Open AccessNbALY916 is involved in potato virus X P25‐triggered cell death in Nicotiana benthamiana
Author(s) -
Yang Xue,
Tian Yanzhen,
Zhao Xing,
Jiang Liangliang,
Chen Ying,
Hu Shuzhen,
MacFarlane Stuart,
Chen Jianping,
Lu Yuwen,
Yan Fei
Publication year - 2020
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12986
Subject(s) - nicotiana benthamiana , potato virus x , biology , gene silencing , potexvirus , virus , tobacco rattle virus , programmed cell death , virology , microbiology and biotechnology , plant virus , apoptosis , gene , rna , genetics , coat protein
Systemic necrosis often occurs during viral infection of plants and is thought mainly to be the result of long‐term stress induced by viral infection. Potato virus X (PVX) encodes the P25 pathogenicity factor that triggers a necrotic reaction during PVX‐potato virus Ysynergistic coinfection. In this study, we discovered that NbALY916, a multifunctional nuclear protein, could interact with P25. When NbALY916 expression was reduced by tobacco rattle virus (TRV)‐based virus‐induced gene silencing, the accumulation of P25 was increased, which would be expected to cause more severe necrosis. However, silencing of NbALY916 reduced the extent of cell death caused by P25. Furthermore, we found that overexpression of NbALY916 increased the accumulation of H 2 O 2 and triggered more extensive cell death when coexpressed with P25, even though accumulation of P25 was itself reduced by the increased expression of NbALY916. Furthermore, transient expression of P25 specifically induced the expression of NbALY916 mRNA, but not the mRNAs of three other ALYs in Nicotiana benthamiana . In addition, we showed that silencing of NbALY916 or transient overexpression of NbALY916 affected the infection of PVX in N. benthamiana . Our results reveal that NbALY916 has an antiviral role that, in the case of PVX, operates by inducing the accumulation of H 2 O 2 and mediating the degradation of P25.