Proteolytic degradation pathways and their role in plant immunity

• Applicant: Professor Dr. Suayib Üstün
• Subject Area: Organismic Interactions, Chemical Ecology and Microbiomes of Plant Systems
• Term: from 2018 to 2024
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 400923110

Autophagy and the ubiquitin-proteasome system (UPS) are two major protein degradation pathways in eukaryotes. They orchestrate many cellular processes during development and in response to environmental stimuli such as microbial infections. In animals, the contribution of autophagy and UPS to anti-bacterial immunity is well documented and several bacteria evolved measures to target and exploit these systems to the benefit of infection. In plants, we have recently identified that the UPS acts as a central hub of immune responses that is subverted by bacteria to enhance virulence. However, the role of autophagy during plant-bacterial interactions is far less understood. Recently we discovered that plant pathogenic bacterium Pseudomonas syringae pv. tomato DC3000 (Pst) induces autophagy to degrade the proteasome eventually leading to proteasome inhibition and enhanced pathogenicity. Based on these findings we conducted a comprehensive analysis of possible targets of pathogen-induced autophagy, which led to the discovery that in addition to the proteasome, other pathways such as RNA metabolism, protein translation and signal transduction might be autophagy targets. Thus, we propose the hypothesis that plant pathogens evolved to target proteolytic pathways to have a broad impact on the plant side. Within this project we aim to distinct and overlapping degradomes of the autophagy and proteasome pathways during plant immunity. Questions that will be addressed within the scope of this project deal with: 1) characterization of recently identified autophagy target after Pst infection and generation of a deep catalogue of potential proteasome and autophagy substrates by a comparative ubiquitylome approach, 2) the potential interplay of the autophagy machinery with protein secretion, 3) how protein translation is modulated as a result of the pathogen-driven cross-talk of autophagy and the proteasome. To obtain a deeper mechanistic understanding of how plant pathogenic bacteria hijack autophagy via the action of type-III effectors, we will utilize these effectors to dissect the autophagy and proteasome pathway. Altogether, these objectives will help us to understand the underlying mechanism of how pathogens evolved to suppress immune responses by exploiting proteolytic degradation mechanisms. Overall, using pathogens and their molecular weapons, the effectors, as a tool to dissect degradation pathways will also help us to understand and identify novel selective autophagy pathways with great implications for a broader community.

• DFG Programme: Independent Junior Research Groups