Abstract
Tomato Atypical Receptor Kinase 1 (TARK1) is a pseudokinase required for postinvasion immunity. TARK1 was originally identified as a target of the Xanthomonas euvesicatoria effector protein Xanthomonas outer protein N (XopN), a suppressor of early defense signaling. How TARK1 participates in immune signal transduction is not well understood. To gain insight into TARK1's role in tomato (Solanum lycopersicum) immunity, we used a proteomics approach to isolate and identify TARK1-associated immune complexes formed during infection. We found that TARK1 interacts with proteins predicted to be associated with stomatal movement. TARK1 CRISPR mutants and overexpression (OE) lines did not display differences in light-induced stomatal opening or abscisic acid-induced stomatal closure; however, they did show altered stomatal movement responses to bacteria and biotic elicitors. Notably, we found that TARK1 CRISPR plants were resistant to Pseudomonas syringae pathovar tomato strain DC3000-induced stomatal reopening, and TARK1 OE plants were insensitive to P syringae pathovar tomato strain DC3118 (coronatine deficit)-induced stomatal closure. We also found that TARK1 OE in leaves resulted in increased susceptibility to bacterial invasion. Collectively, our results indicate that TARK1 functions in stomatal movement only in response to biotic elicitors and support a model in which TARK1 regulates stomatal opening postelicitation.
Highlights
Pathogens have developed a number of different strategies to invade and multiply within host plant tissues and plants have evolved countermeasures to combat encroaching pathogens
Previous work uncovered a role for Tomato Atypical Receptor Kinase 1 (TARK1) in the positive regulation of post-invasion immunity in tomato leaves in response to bacterial infection (Kim et al, 2009)
We hypothesized that TARK1 might interact with pattern recognition receptors (PRRs) or other membrane-associated proteins in leaf cells to regulate and/or amplify defense signal transduction during pathogen-triggered immunity (PTI)
Summary
Pathogens have developed a number of different strategies to invade and multiply within host plant tissues and plants have evolved countermeasures to combat encroaching pathogens. One of the first stages dictating antagonistic interactions between host and pathogen begins with the perception of microbial patterns called microbe-associated molecular patterns (MAMPs), which are detected by cell surface localized pattern recognition receptors (PRRs) (Jones and Dangl, 2006). This response initiates signaling cascades that generate reactive oxygen species (ROS), activate mitogen-activated protein kinases (MAPKs), and transcribe defense related genes aimed to limit pathogen growth and host invasion. One of the primary structures that gate access to the apoplast and restrict pathogen invasion are guard cell pores called stomata. Detection of bacterial MAMPs by PRRs within leaves leads to stomatal closure, a defense response referred to as stomatal immunity (Melotto et al., 2006; Zeng and He, 2010)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
