Mitochondrial contribution to basal plant defenses via proline dehydrogenase (ProDH)

FABRO G; RIZZI YS; ALVAREZ ME

Cordoba

Congreso; LII Reunión Anual SAIB; 2016

The contribution of mitochondria to defense programs against bacterial pathogens has been mostly studied under cell death-triggering conditions. Conversely, its influence over defense programs that trigger broad-spectrum resistance in the absence of cell death has not been established yet. To assess this issue, we monitored PTI (PAMP-triggered immunity) features in wild type tissues treated with inhibitors of the mitochondrial electron transport chain (mETC), and mutants lacking the mitochondrial proline catabolic enzyme ProDH. We found that non-lethal levels of antimycin A or rotenone producing mild mETC alterations, strongly impair PTI. In addition, the absence of ProDH1 or ProDH2 isoenzymes reproduces most of these PTI deffects. Major differences were observed in the generation of reactive oxygen species (ROS) and deposition of callose at the cell wall. Based on these results we used a bacterial flagellin-derived peptide (flg22) to perform a detailed investigation of the requirement of ProDH for ROS generation by the membrane NADPH oxidase homolog D (RBOHD). Surprisingly, the RBOHD function was sensitively dependent on the ProDH activity.