The hyccin-containing protein ECDR1 interacts with PI3K1 and PI4K1 and regulates broad-spectrum disease resistance in rice

生物 程序性细胞死亡 植物免疫 功能(生物学) 突变体 细胞生物学 PI3K/AKT/mTOR通路 基因 植物抗病性 细胞 免疫 植物对草食的防御 调节器 表型 遗传学 疾病 拟南芥 过敏反应 负调节器 自身免疫 T细胞 免疫系统 先天免疫系统 基因组 细胞信号 信号转导 防御机制 突变
作者
Shuang Zhang,Lingzhi Meng,Zhichao Zhao,Changyan Qi,Chen Xie,Xiaokang Jiang,Ling Jiang,Yulong Ren,Zhijun Cheng,Jie Wang,Qibing Lin,Xiuping Guo,Xin Wang,Shanshan Zhu,Cailin Lei,Jianmin Wan
出处
期刊:Plant Physiology [Oxford University Press]
标识
DOI:10.1093/plphys/kiag663
摘要

Programmed cell death and immunity in plants are finely orchestrated to promote antimicrobial defense while preventing autoimmunity. However, the molecular mechanisms involved are not fully understood. Here, we isolated a rice mutant ecdr1 (enhanced cell death and resistance 1) that displayed an autoimmunity phenotype and enhanced resistance to rice blast and bacterial blight, and identified ECDR1 as a new shared component in PI3K and PI4K complexes, linking the hyccin-containing protein with plant defense responses. ECDR1 was expressed at all developmental stages and in all tissues examined. The ECDR1 was highly conserved in function across monocots and dicots. The 113 bp deletion in the ECDR1 promoter reduced its expression, leading to cell death and enhanced disease resistance. The ECDR1 was localized in plasma membrane, and interacted with TPR1 and TPR2 which in turn interacted with both PI4K1 and PI3K1, suggesting that ECDR1 could function as a component associated with not only PI4K complexes but also PI3K complexes to help catalyze PI into PI3P and PI4P. The lethality of all homozygous ecdr1, pi3k1 and tpr1 tpr2 mutants indicated the crucial roles of these genes in plant normal growth, which restricted our understanding of PI3K and PI4K functions. Alternatively, exogenous application of PI3K and PI4K inhibitors could substantially exacerbate the cell death and enhance disease resistance, implying their roles in plant immunity. Our findings provide novel insights into the regulatory mechanisms of ECDR1 in cell death and defense pathways, will aid in understanding the functions of PI3K and PI4K in plant immunity.
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
刚刚
无花果应助Waou采纳,获得10
刚刚
吕布发布了新的文献求助10
刚刚
CC发布了新的文献求助10
刚刚
UNnatural关注了科研通微信公众号
刚刚
跳跃靖发布了新的文献求助50
刚刚
Library发布了新的文献求助10
刚刚
苗条的十三完成签到,获得积分10
1秒前
2秒前
3秒前
3秒前
3秒前
3秒前
4秒前
小白完成签到,获得积分20
4秒前
mqq完成签到,获得积分10
5秒前
beriko发布了新的文献求助10
5秒前
7秒前
科研通AI2S应助吕布采纳,获得10
8秒前
Owen应助狂野的刺猬采纳,获得50
8秒前
9秒前
Akim应助kingmantj采纳,获得10
9秒前
顾矜应助小暑采纳,获得10
10秒前
叶程发布了新的文献求助10
10秒前
10秒前
科研通AI6.4应助于飞采纳,获得10
10秒前
英语六级完成签到,获得积分20
10秒前
11秒前
优秀的半梅完成签到,获得积分10
11秒前
慕青应助fu采纳,获得10
11秒前
黑米粥发布了新的文献求助10
12秒前
宅心仁厚发布了新的文献求助10
12秒前
cdercder应助mqq采纳,获得10
12秒前
v0id应助111采纳,获得10
12秒前
嘀嘀菇菇完成签到,获得积分10
12秒前
Nole应助111采纳,获得30
12秒前
大个应助111采纳,获得10
12秒前
搜集达人应助111采纳,获得10
12秒前
Samuel发布了新的文献求助80
12秒前
万能图书馆应助111采纳,获得10
12秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
The anomeric effect 1314
Principles of town planning: translating concepts to applications 1000
Navigating Normative Orders. Interdisciplinary Perspectives 800
1 Peter and Christ's Descent to the Dead in Its Early Christian Reception 700
Organizational Behavior 510
Management and the Arts 510
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7736518
求助须知:如何正确求助?哪些是违规求助? 9286234
关于积分的说明 20176809
捐赠科研通 7314561
什么是DOI,文献DOI怎么找? 3305321
关于科研通互助平台的介绍 2457655
邀请新用户注册赠送积分活动 2314807