The surveillance complex interacts with the translation release factors to enhance termination and degrade aberrant mRNAs

被引:305
作者
Czaplinski, K
Ruiz-Echevarria, MJ
Paushkin, SV
Han, X
Weng, YM
Perlick, HA
Dietz, HC
Ter-Avanesyan, MD
Peltz, SW [1 ]
机构
[1] Rutgers State Univ, Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Mol Genet & Microbiol, Piscataway, NJ 08855 USA
[2] Rutgers State Univ, Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Grad Program Mol Biosci, Piscataway, NJ 08855 USA
[3] Cardiol Res Ctr, Inst Expt Cardiol, Moscow 121552, Russia
[4] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA
[5] Johns Hopkins Univ, Ctr Med Genet, Dept Pediat Med & Genet, Baltimore, MD 21205 USA
[6] Canc Inst New Jersey, Piscataway, NJ 08854 USA
关键词
mRNA decay; translation termination; release factors; nonsense mutation; ribosome; mRNA surveillance;
D O I
10.1101/gad.12.11.1665
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The nonsense-mediated mRNA decay pathway is an example of an evolutionarily conserved surveillance pathway that rids the cell of transcripts that contain nonsense mutations. The product of the UPF1 gene is a necessary component of the putative surveillance complex that recognizes and degrades aberrant mRNAs. Recent results indicate that the Upf1p also enhances translation termination at a nonsense codon. The results presented here demonstrate that the yeast and human forms of the Upf1p interact with both eukaryotic translation termination factors eRF1 and eRF3. Consistent with Upf1p interacting with the eRFs, the Upf1p is found in the prion-like aggregates that contain eRF1 and eRF3 observed in yeast [PSI+] strains. These results suggest that interaction of the Upf1p with the peptidyl release factors may be a key event in the assembly of the putative surveillance complex that enhances translation termination, monitors whether termination has occurred prematurely, and promotes degradation of aberrant transcripts.
引用
收藏
页码:1665 / 1677
页数:13
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