Research

Broad-spectrum disease resistance mediated by RPW8

Plants have evolved immune receptors to recognize invading pathogens by their conserved molecular patterns or specific effectors, and subsequently trigger defense responses. While pattern-triggered immunity (PTI) stops non- or poorly-adapted pathogens, effector-triggered immunity (ETI) restricts proliferation of adapted pathogens. Intracellular immune receptors that recognize pathogen effectors belong to members of the nucleotide-binding-site and leucine-rich-repeat (NB-LRR) superfamily and are often genetically defined as resistance (R) proteins. In most cases, typical R proteins confer race-specific resistance.  By contrast, the atypical R protein RPW8 from Arabidopsis thaliana confers broad-spectrum resistance against all infectious powdery mildew fungi (Xiao et al., 2001). RPW8 and its tandemly linked homologs are predicted to encode small proteins (18-25 kDa) that contain an N-terminal transmembrane domain or a signal peptide and 1-2 coiled-coil domains. Intriguingly, there exists a small ancient clade of NB-LRRs in many plant families that contain an RPW8-homology N-terminal domain, implying the origin of RPW8.

We recently demonstrated that RPW8 is specifically targeted to the host-pathogen interfacial membrane called the extrahaustorial membrane (EHM) where it activates haustorium-targeted, broad-spectrum mildew resistance. RPW8 is the first protein identified to be localized at the enigmatic EHM, and therefore it provides a unique, powerful tool to interrogate host-pathogen interaction at the interface. Currently, we are taking a combination of cell biological, genetic and biochemical approaches to investigate (i) the structure-function relationship of RPW8 to understand how RPW8 connects and focuses SA-dependent defense to the host-pathogen interface, (ii) the EHM-oriented membrane/protein trafficking pathway, (iii) the origin & biogenesis of the mysterious EHM. We are also using RPW8 as a delivery vehicle to target more generic and effective antimicrobial proteins to the host-pathogen interface to create novel resistance against haustorium-forming pathogens. 

Pathogenicity mechanisms of powdery mildew fungi

Powdery mildew (PM) is one of the most important and widespread crop diseases that constantly reduced plant production.  PM is caused by obligate biotrophic ascomycete fungi in the order of Erysiphales.  Because PM fungi cannot be cultured or transformed, it is very difficult to study this important group of pathogens by conventional genetic approaches. To tackle this challenge, we have recently sequenced the genomes of four dicot PM biotypes. Through a comprehensive comparative analysis of all available PM genomes, we have identified highly conserved as well as lineage-specific candidate pathogenicity genes. Currently, we are conducting comparative genomics-guided, ectopic expression (i.e. in host cells)-enabled, functional studies of key candidate PM genes to understand and intervene PM pathogenesis.

Host nutrient transporters manipulated by powdery mildew

Compared with other ascomycetes, PM fungi have only ~6000 genes, with ~half of their genes lost, explaining why they strictly require living host to complete their life cycle.  This high-level of host dependence implies that many host proteins are required for PM pathogenesis. We are taking forward and reverse genetics approaches to identify host proteins, particularly nutrient transporters, that are targeted by PM effectors for pathogenesis. Understanding how pathogenic fungi manipulate host nutrient machinery can provide novel strategies for developing disease resistance in crop plants.

A summary of current research interests