Ribosome stalling regulates IRES-mediated translation in eukaryotes, a parallel to prokaryotic attenuation

被引:71
作者
Fernandez, J
Yaman, I
Huang, C
Liu, HY
Lopez, AB
Komar, AA
Caprara, MG
Merrick, WC
Snider, MD
Kaufman, RJ
Lamers, WH
Hatzoglou, M [1 ]
机构
[1] Case Western Reserve Univ, Sch Med, Dept Nutr, Cleveland, OH 44106 USA
[2] Case Western Reserve Univ, Sch Med, Dept Biochem, Cleveland, OH 44106 USA
[3] Case Western Reserve Univ, Sch Med, Dept Mol Biol & Microbiol, Cleveland, OH 44106 USA
[4] Univ Michigan, Med Ctr, Howard Hughes Med Inst, Ann Arbor, MI 48109 USA
[5] Sophia Childrens Univ Hosp, Dept Pediat Surg, Erasmus Med Ctr, Rotterdam, Netherlands
关键词
D O I
10.1016/j.molcel.2004.12.024
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It was previously shown that the mRNA for the cat-1 Arg/Lys transporter is translated from an internal ribosome entry site (IRES) that is regulated by cellular stress. Amino acid starvation stimulated cat-1 translation via a mechanism that requires translation of an ORF in the mRNA leader and remodeling of the leader to form an active IRES (the "zipper model" of translational control). It is shown here that slowing of the leader peptide elongation rate, either by cycloheximide or the introduction of rare codons, stimulated translation of the downstream ORF. These results suggest that ribosome stalling in the upstream ORF causes mRNA remodeling and formation of an active IRES. This control is reminiscent of translation attenuation in prokaryotic operons, where inhibition of translation elongation can regulate both mRNA translation and gene transcription by altering mRNA structure.
引用
收藏
页码:405 / 416
页数:12
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