Sachs A B, Davis R W
Department of Biochemistry, Stanford University Medical Center, California 94305.
Cell. 1989 Sep 8;58(5):857-67. doi: 10.1016/0092-8674(89)90938-0.
Depletion of the essential poly(A) binding protein (PAB) in S. cerevisiae by promoter inactivation or by the utilization of a temperature-sensitive mutation (pab1-F364L) results in the inhibition of translation initiation and poly(A) tail shortening. Reversion analysis of pab1-F364L yielded seven independent, extragenic cold-sensitive mutations (spb1-spb7) that also suppress a PAB1 deletion. These mutations allow translation initiation without significantly changing poly(A) tail lengths in the absence of PAB, and they affect the amount of 60S ribosomal subunit. Consistent with this, SPB2 encodes the ribosomal protein L46. These data suggest that the 60S subunit mediates the PAB requirement of translation initiation, thereby ensuring that only intact poly(A)+ mRNA will be translated efficiently in vivo.
通过启动子失活或利用温度敏感突变（pab1-F364L）使酿酒酵母中的必需多聚腺苷酸结合蛋白（PAB）耗竭，会导致翻译起始受到抑制以及多聚腺苷酸尾缩短。对pab1-F364L进行回复分析产生了7个独立的基因外冷敏感突变（spb1-spb7），这些突变也能抑制PAB1缺失。这些突变在没有PAB的情况下允许翻译起始，而不会显著改变多聚腺苷酸尾的长度，并且它们会影响60S核糖体亚基的量。与此一致的是，SPB2编码核糖体蛋白L46。这些数据表明，60S亚基介导了翻译起始对PAB的需求，从而确保只有完整的多聚腺苷酸加尾（poly(A)+）mRNA能在体内被有效翻译。
