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Light‐dependent hypersensitive response and resistance signaling against Turnip Crinkle Virus in Arabidopsis
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Summary
Resistance to Turnip Crinkle Virus (TCV) in Arabidopsis ecotype Dijon (Di)‐17 is conferred by the resistance gene
HRT
and a recessive locus
rrt
. In Di‐17, TCV elicits a hypersensitive response (HR), which is accompanied by increased expression of pathogenesis‐related (
PR
) genes and high levels of salicylic acid (SA). We have previously shown that
HRT
‐mediated resistance to TCV is dependent on SA‐mediated signal transduction and that increased levels of SA confer enhanced resistance to TCV via upregulation of the
HRT
gene. Here we show that
HRT
‐mediated HR and resistance are dependent on light. A dark treatment immediately following TCV inoculation suppressed HR, resistance and activation of the majority of the TCV‐induced genes. However, the absence of light did not affect either TCV‐induced elevated levels of free SA or the expression of
HRT
. Interestingly, in the dark, transgenic plants overexpressing
HRT
showed susceptibility, but overexpression of
HRT
coupled with high levels of endogenous SA resulted in pronounced resistance. Consistent with these results is the finding that exogenous application of SA prior to TCV inoculation partially overcame the requirement for light. Light was also required for
N
gene‐mediated HR and resistance to Tobacco Mosaic Virus, suggesting that it is an important factor which may be generally required during defense signaling.
Title: Light‐dependent hypersensitive response and resistance signaling against Turnip Crinkle Virus in Arabidopsis
Description:
Summary
Resistance to Turnip Crinkle Virus (TCV) in Arabidopsis ecotype Dijon (Di)‐17 is conferred by the resistance gene
HRT
and a recessive locus
rrt
.
In Di‐17, TCV elicits a hypersensitive response (HR), which is accompanied by increased expression of pathogenesis‐related (
PR
) genes and high levels of salicylic acid (SA).
We have previously shown that
HRT
‐mediated resistance to TCV is dependent on SA‐mediated signal transduction and that increased levels of SA confer enhanced resistance to TCV via upregulation of the
HRT
gene.
Here we show that
HRT
‐mediated HR and resistance are dependent on light.
A dark treatment immediately following TCV inoculation suppressed HR, resistance and activation of the majority of the TCV‐induced genes.
However, the absence of light did not affect either TCV‐induced elevated levels of free SA or the expression of
HRT
.
Interestingly, in the dark, transgenic plants overexpressing
HRT
showed susceptibility, but overexpression of
HRT
coupled with high levels of endogenous SA resulted in pronounced resistance.
Consistent with these results is the finding that exogenous application of SA prior to TCV inoculation partially overcame the requirement for light.
Light was also required for
N
gene‐mediated HR and resistance to Tobacco Mosaic Virus, suggesting that it is an important factor which may be generally required during defense signaling.
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