Macroautophagy, hereafter termed autophagy, is a conserved eukaryotic stress-related mechanism. It is classically defined as the degradation of cytoplasmic constituents in the lytic organelle (vacuoles in yeast and plants and lysosomes in mammals). The targets of autophagy vary from long-lived proteins to protein aggregates and even whole organelles. Autophagy begins with the formation of cup-shaped double membranes in the cytoplasm, which expand to form vesicles named autophagosomes, engulfing cargo and transporting it for degradation inside the vacuole. As the autophagosomes arrive at the vacuole, their outer membrane fuses with the tonoplast. The remaining single-membrane vesicles inside the vacuole are termed “autophagic bodies.” The autophagic bodies and their contents are then degraded inside the vacuole, providing recycled materials to build new macromolecules. Originally identified in yeast, autophagy was shown to be involved in nutrient starvation and environmental stress. In animal systems, it was also shown to function in many other processes such as embryonic development, immunological response, and the progression of diseases. In plants, autophagy was shown to take part in the response to nutrient starvation, biotic stress, and abiotic stresses.
Our group aims to study the metabolic effects of nutrient remobilization during development and stress, focusing on autophagy as a model for alternative nutrient supply.
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Studying the interplay between autophagy and sugar metabolism
Autophagy knockout plants (atg mutants) have been shown to display altered metabolic content under both favorable and starvation conditions. Surprisingly, atg mutants seem to accumulate sugars, which is puzzling since they are hypersensitive to carbon starvation. We are interested in understanding how autophagy mediates sugar metabolism and how sugars regulate autophagy. As sugars function as both energy sources and signaling molecules, this co-regultion can be very intricate.
Studying the role of autophagy in seed development and germination
Autophagy has been previously shown to affect nutrient transport into seeds and influence the carbon/nitrogen ratio in seeds. atg mutants also display altered seed development and storage protein processing. However, as atg mutants are knockout plants, it is impossible to know whether these phenotypes stem from autophagy in the mother plant or the developing seed. We are downregulating autophagy in the mother plant or the seed to specifically understand the role of autophagy in each organ to seed development, and also examine the subsequent effect on seed germination.