Kolupaeva V G, Pestova T V, Hellen C U, Shatsky I N
A. N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, 119899 Moscow, Russia.
J Biol Chem. 1998 Jul 17;273(29):18599-604. doi: 10.1074/jbc.273.29.18599.
A complex of eukaryotic initiation factors (eIFs) 4A, 4E, and 4G (collectively termed eIF4F) plays a key role in recruiting mRNAs to ribosomes during translation initiation. The site of ribosomal entry onto most mRNAs is determined by interaction of the 5'-terminal cap with eIF4E; eIFs 4A and 4G may facilitate ribosomal entry by modifying mRNA structure near the cap and by interacting with ribosome-associated factors. eIF4G recruits uncapped encephalomyocarditis virus (EMCV) mRNA to ribosomes without the involvement of eIF4E by binding directly to the approximately 450-nucleotide long EMCV internal ribosome entry site (IRES). We have used chemical and enzymatic probing to map the eIF4G binding site to a structural element within the J-K domain of the EMCV IRES that consists of an oligo(A) loop at the junction of three helices. The oligo(A) loop itself is not sufficient to form stable complexes with eIF4G since alteration of its structural context abolished its interaction with eIF4G. Addition of wild type or trans-dominant mutant forms of eIF4A to binary IRES.eIF4G complexes did not further alter the pattern of chemical/enzymatic modification of the IRES.
真核生物起始因子(eIFs)4A、4E和4G的复合物(统称为eIF4F)在翻译起始过程中将mRNA募集到核糖体中发挥关键作用。核糖体进入大多数mRNA的位点由5'-末端帽与eIF4E的相互作用决定;eIFs 4A和4G可能通过修饰帽附近的mRNA结构以及与核糖体相关因子相互作用来促进核糖体进入。eIF4G通过直接结合约450个核苷酸长的脑心肌炎病毒(EMCV)内部核糖体进入位点(IRES),在不涉及eIF4E的情况下将无帽的EMCV mRNA募集到核糖体。我们使用化学和酶促探测将eIF4G结合位点定位到EMCV IRES的J-K结构域内的一个结构元件上,该元件由三个螺旋交界处的一个寡聚(A)环组成。寡聚(A)环本身不足以与eIF4G形成稳定的复合物,因为其结构背景的改变消除了它与eIF4G的相互作用。向二元IRES.eIF4G复合物中添加野生型或反式显性突变形式的eIF4A并没有进一步改变IRES的化学/酶促修饰模式。