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ARS Home » Pacific West Area » Albany, California » Plant Gene Expression Center » Research » Publications at this Location » Publication #383674
Research Project: Mining Collections of Wild Germplasm and Novel Defense Regulators for Enhanced Plant Defenses

Location: Plant Gene Expression Center

Title: What the wild things do: Mechanisms of plant host manipulation by bacterial type III-secreted effector proteins

Author
item SCHREIBER, KARL - University Of California
item CHAU-LY, ILEA - University Of California
item Lewis, Jennifer

Submitted to: Microorganisms
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/4/2021
Publication Date: 5/11/2021
Citation: Schreiber, K.J., Chau-Ly, I., Lewis, J.D. 2021. What the wild things do: Mechanisms of plant host manipulation by bacterial type III-secreted effector proteins. Microorganisms. 9(5). Article 1029. https://doi.org/10.3390/microorganisms9051029.
DOI: https://doi.org/10.3390/microorganisms9051029

Interpretive Summary: Plant pathogenic bacteria cause significant yield losses in crop plants. Bacteria inject effector proteins into the plant, where they promote virulence of the bacteria, which results in disease. However, plants can evolve to recognize specific effector proteins and induce immune responses. We discuss how effector proteins manipulate the host to promote disease and how plants can recognize the presence or activity of effector proteins. This work will help identify common targets of pathogens in plants as well as potential approaches for preventing disease.

Technical Abstract: Phytopathogenic bacteria possess an arsenal of effector proteins that enable them to subvert host recognition and manipulate the host to promote pathogen fitness. The type III secretion system (T3SS) delivers type III-secreted effector proteins (T3SEs) from bacterial pathogens such as Pseudomonas syringae, Ralstonia solanacearum, and various Xanthomonas species. These T3SEs interact with and modify a range of intracellular host targets to alter their activity and thereby attenuate host immune signaling. Pathogens have evolved T3SEs with diverse biochemical activities, which can be difficult to predict in the absence of structural data. Interestingly, several T3SEs are activated following injection into the host cell. Here, we review the mechanisms by which T3SEs are activated in the cell, as well as how T3SEs modify host targets to promote virulence or trigger immunity. These mechanisms may suggest common enzymatic activities and convergent targets that could be manipulated to protect crop plants from infection.