Cyclic nucleotide-gated ion channel (CNGC)-mediated signal transduction and hormonal crosstalk in plant natural immunity

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BACKGROUND:Due to global population growth, increasing food production is an urgent issue in the world. However, significant amounts of agricultural products are lost annually due to plant disease in spite of the extensive usage of agrochemicals that may harm the environment. Thus, the understanding of plant immunity and finding ways to enhance natural resistance of plans is the key for security of food production and a healthy environment in the future. To date, we have shown that the cyclic nucleotide-gated ion channels CNGC11 and 12 play significant roles in plant immunity and we have analyzed their structure-function relationships. We also used a CNGC mutant to examine signal crosstalk. In animals, CNGCs affect visual and olfactory signal transduction and are regulated by the calcium sensor protein calmodulin (CaM). However, in plants, the regulators of CNGCs and their downstream signal transduction cascades remain largely unknown. RESEARCH OBJECTIVE AND OUTLINE:The long-term goal of my research is to understand the signal transduction pathways and networks integrating environmental stresses with pathogen infection at the molecular level. To this aim, over the next 5 years we will: I) Identify and characterize components of CNGC-mediated signal transduction, II) Investigate the regulation of CNGCs, and III) Investigate hormonal crosstalk and environmental effects on plant immunity.For aim I, we identified rdd1, a suppressor of the CNGC2 null mutant dnd1 (defense no death1), which displays an autoimmune phenotype. Thus, RDD1 likely acts downstream of CNGC2-mediated disease resistance signaling or on a signaling cascade that affects CNGC2 signaling. The proposed work will investigate the involvement of RDD1 in CNGC-mediated resistance signaling at the molecular level. Furthermore, we identified five additional suppressors, which we will characterize and identify. Aim II addresses regulation of CNGCs by CaM. Animal CNGC research showed that CaM binding negatively regulates CNGCs; however, the regulation of plant CNGCs by CaM remains unclear. In this proposal, we will determine the CaM binding domains in plant CNGCs and characterize their binding kinetics upon pathogen infection.Aim III addresses the crosstalk between salicylic acid (SA), abscisic acid (ABA) and auxin. SA is a key signaling molecule in plant immunity and the complex crosstalk among SA, ABA and auxin strongly influences disease resistance. This suggests a coordinated signaling network allowing plants to allocate resources to fight pathogens, respond to abiotic stresses and maintain growth. In addition, our current data indicate that environmental factors affect CNGC signaling. To identify the key nodes in this crosstalk, we conducted a yeast two-hybrid analysis of ABA- and SA-inducible proteins and discovered several candidate interactions that may mediate crosstalk. In this proposal, we will analyze molecular mechanisms of these candidates and conduct another interactome analysis between SA and auxin signaling components.PREDICTED SIGNIFICANCE:The outcome of this proposal will significantly contribute to our understanding of CNGC-mediated plant immune responses. Furthermore, hormonal crosstalk in plant immunity has emerged as an important topic, since it is related to environmental conditions. Currently, plant diseases cause significant annual losses of agricultural products, despite the extensive use of costly agro-chemicals. In addition, unstable climate conditions may increase the frequency of disease outbreaks. Thus, the proposed program will significantly impact agricultural research to improve plant disease resistance for a sustainable human society.