Abstract

Mediator is a highly conserved protein complex that functions as a transcriptional coactivator in RNA polymerase II (RNAPII)-mediated transcription. The Arabidopsis Mediator complex has recently been implicated in plant immune responses. Here, we compared salicylic acid (SA)-, methyl jasmonate (MeJA)-, and the ethylene (ET) precursor 1-aminocyclopropane-1-carboxylic acid (ACC)-induced defense and/or wound-responsive gene expression in 14 Arabidopsis Mediator subunit mutants. Our results show that MED14, MED15, and MED16 are required for SA-activated expression of the defense marker gene PATHOEGNESIS-RELATED GENE1, MED25 is required for MeJA-induced expression of the wound-responsive marker gene VEGATATIVE STORAGE PROTEIN1 (VSP1), MED8, MED14, MED15, MED16, MED18, MED20a, MED25, MED31, and MED33A/B (MED33a and MED33B) are required for MeJA-induced expression of the defense maker gene PLANT DEFENSIN1.2 (PDF1.2), and MED8, MED14, MED15, MED16, MED25, and MED33A/B are also required for ACC-triggered expression of PDF1.2. Furthermore, we investigated the involvement of MED14, MED15, and MED16 in plant defense signaling crosstalk and found that MED14, MED15, and MED16 are required for SA- and ET-mediated suppression of MeJA-induced VSP1 expression. This result suggests that MED14, MED15, and MED16 not only relay defense signaling from the SA and JA/ET defense pathways to the RNAPII transcription machinery, but also fine-tune defense signaling crosstalk. Finally, we show that MED33A/B contributes to the necrotrophic fungal pathogen Botrytis cinerea-induced expression of the defense genes PDF1.2, HEVEIN-LIKE, and BASIC CHITINASE and is required for full-scale basal resistance to B. cinerea, demonstrating a positive role for MED33 in plant immunity against necrotrophic fungal pathogens.

Highlights

  • Salicylic acid (SA), jasmonates (JAs), and ethylene (ET) are the primary defense signal molecules of the plant immune system (Pieterse et al, 2009)

  • To compare the function of different Arabidopsis Mediator subunits in the salicylic acid (SA), JA, and ET signaling pathways, we tested SA-induced expression of the SA pathway marker gene PATHOEGNESIS-RELATED GENE1 (PR1), methyl jasmonate (MeJA)-induced expression of the wound-responsive marker gene VEGATATIVE STORAGE PROTEIN1 (VSP1) and the defense marker gene PLANT DEFENSIN1.2 (PDF1.2), and ACC-induced expression of PDF1.2 in the previously described 13 Mediator subunit mutants except that a med33a/b double mutant was used to replace the med33b single mutant (Wang et al, 2015b)

  • Note that the observation that MeJA-induced PDF1.2 expression was significantly decreased in med18 is in contrast to the previous report (Lai et al, 2014). This discrepancy is probably due to different growth conditions. These results indicate that, among the 14 Mediator subunits, MED14, MED15, and MED16 are required for SA-activated PR1 expression, MED25 is required for MeJA-induced VSP1 expression, MED8, MED14, MED15, MED16, MED18, MED20a, MED25, MED31, and MED33A/B are required for MeJA-induced PDF1.2 expression, and MED8, MED14, MED15, MED16, MED25, and MED33A/B are required for ACC-induced PDF1.2 expression

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Summary

Introduction

Salicylic acid (SA), jasmonates (JAs), and ethylene (ET) are the primary defense signal molecules of the plant immune system (Pieterse et al, 2009). A Role of Mediator in Defense Signaling Crosstalk van Loon et al, 2006; Loake and Grant, 2007) While each of these signal molecules induces a specific defense signaling pathway(s), there is extensive crosstalk among them (Thomma et al, 2001; Glazebrook, 2005; Pieterse et al, 2009). SA and JA signaling mostly antagonize each other, and ET enhances both SA- and JA-mediated defense responses against pathogens, but suppresses JA-mediated wound signaling. Such crosstalk allows plants to prioritize one defense response over others when encountering a specific attacker. Defense signaling crosstalk has been extensively studied in recent years (Pieterse et al, 2009), but the underlying molecular mechanisms still await full characterization

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