Main Content

Cell wall integrity and metabolism in plant-pathogen interactions
(Engelsdorf Lab)

Plant cell walls are essential to support upright growth and provide protection against biotic and abiotic stress. This is not only accomplished by the provision of mechanical strength, but also by a remarkable plasticity and adaptability. When damage is caused to the wall, specific adjustments are made to plant metabolism and cell wall structure. Functionally, this calls for a mechanism capable of detecting damage, activating signaling pathways and initiating compensatory responses. In recent years, we have started to get an idea of a mechanism meeting these criteria, termed the cell wall integrity (CWI) maintenance mechanism.

When plants are attacked by pathogens, the cell wall serves as protecting shell, where the specific composition determines sensitivity to penetration and degradation by cell wall-degrading enzymes (CWDEs). Cell wall composition is strongly influenced by the plant primary metabolism, in particular carbohydrate metabolism. Under starvation conditions, cell wall formation is restricted and carbon potentially remobilized to support cellular metabolism. CWDE activity leads to the release of cell wall fragments that might be detected by receptors located at the plasma membrane (PM). Other PM receptor proteins detect pathogen-associated molecular patterns (PAMPs) or plant elicitor peptides (PEPs) that are induced in response to damage or PAMP recognition.

Fig.1: Model of plant cell wall dynamics under stress conditions. Cell wall-penetrating fungal pathogens secrete cell wall-degrading enzymes (CWDEs), which lead to the generation of cell wall fragments. CWDEs are also released by the plant to modify cell wall structure and enable carbohydrate salvage, e.g. during growth or under starvation conditions. Cell wall fragments, small secreted plant peptides and pathogen-associated molecular patterns (PAMPs) can be recognized by receptor kinases. Inhibition of cellulose biosynthesis with isoxaben impairs cell wall integrity by reducing cellulose abundance.

We are currently addressing the following questions:

  • How does CWI signaling contribute to pathogen defense and how is it coordinated with other defense responses?

  • How is PEP signaling initiated upon cell wall damage and how is it coordinated with CWI signaling?

  • How are cell wall structures modified under starvation conditions? Which polymer modifications are most relevant for pathogen susceptibility?

Contact

phone (office): +49 6421 28-22042
phone (lab): +49 6421 28-22013
email: