Figure 2. The impact of two incompatible pv’s of P. syringae on the mitochondria of tobacco leaf mesophyll cells. (A) Infection with the HR-inducing pv maculicola results in an early and persistent burst of O2- in the mitochondrial matrix that may have a signaling role in support of the HR. (B) Infection with pv phaseolicola, that causes induction of plant defenses but not including the HR, lacks a matrix O2- burst. The differential effect of the two pv’s is supported by a coordinated response of the major ETC mechanism to avoid O2- generation (AOX) and the sole enzymatic means to scavenge matrix O2- (MnSOD). In response to pv phaseolicola, AOX is strongly induced and MnSOD activity remains high, while in response to pv maculicola MnSOD activity declines and AOX remains low. As a result, the two bacterial pv’s each generate distinct mitochondrial ROS signatures that may impact defense responses and cell fate.