Plant NLR-type receptors serve as sensitive triggers of host immunity. Their expression has to be well-balanced, due to their interference with various cellular processes and dose-dependency of their defense-inducing activity. A genetic “arms race” with fast-evolving pathogenic microbes requires plants to constantly innovate their NLR repertoires. We previously showed that insertion of the COPIA-R7 retrotransposon into RPP7 co-opted the epigenetic transposon silencing signal H3K9me2 to a new function promoting expression of this Arabidopsis thaliana NLR gene. Recruitment of the histone binding protein EDM2 to COPIA-R7-associated H3K9me2 is required for optimal expression of RPP7. By profiling of genome-wide effects of EDM2, we now uncovered additional examples illustrating effects of transposons on NLR gene expression, strongly suggesting that these mobile elements can play critical roles in the rapid evolution of plant NLR genes by providing the “raw material” for gene expression mechanisms. We further found EDM2 to have a global role in NLR expression control. Besides serving as a positive regulator of RPP7 and a small number of other NLR genes, EDM2 acts as a suppressor of a multitude of additional NLR genes. We speculate that the dual functionality of EDM2 in NLR expression control arose from the need to compensate for fitness penalties caused by high expression of some NLR genes by suppression of others. Moreover, we are providing new insights into functional relationships of EDM2 with its interaction partner, the RNA binding protein EDM3/AIPP1, and its target gene IBM1, encoding an H3K9-demethylase.

植物NLR型受体可作为宿主免疫力的敏感触发因素。由于它们对各种细胞过程的干扰以及其防御诱导活性的剂量依赖性，因此它们的表达必须达到良好的平衡。具有迅速发展的病原微生物的遗传“军备竞赛”要求植物不断创新其NLR组成。我们以前表明，将COPIA-R7逆转录转座子插入RPP7，将表观遗传转座子沉默信号H3K9me2选为促进该拟南芥NLR基因表达的新功能。RPP7的最佳表达需要募集组蛋白结合蛋白EDM2到COPIA- R7相关的H3K9me2。通过对EDM2的全基因组效应进行分析，我们现在发现了其他示例，说明转座子对NLR基因表达的影响，强烈暗示这些可移动元件可通过提供“原始物质”来在植物NLR基因的快速进化中发挥关键作用。基因表达机制。我们进一步发现EDM2在NLR表达控制中具有全局性作用。除了充当RPP7的积极监管者和少数其他NLR基因，EDM2可以抑制许多其他NLR基因。我们推测EDM2在NLR表达控制中的双重功能是由于需要补偿某些NLR基因的高表达而抑制其他基因而导致的适应性损失。此外，我们正在提供有关EDM2及其相互作用伙伴，RNA结合蛋白EDM3 / AIPP1及其编码H3K9-脱甲基酶的目标基因IBM1的功能关系的新见解。