亲爱的研友该休息了!由于当前在线用户较少,发布求助请尽量完整地填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!身体可是革命的本钱,早点休息,好梦!

Signalling requirements for Erwinia amylovora‐induced disease resistance, callose deposition and cell growth in the non‐host Arabidopsis thaliana

胼胝质 拟南芥 生物 欧文氏菌 寄主(生物学) 拟南芥 微生物学 植物抗病性 植物 细胞生物学 细胞壁 遗传学 细菌 基因 突变体
作者
Safae Hamdoun,Min Gao,Manroop Gill,Ashley Kwon,John L. Norelli,Hua Lu
出处
期刊:Molecular Plant Pathology [Wiley]
卷期号:19 (5): 1090-1103 被引量:5
标识
DOI:10.1111/mpp.12588
摘要

Erwinia amylovora is the causal agent of the fire blight disease in some plants of the Rosaceae family. The non-host plant Arabidopsis serves as a powerful system for the dissection of mechanisms of resistance to E. amylovora. Although not yet known to mount gene-for-gene resistance to E. amylovora, we found that Arabidopsis activated strong defence signalling mediated by salicylic acid (SA), with kinetics and amplitude similar to that induced by the recognition of the bacterial effector avrRpm1 by the resistance protein RPM1. Genetic analysis further revealed that SA signalling, but not signalling mediated by ethylene (ET) and jasmonic acid (JA), is required for E. amylovora resistance. Erwinia amylovora induces massive callose deposition on infected leaves, which is independent of SA, ET and JA signalling and is necessary for E. amylovora resistance in Arabidopsis. We also observed tumour-like growths on E. amylovora-infected Arabidopsis leaves, which contain enlarged mesophyll cells with increased DNA content and are probably a result of endoreplication. The formation of such growths is largely independent of SA signalling and some E. amylovora effectors. Together, our data reveal signalling requirements for E. amylovora-induced disease resistance, callose deposition and cell fate change in the non-host plant Arabidopsis. Knowledge from this study could facilitate a better understanding of the mechanisms of host defence against E. amylovora and eventually improve host resistance to the pathogen.

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
22222发布了新的文献求助10
3秒前
4秒前
材料虎完成签到,获得积分10
6秒前
小二郎应助ww960517采纳,获得10
8秒前
材料虎发布了新的文献求助10
9秒前
12秒前
22222完成签到,获得积分10
16秒前
帅气楷瑞完成签到 ,获得积分10
20秒前
30秒前
cheese完成签到,获得积分10
35秒前
36秒前
ddd发布了新的文献求助10
37秒前
41秒前
46秒前
50秒前
1分钟前
1分钟前
ZZQ完成签到 ,获得积分10
1分钟前
醉熏的西牛完成签到 ,获得积分10
1分钟前
山楂梨发布了新的文献求助10
1分钟前
1分钟前
1分钟前
1分钟前
1分钟前
1分钟前
Krsky完成签到,获得积分10
1分钟前
1分钟前
外向的妍完成签到,获得积分10
2分钟前
顺利巨人完成签到,获得积分10
2分钟前
卡拉肖克攀完成签到 ,获得积分10
2分钟前
叠嶂间听云完成签到,获得积分10
2分钟前
咔敏完成签到 ,获得积分10
2分钟前
2分钟前
Kao应助科研通管家采纳,获得20
2分钟前
Akim应助顺利巨人采纳,获得10
2分钟前
2分钟前
优雅愚志完成签到,获得积分10
2分钟前
2分钟前
终止密码子完成签到 ,获得积分10
2分钟前
2分钟前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(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
Molecular Mechanisms of Photosynthesis, 4th Edition 1000
Organic Reactions, Volume 116 1000
Current concepts in cutaneous toxicity : proceedings of the Fourth Conference on Cutaneous Toxicity, Washington, D.C., May 9-11, 1979 1000
The recovery-stress questionnaires : user manual 800
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 7257526
求助须知:如何正确求助?哪些是违规求助? 8879447
关于积分的说明 18757098
捐赠科研通 6937903
什么是DOI,文献DOI怎么找? 3201074
关于科研通互助平台的介绍 2375192
邀请新用户注册赠送积分活动 2176937