Mediator是一种高度保守的蛋白质复合物,在RNA聚合酶II(RNAPII)介导的转录中起转录共激活因子的作用。拟南芥介体复合物最近与植物免疫反应有关。这里,我们比较了水杨酸(SA)-,茉莉酸甲酯(MeJA)-,和乙烯(ET)前体1-氨基环丙烷-1-羧酸(ACC)在14个拟南芥Mediator亚基突变体中诱导的防御和/或伤口响应基因表达。我们的结果表明,MED14,MED15和MED16是SA激活的防御标记基因PATHOEGNESIS相关GENE1的表达所必需的,MED25是MeJA诱导的伤口反应标记基因VEGATATIVESTORAGEPROTEIN1(VSP1)的表达所必需的,MED8,MED14,MED15,MED16,MED18,MED20a,MED25,MED31和MED33A/B(MED33a和MED33B)是MeJA诱导的防御标记基因PLANTDEFENSIN1.2(PDF1.2)表达所必需的,和MED8,MED14,MED15,MED16,MED25和MED33A/B也是ACC触发的PDF1.2表达所必需的。此外,我们调查了MED14,MED15和MED16在植物防御信号串扰中的参与,发现MED14,MED15和MED16是SA和ET介导的抑制MeJA诱导的VSP1表达所必需的。该结果表明MED14,MED15和MED16不仅将SA和JA/ET防御途径的防御信号传递给RNAPII转录机制,而且还微调防御信号串扰。最后,我们表明,MED33A/B有助于坏死性真菌病原体灰霉病菌诱导的防御基因PDF1.2的表达,和基本的甲壳素,并且是全面的基础抗B.cinerea所必需的,证明MED33在植物对坏死性真菌病原体的免疫中具有积极作用。
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.