类的定量分析表明,M蛋白既是转录的直接抑制剂,也是连续转录的衰减剂。