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 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.