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

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

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...

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Bibliographic Details
Published in:Journal of general plant pathology : JGPP Vol. 90; no. 6; pp. 298 - 308
Main Authors: Unung, Okon Odiong, Bensedira, Houssam Eddine Said, Matsuura, Takakazu, Mori, Izumi C., Shimomura, Yuta, Yaeno, Takashi, Kaya, Hidetaka, Kobayashi, Kappei
Format: Journal Article
Language:English
Published: Singapore Springer Nature Singapore 01-11-2024
Springer Nature B.V
Subjects:
Agriculture
Biomedical and Life Sciences
Cell death
Chloroplasts
Chlorosis
Disease resistance
Gene expression
Gene silencing
Host Responses
Interspecific hybridization
Life Sciences
Microbiology
Mortality
Plant immunity
Plant layout
Plant Pathology
Salicylic acid
Signal transduction
Tobacco
Tomatoes
Transcription factors
Chlorosis
Salicylic acid
Tenoxicam
Cell death
silencing
Plant immunity
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Summary: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, nahG A430V , 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 nahG A430V 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.
ISSN:1345-2630
1610-739X
DOI:10.1007/s10327-024-01191-3