Grass D S, Manley J L
J Virol. 1987 Jul;61(7):2331-5. doi: 10.1128/JVI.61.7.2331-2335.1987.
We described previously a simian virus 40 (SV40) mutant, pSVAdL, that was defective in synthesis of the late viral protein VP1. This mutant, which contains a 100-base-pair fragment of adenovirus DNA encompassing the major late promoter inserted in the SV40 late promoter region (SV40 nucleotide 294), efficiently synthesizes agnoprotein, a protein encoded by the leader region of the same mRNA that encodes VP1. When the agnoprotein AUG initiation codon in pSVAdL was mutated to UUG, agnoprotein synthesis was abolished, and VP1 synthesis was elevated to wild-type levels. Because levels of late mRNA synthesis were not affected by this mutation, these results support a scanning model of translation initiation and suggest that internal translational reinitiation does not occur efficiently in this situation.
我们之前描述过一种猿猴病毒40(SV40)突变体pSVAdL,它在晚期病毒蛋白VP1的合成上存在缺陷。该突变体包含一段100个碱基对的腺病毒DNA片段,该片段包含插入到SV40晚期启动子区域(SV40核苷酸294)的主要晚期启动子,它能高效合成agnoprotein,agnoprotein是由与编码VP1的相同mRNA的前导区编码的一种蛋白质。当pSVAdL中的agnoprotein AUG起始密码子突变为UUG时,agnoprotein合成被消除,而VP1合成则升高到野生型水平。由于晚期mRNA合成水平不受此突变影响,这些结果支持翻译起始的扫描模型,并表明在这种情况下内部翻译重新起始不能有效发生。