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Involvement of a Class III Peroxidase and the Mitochondrial Protein TSPO in Oxidative Burst Upon Treatment of Moss Plants with a Fungal Elicitor

¹Plant Pathology Laboratory, Department of Agricultural Sciences, PO Box 27, FI-00014 University of Helsinki, Finland; ²Department of Biotechnological Sciences, Kinki University, Kinokawa, Wakayama, 649-6493, Japan; ³Plant Biotechnology, Faculty of Biology, University of Freiburg, Schaenzlestr. 1, ⁴BIOSS Centre for Biological Signalling Studies, University of Freiburg, Hebelstr. 25, and ⁵FRIAS Freiburg Institute for Advanced Studies, Albertstr. 19, D-79104 Freiburg, Germany

Production of apoplastic reactive oxygen species (ROS), or oxidative burst, is among the first responses of plants upon recognition of microorganisms. It requires peroxidase or NADPH oxidase (NOX) activity and factors maintaining cellular redox homeostasis. Here, PpTSPO1 involved in mitochondrial tetrapyrrole transport and abiotic (salt) stress tolerance was tested for its role in biotic stress in Physcomitrella patens, a nonvascular plant (moss). The fungal elicitor chitin caused an immediate oxidative burst in wild-type P. patens but not in the previously described ΔPrx34 mutants lacking the chitin-responsive secreted class III peroxidase (Prx34). Oxidative burst in P. patens was associated with induction of the oxidative stress-related genes AOX, LOX7, and NOX, and also PpTSPO1. The available ΔPpTSPO1 knockout mutants overexpressed AOX and LOX7 constitutively, produced 2.6-fold more ROS than wild-type P. patens, and exhibited increased sensitivity to a fungal necrotrophic pathogen and a saprophyte. These results indicate that Prx34, which is pivotal for antifungal resistance, catalyzes ROS production in P. patens, while PpTSPO1 controls redox homeostasis. The capacity of TSPO to bind harmful free heme and porphyrins and scavenge them through autophagy, as shown in Arabidopsis under abiotic stress, seems important to maintenance of the homeostasis required for efficient pathogen defense.