Abstract
The present study was designed to investigate the role of plant mitochondria in redox sensing and hypersensitive response in a Nicotiana sylvestris mitochondrial mutant (CMSII mutant) that lacks a functional respiratory complex I. The abundance of compartment-specific transcripts encoding isoforms of superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6) and ascorbate peroxidase (APX; EC 1.11.1.11) was higher in the CMSII mutant. This suggests the presence of redox signalling, originating in the mitochondria, that affects the rest of the cell. In order to explore this further, the hypersensitive response induced in tobacco by harpin—a bacterial elicitor from Erwinia amylovora—was exploited as a model system for programmed cell death. Although the time course of harpin-induced necrosis was similar in the N. sylvestris wild-type and CMSII, several aspects of the hypersensitive response were found to be different in the mutant. For example, the accumulation of autofluorescent compounds, as observed under UV light, was lower in the mutant. In addition, presymptomatic transpiration was absent while cytosolic APX and PAL transcripts were enhanced. These results strongly suggest that mitochondrial functions (possibly mediated by redox changes) participate in the hypersensitive response to bacterial pathogens.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
