Arabidopsis Elongator subunit 2 positively contributes to resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola
The evolutionarily conserved Elongator complex functions in diverse biological processes including salicylic acid-mediated immune response. However, how Elongator functions in jasmonic acid (JA)/ethylene (ET)-mediated defense is unknown. Here, we show that Elongator is required for full induction of the JA/ET defense pathway marker gene PLANT DEFENSIN1.2 (PDF1.2) and for resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola. A loss-of-function mutation in the Arabidopsis Elongator subunit 2 (ELP2) alters B. cinerea-induced transcriptome reprogramming. Interestingly, in elp2, expression of WRKY33,OCTADECANOID-RESPONSIVE ARABIDOPSIS AP2/ERF59 (ORA59), and PDF1.2 is inhibited, whereas transcription of MYC2 and its target genes is enhanced. However, overexpression of WRKY33 or ORA59 and mutation of MYC2 fail to restore PDF1.2 expression andB. cinerea resistance in elp2, suggesting that ELP2 is required for induction of not only WRKY33 and ORA59 but also PDF1.2. Moreover,elp2 is as susceptible as coronatine-insensitive1 (coi1) and ethylene-insensitive2 (ein2) to B. cinerea, indicating that ELP2 is an important player in B. cinerea resistance. Further analysis of the lesion sizes on the double mutants elp2 coi1 and elp2 ein2 and the corresponding single mutants revealed that the function of ELP2 overlaps with COI1 and is additive to EIN2 for B. cinerea resistance. Finally, basal histone acetylation levels in the coding regions of WRKY33, ORA59, and PDF1.2 are reduced in elp2 and a functional ELP2-GFP fusion protein binds to the chromatin of these genes, suggesting that constitutive ELP2-mediated histone acetylation may be required for full activation of the WRKY33/ORA59/PDF1.2 transcriptional cascade.
Learn more about Dr. Mou!
Department of Microbiology and Cell Science University of Florida
Ph.D. (1999) Institute of Genetics, CAS, Beijing, China
Post-doctoral: (2000-2004) DCMB, Department of Biology, Duke University
Description of Research
General area: The signal transduction pathways in plant immunity
Like animals, plants have evolved active defense mechanisms to fight microbial infections. Following pathogen invasion, plants activate multiple signal transduction pathways to mount immunity against the pathogens. We study these signal transduction pathways and their activation mechanisms using the model plant Arabidopsis. Several projects are currently being carried out in the laboratory.
(1) Epigenetic regulation of plant immunity by the Elongator complex
Elongator is a six-subunit complex that has been shown to function in transcription elongation. We identified Elongator mutants (elp) in a genetic screen for suppressors of the npr1 mutant. NPR1 is a key regulator of salicylic acid (SA)-mediated defense responses. The npr1 mutant is completely defective in systemic acquired resistance (SAR), an inducible defense mechanism against a broad-spectrum of pathogens. We found that defense gene activation is delayed in the elp mutants (Defraia et al., 2010). The elp mutants are more susceptible to pathogen infection than wild type, demonstrating a positive role for Elongator in plant immunity. We are using chromatin immunoprecipitation (ChIP), bisulfite sequencing, and microarray to study the epigenetic regulation of defense gene expression by the Elongator complex.
(2) Regulation of plant immunity by extracellular pyridine nucleotides
Our laboratory found for the first time that extracellular NAD(P) activates SA/NPR1-dependent defense responses (Zhang et al., 2009). We are using genetic approaches to identify new components in the extracellular NAD(P)-mediated defense signaling pathway.
(3) Regulation of SA accumulation during pathogen infection
Plants synthesize multiple signal molecules to activate defense responses at and surrounding infection sites. One such signal molecule is SA. Although two mutants that are unable to accumulate SA upon pathogen infection have been identified, it is still not completely understood how SA accumulation is regulated. Our laboratory has developed a high-throughput method for isolation of SA metabolic mutants (Defraia et al., 2008; Marek et al., 2010). Using this method, we are screening for suppressors of npr1, a mutant that accumulates significantly higher levels of SA than wild type. These mutants will be valuable for dissecting the SA-mediated signaling pathway.
(4) Engineering SAR in crop plants
We apply the knowledge gained from the model plant Arabidopsis to agriculturally important crop plants such as citrus. We have transformed the SAR key regulator NPR1 into citrus and found that the transgenic plants exhibited increased resistance to citrus canker (Zhang et al., 2010). We are currently studying/engineering the SAR signaling pathway in citrus to increase resistance to canker and greening, two major diseases threatening Florida’s citrus industry.