Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China.
Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, China; Department of Plant Pathology and Microbiology, University of California, Riverside, Riverside, CA 92521, USA.
Curr Biol. 2017 Apr 3;27(7):981-991. doi: 10.1016/j.cub.2017.02.044. Epub 2017 Mar 16.
Immune response during pathogen infection requires extensive transcription reprogramming. A fundamental mechanism of transcriptional regulation is histone acetylation. However, how pathogens interfere with this process to promote disease remains largely unknown. Here we demonstrate that the cytoplasmic effector PsAvh23 produced by the soybean pathogen Phytophthora sojae acts as a modulator of histone acetyltransferase (HAT) in plants. PsAvh23 binds to the ADA2 subunit of the HAT complex SAGA and disrupts its assembly by interfering with the association of ADA2 with the catalytic subunit GCN5. As such, PsAvh23 suppresses H3K9 acetylation mediated by the ADA2/GCN5 module and increases plant susceptibility. Expression of PsAvh23 or silencing of GmADA2/GmGCN5 resulted in misregulation of defense-related genes, most likely due to decreased H3K9 acetylation levels at the corresponding loci. This study highlights an effective counter-defense mechanism by which a pathogen effector suppresses the activation of defense genes by interfering with the function of the HAT complex during infection.
病原体感染期间的免疫反应需要广泛的转录重编程。转录调控的一个基本机制是组蛋白乙酰化。然而,病原体如何干扰这一过程以促进疾病仍然很大程度上未知。在这里,我们证明了大豆病原体大豆疫霉菌产生的细胞质效应子 PsAvh23 作为植物中组蛋白乙酰转移酶 (HAT) 的调节剂。PsAvh23 与 HAT 复合物 SAGA 的 ADA2 亚基结合,并通过干扰 ADA2 与催化亚基 GCN5 的关联来破坏其组装。因此,PsAvh23 抑制了由 ADA2/GCN5 模块介导的 H3K9 乙酰化,并增加了植物的易感性。PsAvh23 的表达或 GmADA2/GmGCN5 的沉默导致防御相关基因的失调,这很可能是由于相应基因座处的 H3K9 乙酰化水平降低所致。本研究强调了一种有效的反防御机制,即病原体效应子通过在感染过程中干扰 HAT 复合物的功能来抑制防御基因的激活。