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Quantitative and Qualitative Involvement of P3N-PIPO in Overcoming Recessive Resistance against Clover yellow vein virus in Pea Carrying cyv1
Title: | Quantitative and Qualitative Involvement of P3N-PIPO in Overcoming Recessive Resistance against Clover yellow vein virus in Pea Carrying cyv1 |
Authors: | Choi, Sun Hee Browse this author | Hagiwara-Komoda, Yuka Browse this author | Nakahara, Kenji S. Browse this author →KAKEN DB | Atsumi, Go Browse this author | Shimada, Ryoko Browse this author | Hisa, Yusuke Browse this author | Naito, Satoshi Browse this author | Uyeda, Ichiro Browse this author →KAKEN DB |
Keywords: | Potyvirus | Frameshift product | Resistance breaking | Plant pathology |
Issue Date: | Jul-2013 |
Publisher: | American Society for Microbiology |
Journal Title: | Journal of Virology |
Volume: | 87 |
Issue: | 13 |
Start Page: | 7326 |
End Page: | 7337 |
Publisher DOI: | 10.1128/JVI.00065-13 |
Abstract: | In pea carrying cyv1, a recessive gene for resistance to Clover yellow vein virus (ClYVV), ClYVV isolate Cl-no30 was restricted to the initially infected cells, whereas isolate 90-1 Br2 overcame this resistance. We mapped the region responsible for breaking of cyv1-mediated resistance by examining infection of cyv1 pea with chimeric viruses constructed from parts of Cl-no30 and 90-1 Br2. The breaking of resistance was attributed to the P3 cistron, which is known to produce two proteins: P3, from the main open reading frame (ORF), and P3N-PIPO, which has the N-terminal part of P3 fused to amino acids encoded by a small open reading frame (ORF) called PIPO in the +2 reading frame. We introduced point mutations that were synonymous with respect to the P3 protein but nonsynonymous with respect to the P3N-PIPO protein, and vice versa, into the chimeric viruses. Infection of plants with these mutant viruses revealed that both P3 and P3N-PIPO were involved in overcoming cyv1-mediated resistance. Moreover, P3N-PIPO quantitatively affected the virulence of Cl-no30 in cyv1 pea. Additional expression in trans of the P3N-PIPO derived from Cl-no30, using White clover mosaic virus as a vector, enabled Cl-no30 to move to systemic leaves in cyv1 pea. Susceptible pea plants infected with chimeric ClYVV possessing the P3 cistron of 90-1 Br2, and which were therefore virulent toward cyv1 pea, accumulated more P3N-PIPO than did those infected with Cl-no30, suggesting that the higher level of P3N-PIPO in infected cells contributed to the breaking of resistance by 90-1 Br2. This is the first report showing that P3N-PIPO is a virulence determinant in plants resistant to a potyvirus. |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/54599 |
Appears in Collections: | 農学院・農学研究院 (Graduate School of Agriculture / Faculty of Agriculture) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 中原 健二
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