Singh Chingakham Ranjit, Udagawa Tsuyoshi, Lee Bumjun, Wassink Sarah, He Hui, Yamamoto Yasufumi, Anderson James T, Pavitt Graham D, Asano Katsura
Molecular Cellular and Developmental Biology Program, Division of Biology, Kansas State University, Manhattan, KS 66506, USA.
J Mol Biol. 2007 Jul 6;370(2):315-30. doi: 10.1016/j.jmb.2007.04.034. Epub 2007 Apr 19.
In eukaryotic translation initiation, eIF2GTP-Met-tRNA(i)(Met) ternary complex (TC) interacts with eIF3-eIF1-eIF5 complex to form the multifactor complex (MFC), while eIF2GDP associates with eIF2B for guanine nucleotide exchange. Gcn2p phosphorylates eIF2 to inhibit eIF2B. Here we evaluate the abundance of eIFs and their pre-initiation intermediate complexes in gcn2 deletion mutant grown under different conditions. We show that ribosomes are three times as abundant as eIF1, eIF2 and eIF5, while eIF3 is half as abundant as the latter three and hence, the limiting component in MFC formation. By quantitative immunoprecipitation, we estimate that approximately 15% of the cellular eIF2 is found in TC during rapid growth in a complex rich medium. Most of the TC is found in MFC, and important, approximately 40% of the total eIF2 is associated with eIF5 but lacks tRNA(i)(Met). When the gcn2Delta mutant grows less rapidly in a defined complete medium, TC abundance increases threefold without altering the abundance of each individual factor. Interestingly, the TC increase is suppressed by eIF5 overexpression and Gcn2p expression. Thus, eIF2B-catalyzed TC formation appears to be fine-tuned by eIF2 phosphorylation and the novel eIF2/eIF5 complex lacking tRNA(i)(Met).
在真核生物翻译起始过程中,eIF2GTP-甲硫氨酰-tRNA(i)(Met)三元复合物(TC)与eIF3-eIF1-eIF5复合物相互作用形成多因子复合物(MFC),而eIF2GDP则与eIF2B结合以进行鸟嘌呤核苷酸交换。Gcn2p使eIF2磷酸化以抑制eIF2B。在此,我们评估了在不同条件下生长的gcn2缺失突变体中eIFs及其起始前中间复合物的丰度。我们发现核糖体的丰度是eIF1、eIF2和eIF5的三倍,而eIF3的丰度是后三者的一半,因此是MFC形成中的限制成分。通过定量免疫沉淀,我们估计在富含复合物的培养基中快速生长期间,细胞中约15%的eIF2存在于TC中。大部分TC存在于MFC中,重要的是,约40%的总eIF2与eIF5结合但缺乏tRNA(i)(Met)。当gcn2Delta突变体在限定的完全培养基中生长较慢时,TC丰度增加三倍,而不改变每个单独因子的丰度。有趣的是,eIF5过表达和Gcn2p表达可抑制TC的增加。因此,eIF2B催化的TC形成似乎通过eIF2磷酸化和缺乏tRNA(i)(Met)的新型eIF2/eIF5复合物进行微调。