Multiple Roles of WIN3 in Regulating Disease Resistance, Cell Death, and Flowering Time in Arabidopsis      

Abstract

The salicylic acid (SA) regulatory gene HOPW1-1-INTERACTING3 (WIN3) was previously shown to confer resistance to the biotrophic pathogen Pseudomonas syringae. Here, we report that WIN3 controls broad-spectrum disease resistance to the necrotrophic pathogen Botrytis cinerea and contributes to basal defense induced by flg22, a 22-amino acid peptide derived from the conserved region of bacterial flagellin proteins. Genetic analysis indicates that WIN3 acts additively with several known SA regulators, including PHYTOALEXIN DEFICIENT4, NONEXPRESSOR OF PR GENES1 (NPR1), and SA INDUCTION-DEFICIENT2, in regulating SA accumulation, cell death, and/or disease resistance in the Arabidopsis (Arabidopsis thaliana) mutant acd6-1. Interestingly, expression of WIN3 is also dependent on these SA regulators and can be activated by cell death, suggesting that WIN3-mediated signaling is interconnected with those derived from other SA regulators and cell death. Surprisingly, we found that WIN3 and NPR1 synergistically affect flowering time via influencing the expression of flowering regulatory genes FLOWERING LOCUS C and FLOWERING LOCUS T. Taken together, our data reveal that WIN3 represents a novel node in the SA signaling networks to regulate plant defense and flowering time. They also highlight that plant innate immunity and development are closely connected processes, precise regulation of which should be important for the fitness of plants.

Genetic Dissection of Salicylic Acid-Mediated Defense Signaling Networks in Arabidopsis

“…Twenty-five-day-old plants were harvested for SA extraction followed by HPLC analysis as previously described (Wang et al 2011a).…”

“…We previously used the defense-sensitized mutant acd6-1 to elucidate functional relationships between several SA genes (Song et al 2004b;Lu et al 2009;Wang et al 2011a). In this genetic analysis, we introduced two mutations that affect SAmediated defense, each of which is known to cause suppression of acd6-1-conferred phenotypes, into the acd6-1 background and assessed whether the two mutations together result in additive or nonadditive suppression of acd6-1-conferred phenotypes.…”

“…Increasing evidence suggests that defense signaling networks are complex, involving crosstalk to many other signaling pathways (Feys and Parker 2000;Kunkel and Brooks 2002;Wang et al 2007;Koornneef and Pieterse 2008;De Torres Zabala et al 2009) and to plant development (Martinez et al 2004;Endo et al 2009;Wang et al 2011a). A variety of strategies are used to interrogate the topology of defense networks.…”

“…Type III SA genes act downstream of SA accumulation. The best-characterized type III SA gene is NONEXPRESSOR OF PR GENES 1 (NPR1), which is the major SA signal transducer (Cao et al 1997;Ryals et al 1997;Shah et al 1997;Dong 2004 (Martinez et al 2004;Endo et al 2009;Wang et al 2011a). A variety of strategies are used to interrogate the topology of defense networks.…”

Revealing Shared and Distinct Gene Network Organization in Arabidopsis Immune Responses by Integrative Analysis

“…LOV1 is a master regulator of flowering and cold response (Yoo et al, 2007), and its overexpression in switchgrass (Panicum virgatum) induces alterations lignin content and cell wall composition (Xu et al, 2012). Plant development and innate immunity are closely linked, and previous studies have uncovered several genes that can regulate both flowering time and plant immunity, including HOPW1-1-INTERACTING3, NPR1, and Plant U-box protein13 (Wang et al, 2011a;Li et al, 2012). Therefore, we infer that LOV1 is an immune-related candidate gene that warrants further characterization.…”