Research background and focus

Last changed: 14 December 2021

Mechanisms of autophagy and cell death in plant-pathogen interactions

Plants, unlike animals, lack adaptive immune mechanisms and solely rely on a multilayered innate immune system to prevent pathogen infection. One layer engages surface receptors that detect conserved pathogen molecules (“PAMPs”) of bacterial, oomycete or fungal origin to initiate antimicrobial defences known as PAMP-triggered immunity (PTI). Additionally, antiviral immunity involves recognition and degradation of viral genomes by the cellular RNA silencing machinery. Successful pathogens inhibit these basal immune responses by the delivery of effector proteins including silencing suppressors inside the host cell, resulting in pathogen proliferation and the establishment of disease. Plants have therefore developed another defence layer to detect effectors or their modifications of host targets via different immune receptors (resistance or R proteins). These potentiate disease resistance via effector-triggered immune responses (ETI), which often involves a locally contained programmed cell death (PCD) reaction known as the hypersensitive response (HR). PCD is also induced by certain pathogens (e.g., necrotrophs) as part of their virulence strategy, and plants have evolved measures to control and limit both immunity- and disease-related cell death.

One line of our research focuses on the overall question which signals, core components and pathways regulate immunity- and disease-related PCD.

Autophagy (Greek for “self-eating”) is a major intracellular trafficking and degradation system present in all eukaryotes from yeast to humans. A characteristic feature of autophagy is the formation of specialized double-membrane vesicles, termed autophagosomes, which collect and transport cytoplasmic content to digestive compartments (i.e., the vacuole in yeast and plants, or the lysosome in animals) for hydrolytic breakdown. Autophagy is either an unspecific “bulk” process or acts as selective mechanism to remove individual proteins, toxic compounds and damaged organelles. Thus, autophagy plays a fundamental role in cellular renewal and adaptation to stress conditions, but also functions in the regulation and execution of cell death in different eukaryotic organisms. In plants, autophagy has emerged as central process in development, reproduction, metabolism, senescence and tolerance to abiotic and biotic stresses, thereby defining a multitude of important agricultural traits.

We are generally interested in unraveling the molecular mechanisms underlying the survival and death functions of autophagy in the context of pathogen-triggered immunity and disease.

Related reviews:

Üstün, S., Hafren, A., and Hofius, D. (2017). Autophagy as a mediator of life and death in plants. Curr Opin Plant Biol 40, 122-130.
Hofius, D., Li, L., Hafren, A., and Coll, N.S. (2017). Autophagy as an emerging arena for plant-pathogen interactions. Curr Opin Plant Biol 38, 117-123.
Minina, E.A., Bozhkov, P.V., and Hofius, D. (2014). Autophagy as initiator or executioner of cell death. Trends Plant Sci 19, 692-697.
Teh, O.K., and Hofius, D. (2014). Membrane trafficking and autophagy in pathogen-triggered cell death and immunity. J Exp Bot 65, 1297-1312.
Hofius, D., Munch, D., Bressendorff, S., Mundy, J., and Petersen, M. (2011). Role of autophagy in disease resistance and hypersensitive response-associated cell death. Cell Death Differ 18, 1257-1262.
Hofius, D., Tsitsigiannis, D.I., Jones, J.D., and Mundy, J. (2007). Inducible cell death in plant immunity. Semin Cancer Biol 17, 166-187.