Unraveling the interplay between autophagy and respiration and its contribution to plant growth (funded by theGerman-Israeli Foundation for Scientific Research and Development)

In the next years, agricultural production must meet the growing world population's increased nutritional demands and ensure food security worldwide. As agricultural area is limited, further improvements of crop yield are necessary. A common tactic to tackle this problem is increasing plant photosynthetic efficiency; however, much of the fixed carbon is lost by cellular respiration. Thus, optimizing cellular respiration can have positive implications on plant growth and yield and, consequently, on food sustainability. The mitochondrion is the energy hub of all eukaryotic cells, in which metabolites are degraded to produce ATP by cellular respiration. The process is highly regulated, as malfunction leads to the accumulation of reactive oxygen species and cell death. Although altered mitochondrial function has a vast effect on plant viability, our knowledge of mitochondrial regulation is still limited, specifically the management of damaged mitochondria remains unresolved.
Macroautophagy (hereafter termed "autophagy") is a eukaryotic degradation mechanism aimed at the breakdown of cellular components in the lytic organelle (vacuole in yeast and plants, lysosome in animals). Autophagy targets vary from long-lived proteins to protein aggregates and whole organelles. Autophagy has been characterized in plants, with autophagy mutants displaying increased senescence, reduced yield, and hypersensitivity to nutrient starvation. Degradation of mitochondria by autophagy (‘mitophagy’) has been extensively studied in yeast and animals, but almost not at all in plants. Despite that, some evidence exists regarding the function of autophagy in mitochondrial regulation, either by modulating mitochondrial metabolism or by affecting mitochondrial abundance.
Our collaboration aims to understand the interplay between autophagy and respiration in plants. In the scope of this project, we will perturb cellular respiration in autophagy-related mutants and autophagy in respiration mutants of the model plant Arabidopsis thaliana and study their physiological response and mitochondrial abundance. We will also establish double-mutants of autophagy and cellular respiration for long-term research in the scope of this collaboration. The data gained from this analysis will provide insights regarding the possible mechanisms affected by autophagy during mitochondrial damage and lay the ground for future research.