Location: Plant, Soil and Nutrition ResearchTitle: The raf-like kinase ILK1 and the high affinity K+ transporter HAK5 are required for innate immunity and abiotic stress response
|BRAUER, ELIZABETH - Boyce Thompson Institute|
|AHSAN, NAGIB - Cornell University - New York|
|DALE, RENEE - Louisiana State University|
|KATO, NAOHIRO - Louisiana State University|
|COLUCCIO, ALISON - Boyce Thompson Institute|
|THELEN, JAY - University Of Missouri|
|POPESCU, SORINA - Boyce Thompson Institute|
Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/29/2016
Publication Date: 5/2/2016
Citation: Brauer, E.K., Ahsan, N., Dale, R., Kato, N., Coluccio, A.E., Pineros, M., Kochian, L.V., Thelen, J.J., Popescu, S. 2016. The raf-like kinase ILK1 and the high affinity K+ transporter HAK5 are required for innate immunity and abiotic stress response. Plant Physiology. doi: 10.1104/pp.16.00035.
Interpretive Summary: Plants, like humans and animals, have an immune system that identifies molecular components of invading pathogens which activates defense systems to inhibit pathogen entry and multiplication in the plant. A number of the early responses involve the transport of ions including calcium ions and protons into and out of the plant cells under pathogen attack. This study focuses on the identification of the molecular components that mediate the pathogen-induced ion transport processes. Here we report on the identification of a signaling protein called integrin-linked kinase (ILK) that is a controller of ion transport mediated signal responses involving potassium transport. In this study we discovered that the ILK1 protein interacts with a novel potassium uptake transport protein, HAK5, to mediate changes in ion homeostasis associated with pathogen signaling and defense. We also found that the ILK1 protein plays a role in tolerance to plant response to the toxic metal ion, Na+, during salt stress. When the expression of the gene encoding ILK1 is reduced, plant tolerance to salt stress increases. These findings improve our understanding of the early events in plant response to pathogen attack, which in turn may assist researchers in using molecular approaches to improve plant tolerance and resistance to pathogens that can greatly reduce crop yields.
Technical Abstract: Plants combat bacterial infection by detecting conserved molecular signatures called pathogen-associated molecular patterns (PAMPs) and producing defensive compounds to restrict pathogen entry and reproduction. Numerous ion fluxes are activated within minutes of PAMP perception, including Ca2+ influx and anion efflux, which are required for membrane depolarization and gene induction. However, the molecular components that mediate these ion fluxes are unknown. Here, we report that the INTEGRIN-LINKED KINASE1 (ILK1) promotes signaling responses to the PAMP flg22 through its contribution to K+ homeostasis and plasma membrane depolarization. We confirmed our previous findings that ILK1 interacts with CML9, a Ca2+-sensing calmodulin-like protein, and demonstrate that ILK1 activity is repressed by CML9. ILK1 promotes basal immunity and response to osmotic stress and flg22. ILK1 also interacts with the HAK5 high affinity K+ transporter and contributes to dynamic changes in ion homeostasis induced by flg22 and NaCl, including changes in K+ content. Both HAK5 and ILK1 affect the rate of flg22-induced plasma membrane depolarization, K+ transport and gene induction in leaf cells where depolarization could also be delayed by applying chemical K+ transport inhibitors. Furthermore, we demonstrated that HAK5 protein accumulation is significantly enhanced by the presence of both ILK1 and CML9 in planta. Together, our data indicate that flagellin-induced signaling responses are influenced by ILK1- and HAK5-mediated K+ transport at the plasma membrane. These findings reveal a previously unidentified role for potassium nutrition in modulating PAMP-activated gene expression and shed light on the mechanisms regulating membrane depolarization dynamics during immunity.