Abstract:
:Messenger RNAs with premature translation termination codons (PTCs) are degraded by nonsense-mediated mRNA decay (NMD). In mammals, PTCs are discriminated from physiological stop codons by a process thought to involve the splicing-dependent deposition of an exon junction complex (EJC), EJC-mediated recruitment of Upf3, and Upf2 binding to the N terminus of Upf3. Here, we identify a conserved domain of hUpf3b that mediates an interaction with the EJC protein Y14. Tethered function analysis shows that the Y14/hUpf3b interaction is essential for NMD, while surprisingly the interaction between hUpf3b and hUpf2 is not. Nonetheless, hUpf2 is necessary for NMD mediated by tethered Y14. RNAi-induced knockdown and Y14 repletion of siRNA-treated cells implicates Y14 in the degradation of beta-globin NS39 mRNA and demonstrates that Y14 is required for NMD induced by tethered hUpf3b. These results uncover a direct role of Y14 in NMD and suggest an unexpected hierarchy in the assembly of NMD complexes.
journal_name
Mol Celljournal_title
Molecular cellauthors
Gehring NH,Neu-Yilik G,Schell T,Hentze MW,Kulozik AEdoi
10.1016/s1097-2765(03)00142-4subject
Has Abstractpub_date
2003-04-01 00:00:00pages
939-49issue
4eissn
1097-2765issn
1097-4164pii
S1097-2765(03)00142-4journal_volume
11pub_type
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