莫洛尼鼠白血病病毒感染在体内不会增加琥珀酸终止密码子通读。
UAG readthrough is not increased in vivo by Moloney murine leukemia virus infection.
作者信息
Berteaux V, Rousset J P, Cassan M
机构信息
URA CNRS 1354, Université Paris 11, Orsay, France.
出版信息
Biochimie. 1991 Oct;73(10):1291-3. doi: 10.1016/0300-9084(91)90091-e.
Expression of the pol gene of the murine leukemia viruses is subject to translational control at the UAG termination codon of the upstream gene gag. Previous experiments have suggested that: i) Moloney murine leukemia virus infection induces a tRNA(Gln)iii) in an in vitro system using the tobacco mosaic virus as template, this tRNA is able to increase readthrough at the UAG codon [1]. Here we demonstrate that, in vivo, Moloney murine leukemia virus infection does not increase translational readthrough at either the tobacco mosaic virus or the Moloney murine leukemia virus UAG stop codons.
鼠白血病病毒pol基因的表达在上游基因gag的UAG终止密码子处受到翻译控制。先前的实验表明：i）莫洛尼鼠白血病病毒感染可诱导tRNA（Gln）iii）在以烟草花叶病毒为模板的体外系统中，这种tRNA能够增加UAG密码子处的通读[1]。在此我们证明，在体内，莫洛尼鼠白血病病毒感染不会增加烟草花叶病毒或莫洛尼鼠白血病病毒UAG终止密码子处的翻译通读。
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