The role of NADPH oxidase - mediated ROS in interaction between plant and nematodes

• Applicant: Professor Dr. Florian M. W. Grundler, since 3/2019
• Subject Area: Plant Breeding and Plant Pathology
• Term: from 2015 to 2023
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 287570125

The oxidative burst, production of Reactive Oxygen species (ROS) in response to pathogen attack, is an important component of plant defence mechanisms. It is now generally recognised that the major source of ROS during an oxidative burst in plants is plasma membrane-bound NADPH oxidase (nicotinamide adeninedinucleotide phosphate). Plant NADPH oxidases have been named as respiratory burst oxidase homolog (Rboh) and possess six transmembrane-spanning domains corresponding to the domains that have been identified in the gp91phox subunit in mammals. Genetic analysis of plants disrupted in Rboh functions suggested that they are required for the production of a full oxidative burst in response to a variety of pathogens. Yet, this lack of ROS production by NADPH oxidase has variable effects on plant responses to pathogens in terms of cell death and resistance. Nevertheless, the mechanistic details on the pathosystem-specific role of Rboh-mediated ROS are not yet known. Heterodera schachtii is a cyst nematode that establishes a long-term biotrophic relationship with the host plants, including Arabidopsis thaliana. Infective stage juveniles of nematodes (J2s) invade the roots and move towards the vascular cylinder where they establish a syncytial nurse cell system. Syncytium is the only source of nutrients for nematodes throughout their life-span of several weeks. We used loss-of-function mutants for Arabidopsis Rboh genes and found that the number of nematodes, the size of female nematodes, and the size of syncytium decreased greatly in rbohD and rbohD/F compared with Col-0 plants. A detailed microscopic, molecular and biochemical analysis showed that Rboh-dependent ROS are not required for root invasion; however, the syncytial establishment and development is impaired in the absence of ROS. To understand the mechanism underlying the Rboh-mediated resistance to nematodes, we performed a genome-wide comparative transcriptome analysis between Col-0 and rbohD/F during early stages of infection. The gene that was most strongly downregulated encode for a vacuolar auxin transporter, Walls Are Thin 1 (WAT1). Genetic disruption of WAT1 led to similar changes in nematode susceptibility as in rbohD/F; thus suggesting that Rboh-mediated resistance to nematode is dependent on WAT1. Further analyses showed a link between Rboh-mediated resistance phenotypes and auxin metabolism in infected tissues. The objective of this research proposal is to deliver a mechanistic understanding for the role of ROS as signals to promote nematode and other pathogen infections. Moreover, we will also get insights into the role of ROS in the regulation of trade-offs between plant growth and immunity.

• DFG Programme: Research Grants
• Ehemaliger Antragsteller: Dr. Shahid Siddique, until 2/2019