Methyl Salicylate Glucosylation Regulates Plant Defense Signaling and Systemic Acquired Resistance

丁香假单胞菌 系统获得性抵抗 水杨酸 拟南芥 拟南芥 生物 突变体 植物抗病性 病菌 微生物学 植物对草食的防御 生物化学 基因
作者
Lu Chen,Wen-Shuai Wang,Ting Wang,Xia‐Fei Meng,Tingting Chen,Xu‐Xu Huang,Yanjie Li,Bingkai Hou
出处
期刊:Plant Physiology [Oxford University Press]
卷期号:180 (4): 2167-2181 被引量:91
标识
DOI:10.1104/pp.19.00091
摘要

Plant systemic acquired resistance (SAR) provides an efficient broad-spectrum immune response to pathogens. SAR involves mobile signal molecules that are generated by infected tissues and transported to systemic tissues. Methyl salicylate (MeSA), a molecule that can be converted to salicylic acid (SA), is an essential signal for establishing SAR, particularly under a short period of exposure to light after pathogen infection. Thus, the control of MeSA homeostasis is important for an optimal SAR response. Here, we characterized a uridine diphosphate-glycosyltransferase, UGT71C3, in Arabidopsis (Arabidopsis thaliana), which was induced mainly in leaf tissue by pathogens including Pst DC3000/avrRpt2 (Pseudomonas syringae pv tomato strain DC3000 expressing avrRpt2). Biochemical analysis indicated that UGT71C3 exhibited strong enzymatic activity toward MeSA to form MeSA glucosides in vitro and in vivo. After primary pathogen infection by Pst DC3000/avrRpt2, ugt71c3 knockout mutants exhibited more powerful systemic resistance to secondary pathogen infection than that of wild-type plants, whereas systemic resistance in UGT71C3 overexpression lines was compromised. In agreement, after primary infection of local leaves, ugt71c3 knockout mutants accumulated significantly more systemic MeSA and SA than that in wild-type plants. whereas UGT71C3 overexpression lines accumulated less. Our results suggest that MeSA glucosylation by UGT71C3 facilitates negative regulation of the SAR response by modulating homeostasis of MeSA and SA. This study unveils further SAR regulation mechanisms and highlights the role of glucosylation of MeSA and potentially other systemic signals in negatively modulating plant systemic defense.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
外套waitlen发布了新的文献求助10
刚刚
简单的思菱完成签到 ,获得积分10
1秒前
xxj完成签到 ,获得积分10
2秒前
我瞎蒙完成签到,获得积分10
2秒前
3秒前
喜悦的板凳完成签到 ,获得积分10
4秒前
张小度ever完成签到 ,获得积分10
4秒前
5秒前
钟sss完成签到 ,获得积分10
5秒前
踏实采波完成签到,获得积分10
7秒前
7秒前
kaka发布了新的文献求助10
7秒前
gaga发布了新的文献求助10
9秒前
zzl1111完成签到,获得积分10
9秒前
外套waitlen完成签到,获得积分20
9秒前
mrjohn完成签到,获得积分10
10秒前
钟sss关注了科研通微信公众号
11秒前
yueyueyue完成签到,获得积分10
11秒前
沟通亿心完成签到,获得积分10
11秒前
叶雨思空完成签到 ,获得积分10
13秒前
13秒前
谢花花完成签到 ,获得积分10
14秒前
SHuEvan完成签到,获得积分10
14秒前
小男孩完成签到,获得积分10
14秒前
加油加油完成签到 ,获得积分10
14秒前
隐形的迎南完成签到,获得积分10
15秒前
阿巴阿巴完成签到,获得积分10
15秒前
金先生发布了新的文献求助10
16秒前
棵虫完成签到,获得积分10
16秒前
nong12123完成签到,获得积分10
18秒前
星空完成签到 ,获得积分10
18秒前
席涑完成签到,获得积分10
21秒前
隐形竺完成签到,获得积分10
21秒前
lhl完成签到,获得积分10
22秒前
英姑应助nong12123采纳,获得10
22秒前
songf11完成签到,获得积分10
23秒前
meiqiu完成签到 ,获得积分10
23秒前
麦麦完成签到,获得积分10
23秒前
倪小呆完成签到 ,获得积分10
23秒前
薄荷味完成签到 ,获得积分0
24秒前
高分求助中
Technologies supporting mass customization of apparel: A pilot project 600
Izeltabart tapatansine - AdisInsight 500
Chinesen in Europa – Europäer in China: Journalisten, Spione, Studenten 500
Arthur Ewert: A Life for the Comintern 500
China's Relations With Japan 1945-83: The Role of Liao Chengzhi // Kurt Werner Radtke 500
Two Years in Peking 1965-1966: Book 1: Living and Teaching in Mao's China // Reginald Hunt 500
Epigenetic Drug Discovery 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3815941
求助须知:如何正确求助?哪些是违规求助? 3359417
关于积分的说明 10402560
捐赠科研通 3077261
什么是DOI,文献DOI怎么找? 1690255
邀请新用户注册赠送积分活动 813693
科研通“疑难数据库(出版商)”最低求助积分说明 767743