Plants and microbial pathogens co-evolve their mechanisms of detection and evasion, respectively. Plants detect the presence of conserved Pathogen Associated Molecular Patterns (PAMPs) via cell surface localised pattern-recognition receptors and activate PAMP-triggered immunity (PTI). Pathogens, however, have evolved mechanisms to suppress PTI by delivering ‘effector’ proteins into the host cell. Effectors attenuate plant immunity by interfering with the function of their host target proteins. In turn, plants evolved disease resistance (R) proteins that can recognize corresponding effectors (thereafter termed avirulent effector) and activate a strong defence system known as effector-triggered immunity (ETI), which includes rapid transcriptional reprogramming and programmed cell death in the infected cells.
We are interested in understanding the mechanisms of plant innate immunity and microbial pathogenesis. In particular, we focus on the following topics.
1. What is the molecular basis of activation and suppression of HopZ5-triggered immunity in Arabidopsis?
Pseudomonas-Arabidopsis pathosystem is a well-studied model system for investigating molecular basis of various pathogen effector recognition in plants. A kiwifruit pathogen Pseudomonas syringae pv. actinidiae effector HopZ5 triggers immune responses in Arabidopsis. HopZ5 possesses acetyltransferase activity which is required for its avirulence in planta. However, in most of Arabidopsis accession, an immune suppressor gene SOBER1 (Suppressor of AvrBsT-elicited resistance 1) suppresses HopZ5-triggered immunity presumably by deacetylation of the HopZ5 avirulence target(s).
Our research aim is to understand how HopZ5 activates the plant immune system and how SOBER1 can effectively suppress the HopZ5-triggered immunity in Arabidopsis. For this end, we focus on genetic mapping of HopZ5 immune receptor and investigation of biochemical interaction between HopZ5, SOBER1 and the HopZ5 immune receptor.
2. What are the key mechanisms underpinning RRS1/RPS4-mediated immunity in response to pathogen effectors?
Plants deploy a complex innate immune system to protect themselves against invading pathogens. Inside of the plant cell, nucleotide-binding domain and leucine-rich repeat (NLR) proteins encoded by resistance (R) genes specifically detect proteins secreted from pathogens (effectors) leading to resistance. Since a constantly “on” immune system has several penalties, precise activation of immunity in response to effectors is critical.
While NLR activation in response to effectors is a well-studied area, the mechanistic underpinnings of NLR signaling and immune activation remain intriguingly mysterious. The NLR pair of RRS1 and RPS4 contribute to immunity in Arabidopsis- effectors (AvrRps4 or PopP2) are perceived by the “sensor” RRS1 which leads to immune signaling by the “activator” RPS4. An allele of RRS1 with a Leucine insertion in its C-terminal WRKY domain (slh1) leads to temperature and RPS4-dependent autoimmunity. A suppressor screen identified intragenic mutations in both RPS4 and RRS1 which suppress autoimmunity. Tantalizingly, a set of mutations which suppress autoimmunity and are not in RPS4 or RRS1 also exist. We hypothesize that these unknown mutations will uncover novel genes important to the suppression of immunity in the absence of pathogen threats and to appropriate, precise immune activation.
3. How does guardee protein, RIN4, mediate the recognition of two distinct avirulent effectors, AvrRpt2 and AvrRpm1?
Resistance to Pseudomonas syringae 2 (RPS2), a well-characterized CC-NB-LRR class plant immune receptor, confers disease resistance against Pseudomonas syringae strains carrying a type III secretion-dependent avirulent effector avrRpt2. Erwinia amylovora, an important pathogen of apple and pear, also carries avrRpt2. Recently, it was reported that MR5, another CC-NB-LRR found in an apple, recognize avrRpt2. Recognition of avrRpt2 in Arabidopsis and apple both require an guardee protein, RPM1 interacting protein4 (RIN4). RIN4 is also known to mediate the recognition of avirulent effector, avrRpm1 by RPM1.
Comparative analysis between Arabidopsis RIN4 and apple RIN4 showed that RPS2 and MR5 recognize avrRpt2 in distinct ways. Also, we found that two critical residues of RIN4 are important in the repression or activation of RPS2, RPM1, or MR5 in variant-dependent manner. These discoveries suggest that not only NLRs but also decoy/guardee proteins are possibly under diversifying selection and play an important role in the coevolution between plants and pathogens in nature.
4. How do we develop Bacterial wilt-resistant crops?
Ralstonia solanacearum is a challenging bacterial pathogen causing lethal bacterial wilt disease in a wide range of hosts and is particularly devastating in crops like tomato, potato, peppers etc. Owing to large genetic diversity and limited resistant resources, breeding resistance against Ralstonia solanacearum has been difficult to achieve. Our lab is interested in understanding various aspects of Ralstonia solanacearum interaction with hosts such as Capsicum annum (pepper) and Solanum americanum (black nightshade). We focus on identifying the genetic determinants of bacterial wilt disease and further characterizing their molecular interaction. The long-term goal of this project is to discover important NLRs against Ralstonia solanacearum avirulence effectors and incorporate the resistance genes into elite commercial cultivars leading to improved crop production through rational crop protection design.