Genome-wide suppression of aberrant mRNA-like noncoding RNAs by NMD in Arabidopsis. Export

@article{citeulike:6061244, abstract = {The nonsense-mediated mRNA decay (NMD) pathway is a well-known eukaryotic surveillance mechanism that eliminates aberrant mRNAs that contain a premature termination codon (PTC). The UP-Frameshift (UPF) proteins, UPF1, UPF2, and UPF3, are essential for normal NMD function. Several NMD substrates have been identified, but detailed information on NMD substrates is lacking. Here, we noticed that, in Arabidopsis, most of the mRNA-like nonprotein-coding RNAs (ncRNAs) have the features of an NMD substrate. We examined the expression profiles of 2 Arabidopsis mutants, upf1-1 and upf3-1, using a whole-genome tiling array. The results showed that expression of not only protein-coding transcripts but also many mRNA-like ncRNAs (mlncRNAs), including natural antisense transcript RNAs (nat-RNAs) transcribed from the opposite strands of the coding strands, were up-regulated in both mutants. The percentage of the up-regulated mlncRNAs to all expressed mlncRNAs was much higher than that of the up-regulated protein-coding transcripts to all expressed protein- coding transcripts. This finding demonstrates that one of the most important roles of NMD is the genome-wide suppression of the aberrant mlncRNAs including nat-RNAs.}, author = {Kurihara, Yukio and Matsui, Akihiro and Hanada, Kousuke and Kawashima, Makiko and Ishida, Junko and Morosawa, Taeko and Tanaka, Maho and Kaminuma, Eli and Mochizuki, Yoshiki and Matsushima, Akihiro and Toyoda, Tetsuro and Shinozaki, Kazuo and Seki, Motoaki}, citeulike-article-id = {6061244}, citeulike-linkout-0 = {http://dx.doi.org/10.1073/pnas.0808902106}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19181858}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19181858}, day = {17}, doi = {10.1073/pnas.0808902106}, issn = {1091-6490}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, keywords = {nmd}, month = {February}, number = {7}, pages = {2453--2458}, posted-at = {2009-11-03 18:05:47}, priority = {2}, title = {Genome-wide suppression of aberrant mRNA-like noncoding RNAs by NMD in Arabidopsis.}, url = {http://dx.doi.org/10.1073/pnas.0808902106}, volume = {106}, year = {2009} }

TY - JOUR ID - citeulike:6061244 L3 - citeulike-article-id:6061244 N2 - The nonsense-mediated mRNA decay (NMD) pathway is a well-known eukaryotic surveillance mechanism that eliminates aberrant mRNAs that contain a premature termination codon (PTC). The UP-Frameshift (UPF) proteins, UPF1, UPF2, and UPF3, are essential for normal NMD function. Several NMD substrates have been identified, but detailed information on NMD substrates is lacking. Here, we noticed that, in Arabidopsis, most of the mRNA-like nonprotein-coding RNAs (ncRNAs) have the features of an NMD substrate. We examined the expression profiles of 2 Arabidopsis mutants, upf1-1 and upf3-1, using a whole-genome tiling array. The results showed that expression of not only protein-coding transcripts but also many mRNA-like ncRNAs (mlncRNAs), including natural antisense transcript RNAs (nat-RNAs) transcribed from the opposite strands of the coding strands, were up-regulated in both mutants. The percentage of the up-regulated mlncRNAs to all expressed mlncRNAs was much higher than that of the up-regulated protein-coding transcripts to all expressed protein- coding transcripts. This finding demonstrates that one of the most important roles of NMD is the genome-wide suppression of the aberrant mlncRNAs including nat-RNAs. IS - 7 JF - Proceedings of the National Academy of Sciences of the United States of America SN - 1091-6490 EP - 2458 TI - Genome-wide suppression of aberrant mRNA-like noncoding RNAs by NMD in Arabidopsis. VL - 106 SP - 2453 KW - nmd AU - Kurihara, Yukio AU - Matsui, Akihiro AU - Hanada, Kousuke AU - Kawashima, Makiko AU - Ishida, Junko AU - Morosawa, Taeko AU - Tanaka, Maho AU - Kaminuma, Eli AU - Mochizuki, Yoshiki AU - Matsushima, Akihiro AU - Toyoda, Tetsuro AU - Shinozaki, Kazuo AU - Seki, Motoaki PY - 2009/02/17/ UR - http://dx.doi.org/10.1073/pnas.0808902106 ER -