大肠杆菌的宿主因子Hfq通过多聚腺苷酸聚合酶I刺激多聚腺苷酸尾的延长。
Host factor Hfq of Escherichia coli stimulates elongation of poly(A) tails by poly(A) polymerase I.
作者信息
Hajnsdorf E, Régnier P
机构信息
Institut de Biologie Physico-Chimique, 13 rue Pierre et Marie Curie, 75005 Paris, France.
出版信息
Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1501-5. doi: 10.1073/pnas.040549897.
Abstract
Current evidence suggests that the length of poly(A) tails of bacterial mRNAs result from a competition between poly(A) polymerase and exoribonucleases that attack the 3' ends of RNAs. Here, we show that host factor Hfq is also involved in poly(A) tail metabolism. Inactivation of the hfq gene reduces the length of poly(A) tails synthesized at the 3' end of the rpsO mRNA by poly(A) polymerase I in vivo. In vitro, Hfq stimulates synthesis of long tails by poly(A) polymerase I. The strong binding of Hfq to oligoadenylated RNA probably explains why it stimulates elongation of primers that already harbor tails of 20-35 A. Polyadenylation becomes processive in the presence of Hfq. The similar properties of Hfq and the PABPII poly(A) binding protein, which stimulates poly(A) tail elongation in mammals, indicates that similar mechanisms control poly(A) tail synthesis in prokaryotes and eukaryotes.
摘要
目前的证据表明，细菌mRNA的聚腺苷酸（poly(A)）尾长度是由聚(A)聚合酶和攻击RNA 3'末端的外切核糖核酸酶之间的竞争所导致的。在此，我们表明宿主因子Hfq也参与了聚(A)尾代谢。hfq基因的失活会降低体内聚(A)聚合酶I在rpsO mRNA 3'末端合成的聚(A)尾的长度。在体外，Hfq会刺激聚(A)聚合酶I合成长尾。Hfq与寡聚腺苷酸化RNA的强结合可能解释了它为何能刺激已带有20 - 35个A尾巴的引物的延伸。在Hfq存在的情况下，聚腺苷酸化变得具有持续性。Hfq与刺激哺乳动物中聚(A)尾延伸的PABPII聚(A)结合蛋白具有相似的特性，这表明原核生物和真核生物中控制聚(A)尾合成的机制相似。
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