A Phytophthora Effector Manipulates Host Histone Acetylation and Reprograms Defense Gene Expression to Promote Infection

• Published in: Current biology 2017-04, Vol.27 (7), p.981-991
• Main Authors: Kong, Liang, Qiu, Xufang, Kang, Jiangang, Wang, Yang, Chen, Han, Huang, Jie, Qiu, Min, Zhao, Yao, Kong, Guanghui, Ma, Zhenchuan, Wang, Yan, Ye, Wenwu, Dong, Suomeng, Ma, Wenbo, Wang, Yuanchao
• Format: Article
• Language: English
• Subjects: Acetylation; defense gene expression; Fungal Proteins - genetics; Fungal Proteins - metabolism; Gene Expression Regulation, Plant; Glycine max - genetics; Glycine max - immunology; Glycine max - microbiology; H3K9ac; histone acetylation; Host-Pathogen Interactions; Nicotiana - genetics; Nicotiana - immunology; Nicotiana - microbiology; Phytophthora; Phytophthora - pathogenicity; Phytophthora - physiology; Plant Immunity; PsAvh23; Transcription, Genetic; Virulence
• ISSN: 0960-9822; 1879-0445
• DOI: 10.1016/j.cub.2017.02.044

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. [Display omitted] •PsAvh23 is an essential effector for full virulence of Phytophthora sojae•Binding to ADA2, PsAvh23 disrupts the formation of the ADA2-GCN5 subcomplex•PsAvh23 suppresses host ADA2/GCN5-mediated H3K9ac levels to enhance susceptibility•Misregulation of defense genes is most likely due to the decrease of H3K9ac levels Kong et al. find that Phytophthora effector PsAvh23 competitively binds to ADA2 to disrupt ADA2-GCN5 subcomplex formation and subsequently represses the expression of defense genes by decreasing GCN5-mediated H3K9ac levels, suggesting that the pathogen manipulates host histone acetylation to gain virulence.