Possible roles of immunity-related response in modulating chlorosis induced by the silencing of chloroplast HSP90C in tobacco models

IF 1 4区 农林科学 Q3 PLANT SCIENCES Journal of General Plant Pathology Pub Date : 2024-07-22 DOI:10.1007/s10327-024-01191-3
Okon Odiong Unung, Houssam Eddine Said Bensedira, Takakazu Matsuura, Izumi C. Mori, Yuta Shimomura, Takashi Yaeno, Hidetaka Kaya, Kappei Kobayashi
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Abstract

In the inducible chlorosis model tobacco, i-hpHSP90C, the silencing of HSP90C activated both salicylic acid (SA)- and cell death-related gene expression and sporadic cell death, resulting in severe chlorosis. In this model plant, we found a transient SA accumulation to a significantly high level at 8 h after induction of HSP90C silencing and consistent upregulation of CBP60-type transcription factors and some SA biosynthetic genes. Exogenous treatment of the model plant with SA alone did not induce chlorosis. The introgression of a gene encoding SA-degrading enzyme, nahGA430V, into tobacco plants with functional N′ tobamovirus resistance gene partially compromised their resistance to tomato mosaic virus but without a clear reduction in SA levels. Expression of nahGA430V stochastically alleviated chlorosis and, subsequently, sporadic cell death upon induction of HSP90C silencing. We applied tenoxicam, a potent inhibitor of the NPR1-dependent SA signaling pathway in Arabidopsis, and found that it alleviated chlorosis in i-hpHSP90C, which accompanied a reduced expression of a CBP60-type transcription factor. However, the expression of PR1a, a well-characterized SA signal marker, was not suppressed by tenoxicam in the i-hpHSP90 plants with alleviated chlorosis. The findings collectively suggest that the plant immunity-related response, including SA production, could have a role in increasing the severity of chlorosis, although the underlying mechanisms remain to be elucidated.

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在烟草模型中,免疫相关反应在调节叶绿体 HSP90C 沉默诱导的萎黄病中可能发挥的作用
在诱导性萎黄病模型烟草 i-hpHSP90C 中,HSP90C 的沉默激活了水杨酸(SA)和细胞死亡相关基因的表达以及零星的细胞死亡,导致严重的萎黄病。在该模式植物中,我们发现在诱导 HSP90C 沉默 8 小时后,一过性的 SA 积累达到明显的高水平,CBP60 型转录因子和一些 SA 生物合成基因持续上调。仅用 SA 对模型植物进行外源处理不会诱导叶枯病。将编码 SA 降解酶的基因 nahGA430V 导入具有 N′ tobamovirus 抗性功能基因的烟草植株,部分削弱了它们对番茄花叶病毒的抗性,但并未明显降低 SA 水平。在诱导 HSP90C 沉默后,nahGA430V 的表达随机缓解了萎黄病,并随后缓解了零星的细胞死亡。我们应用了拟南芥中依赖于 NPR1 的 SA 信号通路的强效抑制剂替诺昔康,发现它缓解了 i-hpHSP90C 的叶绿素沉降,同时 CBP60 型转录因子的表达也有所减少。然而,在萎黄病得到缓解的 i-hpHSP90 植株中,PR1a(一种特征明显的 SA 信号标记)的表达并未受到替诺昔康的抑制。这些发现共同表明,植物免疫相关反应(包括 SA 的产生)可能在加重萎黄病的严重程度方面发挥作用,但其潜在机制仍有待阐明。
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来源期刊
CiteScore
2.40
自引率
8.30%
发文量
60
审稿时长
6 months
期刊介绍: The Journal of General Plant Pathology welcomes all manuscripts dealing with plant diseases or their control, including pathogen characterization, identification of pathogens, disease physiology and biochemistry, molecular biology, morphology and ultrastructure, genetics, disease transmission, ecology and epidemiology, chemical and biological control, disease assessment, and other topics relevant to plant pathological disorders.
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