Lee Sanghun, Fu Fuyou, Xu Siming, Lee Sang Yeol, Yun Dae-Jin, Mengiste Tesfaye
Department of Botany and Plant Pathology, Purdue University, West Lafayette, Indiana 47907.
Division of Applied Life Sciences (BK 21 Program), Gyeongsang National University, Jinju City 660-701, Korea.
Plant Cell. 2016 Jul;28(7):1640-61. doi: 10.1105/tpc.16.00012. Epub 2016 Jun 27.
Posttranslational modification of histones modulates gene expression affecting diverse biological functions. We showed that the Arabidopsis thaliana histone methyl transferases SET DOMAIN GROUP8 (SDG8) and SDG25 regulate pep1-, flg22-, and effector-triggered immunity as well as systemic acquired resistance. Genome-wide basal and induced transcriptome changes regulated by SDG8 and/or SDG25 showed that two genes of the SDG-dependent transcriptome, CAROTENOID ISOMERASE2 (CCR2) and ECERIFERUM3 (CER3), were also required for plant immunity, establishing mechanisms in defense functions for SDG8 and SDG25. CCR2 catalyzes the biosynthesis of carotenoids, whereas CER3 is involved in the biosynthesis of cuticular wax. SDG8 and SDG25 affected distinct and overlapping global and locus-specific histone H3 lysine 4 (H3K4) and histone H3 lysine 36 (H3K36) methylations. Loss of immunity in sdg mutants was attributed to altered global and CCR2- and CER3-specific histone lysine methylation (HLM). Loss of immunity in sdg, ccr2, and cer3 mutants was also associated with diminished accumulation of lipids and loss of cuticle integrity. In addition, sdg8 and sdg25 mutants were impaired in H2B ubiquitination (H2Bubn) at CCR2, CER3, and H2Bubn regulated R gene, SNC1, revealing crosstalk between the two types of histone modifications. In summary, SDG8 and SDG25 contribute to plant immunity directly through HLM or indirectly through H2Bubn and by regulating expression of plant immunity genes, accumulation of lipids, biosynthesis of carotenoids, and maintenance of cuticle integrity.
组蛋白的翻译后修饰可调节基因表达，影响多种生物学功能。我们发现，拟南芥组蛋白甲基转移酶SET结构域组8（SDG8）和SDG25可调节肽聚糖1（pep1）、鞭毛蛋白22（flg22）和效应子触发的免疫反应以及系统获得性抗性。由SDG8和/或SDG25调控的全基因组基础转录组和诱导转录组变化表明，SDG依赖转录组中的两个基因，类胡萝卜素异构酶2（CCR2）和蜡质3（CER3），也是植物免疫所必需的，从而确立了SDG8和SDG25在防御功能中的作用机制。CCR2催化类胡萝卜素的生物合成，而CER3参与角质层蜡质的生物合成。SDG8和SDG25影响不同且部分重叠的全基因组和基因座特异性组蛋白H3赖氨酸4（H3K4）和组蛋白H3赖氨酸36（H3K36）甲基化。sdg突变体中免疫功能的丧失归因于全基因组以及CCR2和CER3特异性组蛋白赖氨酸甲基化（HLM）的改变。sdg、ccr2和cer3突变体中免疫功能的丧失还与脂质积累减少和角质层完整性丧失有关。此外，sdg8和sdg25突变体在CCR2、CER3处的H2B泛素化（H2Bubn）以及H2Bubn调控的R基因SNC1中受损，揭示了两种组蛋白修饰之间的相互作用。总之，SDG8和SDG25通过HLM直接或通过H2Bubn间接促进植物免疫，并通过调节植物免疫基因的表达、脂质积累、类胡萝卜素生物合成和维持角质层完整性来实现。
