Abstract
Hypersenitive response (HR) is a plant-specific defense response, which involves both autonomous cell death and defense activation. Decreased photosynthetic activity was observed before HR cell death, but the contribution of the chloroplast (dys)-function upon HR was not elucidated. Upon HR mediated by tobacco mosaic virus resistance gene N, decreased photosynthetic activity was observed after loss of mitochondrial membrane potential. Expression of constitutive active mutant of MAPK kinase MEK2DD, which activates the tobacco MAPKs WIPK and SIPK, and animal pro-apoptotic gene Bax, which induces mitochondrial dysfunction, also reduced photosynthetic rate. Light condition as well as treatment of DCMU, an inhibitor of photosynthesis, did not affect timing of HR cell death, but TMV multiplication was enhanced in the dark. These results suggest that chloroplast dysfunction was induced downstream of mitochondrial dysfunction. Further, alteration of chloroplast function is dispensable for HR cell death but required for suppression of TMV.
