He, Sheng Yang

Sheng Yang He

University Distinguished Professor
Ph.D., Cornell University

MSU-DOE Plant Research Laboratory
Room 4245 Molecular Plant Sciences
East Lansing, MI 48824
 Phone: (517) 353-9181


Molecular Biology of Plant-Pathogen Interactions

How microbial pathogens cause diseases in higher eukaryotes is a major unresolved question in biology. Our research is focused on the interaction between Arabidopsis thaliana and Pseudomonas syringae. In this model interaction, both the host and the pathogen are genetically and genomically amenable, making it a fascinating system for dissecting the molecular details of bacterial virulence, host defense, and host-pathogen co-evolution. We are currently pursuing four lines of research: (1) We investigate host proteins and pathways targeted by P. syringae virulence proteins. (2) We study the role of stomate-based defense and counter-defense in host- P. syringae interactions. (3) We explore novel strategies to produce disease-resistant plants, based on our basic understanding of the Arabidopsis - P. syringae interaction. ( 4) We study the hrp gene-encoded type III protein secretion system, which injects bacterial virulence proteins directly into the host cell. Our research is driven by scientific questions. All available and proper technologies are used to solve specific questions. This lab provides a supportive environment for students and postdocs to gain experience in molecular biology, genetics, cell biology, and biochemistry, with a specialization in plant-microbe interactions.

The ability of P. syringae to cause disease in susceptible plants or to elicit the hypersensitive response (HR, a rapid plant cell death response associated with plant resistance) in resistant plants is dependent on a cluster of highly conserved bacterial genes, known as hrp genes. Research from our laboratory is contributing to the elucidation of the structure and function of hrp genes. It is now clear that most hrp gene products are involved in the assembly of a type III secretion apparatus in the interface between the infecting bacteria and plant cells. Bacterial virulence proteins (type III effector proteins) traverse the type III secretion apparatus from bacteria directly into the plant cell interior to affect plant physiology, leading to disease.

Host targets of P. syringae type III effector proteins

What do P. syringae type III effector proteins do inside the Arabidopsis cell? What host proteins and pathways are targeted by these bacterial ‘smart bombs? ‘ Answering these questions is fundamental to our understanding of disease development. This is an exciting new area in the field of molecular plant-pathogen interactions. Our recent studies suggest that a major function of P. syringae effector proteins is suppression of host innate immune response (basal defense). Using transgenics, global gene profiling, protein structure, and yeast two-hybrid protein trap methods, we are elucidating the molecular mechanisms by which some of these effector proteins suppress host defense.

Stomate-based defense against bacterial invasion into host tissue

Bacterial invasion into plant tissue is a critical first step in causing infection. It has long been assumed that microscopic surface openings, such as stomata, serve as passive ports of bacterial entry during infection. Surprisingly, we found that stomatal closure is part of a plant defense response to restrict bacterial invasion. To circumvent this host defense, some P. syringae strains produce a polyketide toxin, coronatine, to effectively cause stomatal reopening as an important pathogenesis strategy. We are interested in dissecting the molecular mechanisms underlying the stomata-based host defense and the molecular action of coronatine in the stomatal guard cell.


Producing disease-resistant crop plants is a major goal of the basic research on plant-pathogen interactions. To this end, we are producing plants expressing nonfunctional type III effectors to interfere with the normal interaction of functional type III effectors and their host targets.

Bacterial type III protein secretion mechanism

The molecular mechanism of the Hrp-mediated type III protein secretion from bacteria to plant cells is poorly understood and is an exciting area of research in the fields of microbiology and plant-pathogen interactions. We found that a key feature of this secretion system is the construction of a surface filamentous appendage-the Hrp pilus. Accumulating evidence suggests that the Hrp pilus functions as a conduit (tube) for transporting type III effector protein into the host cell.


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