Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/27/2010
Publication Date: 5/1/2011
Citation: Wu, S., Lu, D., Kabbage, M., Wei, H., Swingle, B.M., Dickman, M., He, P., Shan, L. 2011. Bacterial effector HopF2 interacts with AvrPto and suppresses Arabidopsis innate immunity at the plasma membrane. Molecular Plant-Microbe Interactions. 24(5):585-593. Interpretive Summary: Plants have immune systems to protect them from infection with pathogens such as bacteria. The bacteria, on the other hand, have systems to counteract the plants immune response. One way that bacteria do this is by preventing the plants from being able to sense that they have been infected. This paper describes experiments that were aimed at understanding the molecular details of how the bacteria evade detection by the plant and finds that multiple proteins are secreted by the bacteria and that these proteins work together to prevent the plant from sensing the bacteria.
Technical Abstract: Plant pathogenic bacteria inject a cocktail of effector proteins into host plant cells to modulate the host immune response, thereby promoting pathogenicity. How or whether these effectors work cooperatively is largely unknown. The Pseudomonas syringae DC3000 effector HopF2 suppresses the host plants ability to sense the presence of factors associated with the pathogen (i.e., bacterial flagellin, elongation factor Tu, peptidoglycan, lipopolysaccharide and harpin and fungal chitin). Expression of HopF2 in plants potently diminished the flagellin-induced phosphorylation of BIK1, a plasma membrane-associated cytoplasmic kinase. Thus, HopF2 likely intercepts signaling at the plasma membrane immediately upon signal perception. Consistent with the potent suppression function of multiple signaling systems, expression of HopF2 in transgenic plants compromised plant immunity to other microbes (bacteria and fungi) that are not normally capable of producing a pathogenic infection in these plants. Additionally, this paper reports that HopF2 physically interacts with AvrPto (a well known effector), and proposes that the physical interaction enhances the suppressing activity of both AvrPto and HopF2.