The fungus Fusarium oxysporum is a major threat to agriculture, causing vascular wilt disease in over a hundred different crop species. This soil-borne pathogen infects roots and colonises the vasculature causing wilting, stunting and eventually plant death. Whereas the immune system in shoots is well studied, it is poorly understood how a xylem dwelling pathogen overcomes plant immunity to cause disease.
During infection, Fusarium secretes so called SIX (Secreted in Xylem) proteins. Many of these proteins have been shown to contribute to fungal virulence, as their loss typically renders the fungus less pathogenic. One of these effectors, SIX3, was previously shown to be required for full fungal virulence. Since this effector can be recognised by the tomato immune receptor I-2, SIX3 has been renamed AVR2. Here, we set out to investigate the function of AVR2 for the fungus.
The plant immune system can be activated by extracellular localised immune receptors that recognise pathogen derived molecules (PAMPS) such as those released from flagella. Recognition of PAMPs such as the Flagellin 22 peptide (Flg22) by these so-called PRR (PAMP recognition Receptors) receptors triggers a phosphorylation cascade in which the receptor (e.g FLS2) and co-receptor (BAK1) are both phosphorylated. Subsequently, the activated complex phosphorylates downstream cytoplasmic signalling kinases that convey the signal to e.g., a reactive oxygen generating protein complex, a MAPkinase cascade and a set of transcription factors. To interact with these signalling components, the phosphorylated cytoplasmic kinases (such as BIK1) need to dissociate from the plasma membrane. Release from the membrane localised FLS2-BAK1 complex by phosphorylated BIK1 requires the kinase to become mono-ubiquitinylated.
We here show that Avr2 prevents this last step and blocks addition of a mono-ubiquitin. By retaining BIK1 at the plant plasma membrane, the kinase cannot activate the immune system upon pathogen perception, allowing disease. The finding that BIK1 is manipulated by a root-vascular pathogen identifies this protein as a conserved key component for both root and shoot immunity. This new insight provides leads to develop new strategies to protect our crops.
Mila C. Blekemolen, Zunyong Liu, Martin Stegman, Cyril Zipfel, Libo Shan and Frank L. W. Takken published this study in Molecular Plant Pathology:
TITLE IMAGE: Diagram of the plant membrane following activation of FLS2 receptor (green structure) and BAK1 co-receptor (purple structure) by flagellin/flg22 (yellow star); comparing the action of BIK1 kinase (orange circle) in the presence and absence of Avr2 (green pakman) . All images used with permission of the author.
