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Orchestration of hydrogen peroxide and nitric oxide in brassinosteroid‐mediated systemic virus resistance in Nicotiana benthamiana
Author(s) -
Deng XingGuang,
Zhu Tong,
Zou LiJuan,
Han XueYing,
Zhou Xue,
Xi DeHui,
Zhang DaWei,
Lin HongHui
Publication year - 2016
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.13120
Subject(s) - nicotiana benthamiana , systemic administration , gene silencing , nadph oxidase , nitric oxide , chemistry , biology , virus , biochemistry , enzyme , gene , virology , in vivo , microbiology and biotechnology , organic chemistry
Summary Brassinosteroids ( BR s) play essential roles in modulating plant growth, development and stress responses. Here, involvement of BR s in plant systemic resistance to virus was studied. Treatment of local leaves in Nicotiana benthamiana with BR s induced virus resistance in upper untreated leaves, accompanied by accumulations of H 2 O 2 and NO . Scavenging of H 2 O 2 or NO in upper leaves blocked BR ‐induced systemic virus resistance. BR ‐induced systemic H 2 O 2 accumulation was blocked by local pharmacological inhibition of NADPH oxidase or silencing of respiratory burst oxidase homolog gene Nb RBOHB , but not by systemic NADPH oxidase inhibition or Nb RBOHA silencing. Silencing of the nitrite‐dependent nitrate reductase gene Nb NR or systemic pharmacological inhibition of NR compromised BR ‐triggered systemic NO accumulation, while local inhibition of NR , silencing of Nb NOA 1 and inhibition of NOS had little effect. Moreover, we provide evidence that BR ‐activated H 2 O 2 is required for NO synthesis. Pharmacological scavenging or genetic inhibiting of H 2 O 2 generation blocked BR ‐induced systemic NO production, but BR ‐induced H 2 O 2 production was not sensitive to NO scavengers or silencing of Nb NR . Systemically applied sodium nitroprusside rescued BR ‐induced systemic virus defense in Nb RBOHB ‐silenced plants, but H 2 O 2 did not reverse the effect of Nb NR silencing on BR ‐induced systemic virus resistance. Finally, we demonstrate that the receptor kinase BRI 1(BR insensitive 1) is an upstream component in BR ‐mediated systemic defense signaling, as silencing of Nb BRI 1 compromised the BR ‐induced H 2 O 2 and NO production associated with systemic virus resistance. Together, our pharmacological and genetic data suggest the existence of a signaling pathway leading to BR ‐mediated systemic virus resistance that involves local Respiratory Burst Oxidase Homolog B (RBOHB)‐dependent H 2 O 2 production and subsequent systemic NR ‐dependent NO generation.