Metabolic Signals in Systemic Acquired Resistance
by Dmitrij Aleksandrovic Rekhter
Date of Examination:2019-05-08
Date of issue:2019-08-26
Advisor:Prof. Dr. Ivo Feussner
Referee:Prof. Dr. Ivo Feussner
Referee:Prof. Dr. Christiane Gatz
Referee:Prof. Dr. Yuelin Zhang
Persistent Address:
http://dx.doi.org/10.53846/goediss-7618
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Abstract
English
Plants are sessile organisms and therefore, they cannot escape from potential threats. Moreover, plants do not possess specialized mobile immune cells, which would maintain the immune system, as we know from mammals. In order to cope with pathogen attackers, plants developed a complex and multilayered defense system (Fu and Dong, 2013; Bacete et al., 2018). To coordinate the immune response, plants produce a number of signaling compounds. These metabolites regulate on the one hand the processes in infected tissues and spread on the other hand through the plant to alarm distal organs (Fu and Dong, 2013; van Loon, 2016). The exact spatiotemporal organized biosynthesis of these signaling compounds is crucial for the establishment of an efficient defense against the corresponding pathogens, without wasting important resources. Against biotrophic pathogen, salicylic acid (SA) and pipecolic acid (Pip) respectively N-hydroxy pipecolic acid (NHP) are the most important signaling compounds. Although the importance of these small metabolites in plants has been known for decades, parts of their biosynthesis stayed elusive so far (Hartmann and Zeier, 2018; Klessig et al., 2018). This motivated the work presented here, to study metabolic pathways that are responsible for the biosynthesis of these signaling compounds. Utilizing immune deficient mutant lines of the model organism Arabidopsis thaliana, untargeted metabolite fingerprint analysis was performed in order to identify yet missing links in the biosynthesis pathways of SA and Pip/NHP. Subsequent in vitro protein assays enabled the identification of systemic acquired resistance-deficient 4 (SARD4) as the yet missing ketimine reductase in the pathogen induced biosynthesis of Pip (Article I) in systemic leaves. In case of SA biosynthesis, it was shown previously that the formation of isochorismic acid (ISC) is crucial for the pathogen induced accumulation of SA (Garcion et al., 2008). However, the enzymatic step from ISC to SA remained elusive in plants. We found that avrPphB susceptible 3 (PBS3) catalyzes the conjugation of ISC with glutamic acid to yield ISC-9-glutamate (ISC-9-Glu). This compound decays non-enzymatically to give rise to SA (Article II). Both, Pip and ISC, are synthesized in plastids, whereas their metabolism occurs in the cytosol (Dempsey et al., 2011). A plastidial exporter is therefore required to transport these compounds into the cytosol (Hartmann and Zeier, 2018). We gathered strong evidences that enhanced disease susceptibility 5 (EDS5) is responsible for the export of both, ISC and Pip (Article III). Together, these studies improved the understanding of the biosynthesis as well as the spatial distribution of the signaling compounds SA and Pip/NHP, which are key regulators of plant immunity.
Keywords: Systemic acquired resistance; plant immunity; salicylic acid; pipecolic acid