Arabidopsis HOOKLESS1 Regulates Responses to Pathogens and Abscisic Acid through Interaction with MED18 and Acetylation of WRKY33 and ABI5 Chromatin

被引:76
|
作者
Liao, Chao-Jan [1 ]
Lai, Zhibing [2 ]
Lee, Sanghun [1 ]
Yun, Dae-Jin [3 ]
Mengiste, Tesfaye [1 ]
机构
[1] Purdue Univ, Dept Bot & Plant Pathol, W Lafayette, IN 47907 USA
[2] Huazhong Agr Univ, Natl Key Lab Crop Genet Improvement, Wuhan 430070, Peoples R China
[3] Gyeongsang Natl Univ, Div Appl Life Sci, BK Program 21, Jinju 660701, South Korea
来源
PLANT CELL | 2016年 / 28卷 / 07期
基金
美国国家科学基金会;
关键词
REVERSIBLE HISTONE ACETYLATION; SYSTEMIC ACQUIRED-RESISTANCE; PLANT DEFENSIN GENE; SALICYLIC-ACID; ANTAGONISTIC INTERACTION; INDEPENDENT FUNCTIONS; TRANSCRIPTION FACTOR; ANTIOXIDANT DEFENSE; TRIGGERED IMMUNITY; SIGNALING PATHWAY;
D O I
10.1105/tpc.16.00105
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Arabidopsis thaliana HOOKLESS1 (HLS1) encodes a putative histone acetyltransferase with known functions in seedling growth. Here, we show that HLS1 regulates plant responses to pathogens and abscisic acid (ABA) through histone acetylation at chromatin of target loci. The hls1 mutants show impaired responses to bacterial and fungal infection, accelerated senescence, and impaired responses to ABA. HLS1 modulates the expression of WRKY33 and ABA INSENSITIVE5 (ABI5), known regulators of pathogen and ABA responses, respectively, through direct association with these loci. Histone 3 acetylation (H3Ac), a positive mark of transcription, at WRKY33 and ABI5 requires HLS1 function. ABA treatment and pathogen infection enhance HLS1 recruitment and H3Ac at WRKY33. HLS1 associates with Mediator, a eukaryotic transcription coregulatory complex, through direct interaction with mediator subunit 18 (MED18), with which it shares multiple functions. HLS1 recruits MED18 to the WRKY33 promoter, boosting WKRY33 expression, suggesting the synergetic action of HLS1 and MED18. By contrast, MED18 recruitment to ABI5 and transcriptional activation are independent of HLS1. ABA-mediated priming of resistance to fungal infection was abrogated in hls1 and wrky33 mutants but correlated with ABA-induced HLS1 accumulation. In sum, HLS1 provides a regulatory node in pathogen and hormone response pathways through interaction with the Mediator complex and important transcription factors.
引用
收藏
页码:1662 / 1681
页数:20
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