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Wiley InterScience | ||
![]() The Plant JournalVolume 43 Issue 4, Pages 530 - 540 Published Online: 7 Jul 2005 Journal compilation © 2010 Blackwell Publishing Ltd and the Society for Experimental Biology Published in association with the Society for Experimental Biology
Abstract | References | Full Text: HTML, PDF (Size: 556K) | Supporting Information | Related Articles | Citation Tracking UPF3 suppresses aberrant spliced mRNA in Arabidopsis Copyright 2005 Blackwell Publishing Ltd KEYWORDS alternative splicing • nonsense-mediated decay • post-transcriptional regulation • mRNA surveillance • premature termination codon • aberrant mRNA ABSTRACTIt has been reported that eukaryotic organisms have a nonsense-mediated mRNA decay (NMD) system to exclude aberrant mRNAs that produce truncated proteins. NMD is an RNA surveillance pathway that degrades mRNAs possessing premature translation termination codons (PTCs), thus avoiding production of possibly toxic truncated proteins. Three interacting proteins, UPF1, UPF2 and UPF3, are required for NMD in mammals and yeasts, and their amino acid sequences are well conserved among most eukaryotes, including plants. In this study, 'The Arabidopsis Information Resource' database was searched for mRNAs with premature termination codons. We selected five of these mRNAs and checked for the presence of PTCs in these mRNAs when translated in vivo. As a result we identified aberrant mRNAs produced by alternative splicing for each gene. These genes produced at least one alternative splicing variant including a PTC (PTC+) and another variant without a PTC (PTC−). We analyzed their PTC+/PTC− ratios in wild-type Arabidopsis and upf3 mutant plants and showed that the PTC+/PTC− ratios were higher in atupf3 mutant plants than wild-type plants and that the atupf3 mutant was less able to degrade mRNAs with premature termination codons than wild-type plants. This indicated that the AtUPF3 gene is required by the plant NMD system to obviate aberrantly spliced mRNA. Received 18 January 2005; revised 17 May 2005; accepted 26 May 2005. |