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Published online July 14, 2008
doi:10.1083/jcb.200801196
The Journal of Cell Biology, Vol. 182, No. 1, 89-101
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Zheng et al.
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Article

 Deadenylation is prerequisite for P-body formation and mRNA decay in mammalian cells

Dinghai Zheng1, Nader Ezzeddine1, Chyi-Ying A. Chen1, Wenmiao Zhu1, Xiangwei He2, and Ann-Bin Shyu1

1 Department of Biochemistry and Molecular Biology, The University of Texas Medical School, Houston, TX 77030
2 Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030

Correspondence to Ann-Bin Shyu: Ann-Bin.Shyu{at}uth.tmc.edu.

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.

D. Zheng and N. Ezzeddine contributed equally to this paper.

Abbreviations used in this paper: ARE, AU-rich element; miRNA, microRNA; NMD, nonsense-mediated decay; PTC, premature translation-termination codon.


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