| First Author | Zheng D | Year | 2008 |
| Journal | J Cell Biol | Volume | 182 |
| Issue | 1 | Pages | 89-101 |
| PubMed ID | 18625844 | Mgi Jnum | J:139263 |
| Mgi Id | MGI:3807625 | Doi | 10.1083/jcb.200801196 |
| Citation | Zheng D, et al. (2008) Deadenylation is prerequisite for P-body formation and mRNA decay in mammalian cells. J Cell Biol 182(1):89-101 |
| abstractText | Deadenylation is the major step triggering mammalian mRNA decay. One consequence of deadenylation is the formation of nontranslatable messenger RNA (mRNA) protein complexes (messenger ribonucleoproteins [mRNPs]). Nontranslatable mRNPs may accumulate in P-bodies, which contain factors involved in translation repression, decapping, and 5'-to-3' degradation. We demonstrate that deadenylation is required for mammalian P-body formation and mRNA decay. We identify Pan2, Pan3, and Caf1 deadenylases as new P-body components and show that Pan3 helps recruit Pan2, Ccr4, and Caf1 to P-bodies. Pan3 knockdown causes a reduction of P-bodies and has differential effects on mRNA decay. Knocking down Caf1 or overexpressing a Caf1 catalytically inactive mutant impairs deadenylation and mRNA decay. P-bodies are not detected when deadenylation is blocked and are restored when the blockage is released. When deadenylation is impaired, P-body formation is not restorable, even when mRNAs exit the translating pool. These results support a dynamic interplay among deadenylation, mRNP remodeling, and P-body formation in selective decay of mammalian mRNA. |
