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P3N-PIPO, a Frameshift Product fromP3, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

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Title: P3N-PIPO, a Frameshift Product fromP3, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas
Authors: Atsumi, Go Browse this author
Suzuki, Haruka Browse this author
Miyashita, Yuri Browse this author
Choi, Sun Hee Browse this author
Hisa, Yusuke Browse this author
Rihei, Shunsuke Browse this author
Shimada, Ryoko Browse this author
Jeon, Eun Jin Browse this author
Abe, Junya Browse this author
Nakahara, Kenji S Browse this author →KAKEN DB
Uyeda, Ichiro Browse this author →KAKEN DB
Issue Date: Aug-2016
Journal Title: Journal of Virology
Volume: 90
Issue: 16
Start Page: 7388
End Page: 7404
Publisher DOI: 10.1128/JVI.00190-16
Abstract: Peas carrying the cyv1 recessive resistance gene are resistant to clover yellow vein virus (ClYVV) isolates No. 30 and 90-1 (Cl-No.30 and Cl-90-1), but can be infected by a derivative of Cl-90-1 (Cl-90-1 Br2). The main determinant for the breaking of cyv1 resistance by Cl-90-1 Br2 is P3N-PIPO produced from the P3 gene via transcriptional slippage, and the higher level of P3N-PIPO produced by Cl-90-1 Br2 than by Cl-No.30 contributes to the breaking. Here we show that P3N-PIPO is also a major virulence determinant in susceptible peas that possess another resistance gene, Cyn1, which does not inhibit systemic infection with ClYVV but causes hypersensitive reaction–like lethal systemic cell death. We previously assumed that the susceptible pea cultivar PI 226564 has a weak allele of Cyn1. Cl-No.30 did not induce cell death but Cl-90-1 Br2 killed the plants. Our results suggest that P3N-PIPO is recognized by Cyn1 and induces cell death. Unexpectedly, heterologously strongly expressed P3N-PIPO of Cl-No.30 appears to be recognized by Cyn1 in PI 226564. P3N-PIPO accumulation from the P3 gene of Cl-No.30 was significantly lower than that from Cl-90-1 Br2 in a Nicotiana benthamiana transient assay. Therefore, Cyn1-mediated cell death also appears to be determined by the level of P3N-PIPO. The more efficiently a ClYVV isolate broke cyv1 resistance, the more it induced cell death systemically (resulting in a loss of environment for virus accumulation) in susceptible peas carrying Cyn1, suggesting that antagonistic pleiotropy of P3N-PIPO controls the resistance breaking of ClYVV.
Type: article (author version)
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)

Submitter: 中原 健二

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