Research

Lewis Lab Research

We are interested in understanding the molecular mechanisms of plant immunity, how pathogens adapt to host recognition and how pathogens suppress host immune signaling. Our research focuses on Pseudomonas syringae, a Gram-negative bacterial pathogen that can infect more than 100 plant species. Pathogen-associated molecular patterns (PAMPs) can elicit pattern-triggered immunity in plants to prevent disease (Figure 1A) P. syringae uses the type III secretion system to secrete and translocate effector proteins into the plant (Figure 1B). Many of these effector proteins function primarily in the suppression of host defense signaling (Figure 1B). However recognition of these effector proteins by Nod-like receptors (NLR) (also called resistance (R) proteins) induces immunity (Figure 1C).

Figure 1: Zigzag model of plant-pathogen interactions. A) P. syringae carries Pathogen-Associated Molecular Patterns (PAMPs) like flagellin that are recognized by host Pattern Recognition Receptors (PRRs), resulting in PRR-Triggered Immunity (PTI). B) P. syringae injects type III secreted effectors (T3SEs) into the host using the type III secretion system. T3SEs suppress PTI and resulting in disease. C) Plants evolve nucleotide-binding site leucine-rich repeat containing receptor (NLR) proteins that recognize specific T3SEs, resulting in Effector-Triggered Immunity (ETI). Recognition may occur when the NLR detects the modification made by the T3SE to the guardee (modified guardee in red).

ZAR1 immune receptor is a highly conserved NLR that recognizes many effector proteins

Pathogen effector proteins can be recognized by NOD-like receptors (also called nucleotide-binding leucine-rich repeat receptors), resulting in rapid defense responses. We found that the Pseudomonas syringae type III effector protein HopZ1a is recognized by ZAR1 through its activity on the pseudokinase ZED1. ZAR1 is a highly conserved and ancient Resistance protein that is found in many plant species. We continue to be interested in understanding this system and in engineering recognition of effectors. We also developed ARTIC, the Arabidopsis Resistance gene T-DNA Insertion Collection, as a robust reverse genetic approach to identify NLRs that recognize specific effector proteins.

Bolstering immunity in crop species

Pathogens cause significant crop losses in the absence of durable resistance. This can be exacerbated as pathogens move into new territories. We are using natural genetic diversity in wild relatives of crop species to identify genes that can protect plants from pathogens.

Pathogens manipulate host immune pathways to promote virulence

Pathogens deliver effector proteins to plants primarily to suppress host immune signaling pathways and promote bacterial virulence. We have identified susceptibility hubs that are targeted by P. syringae effectors. We have characterized the interactions between host and bacterial proteins to determine the mechanisms of virulence promotion. We have developed random barcoded transposon-based mutants in bacterial pathogens to identify additional genes that contribute to virulence.

Pathogen molecules elicit basal immune responses

Pathogen-associated molecular patterns can elicit basal immune responses that protect against disease. We identified putative PAMPs in Candidatus Liberibacter species, that cause a devastating disease in citrus called citrus greening. Some PAMPs were able to elicit immune responses in several species, and bolster immunity against infection by an unrelated pathogen.

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