The enigmatic hypersensitive response: induction, execution and role
The enigmatic hypersensitive response: induction, execution and role
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神秘的超敏反应：诱导、执行和角色
DOI：
10.1006/pmpp.1999.0217
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发表时间：
1999
影响因子：
2.7
通讯作者：
M. C. Heath
中科院分区：
文献类型：
--
作者：
M. C. Heath
对于新格式的第一期PMPP，也许在这篇社论和两篇特邀文章中，我们采取了一些不同的，如果不是完全的偶像崇拜，看看植物病理学的一个长期谜团-过敏反应（HR）。为什么植物中的抗病性几乎普遍与快速、局部的植物细胞死亡相关，自从1915年Stakman首次明确发现HR以来，一直是争论的焦点[18]。1976年，作为一名年轻而热情的研究人员，当时关于HR作用的争论促使我给编辑写了一封题为“超敏反应：防锈的原因或后果？”的信。在这篇文章中，我警告说，不要假设人力资源是一个单一的现象，只有一个角色[9]。从概念上讲，在过去的23年里没有太大的变化，在这个问题的评论中，Richael和Gilchrist [16]重新审视了超敏细胞死亡在抗病性中的作用，并指出在我们如何看待这种反应方面，感知和现实之间仍然存在差距。人们早就认识到，过敏性细胞死亡可以产生导致植物局部或系统变化的信号。从一个有点不寻常的角度来看，Graham和Graham [6]在本期回顾的数据表明，超敏细胞死亡是触发周围活细胞对防御反应激发子做出反应的能力所必需的。他们还提出了一个有趣的假设，即这些“有能力”的周围细胞进入了一个超敏的细胞死亡程序，该程序被活性氧的清除剂“拯救”，这是细胞执行与局部组织防御相关的代谢功能所必需的。
For the first issue of PMPP in its new format, it is perhaps fitting that in this editorial and in two invited articles we take a somewhat dierent, if not totally iconoclastic, look at a long-standing enigma of plant pathology—the hypersensitive response (HR). Why disease resistance in plants should be almost ubiquitously associated with rapid, localized plant cell death has been a source of debate ever since the HR was first clearly identified by Stakman in 1915 [18]. In 1976, as a young and enthusiastic researcher, the then current controversy over the role of the HR moved me to write a Letter to the Editor entitled ‘‘Hypersensitivity: the cause or the consequence of rust resistance?’’ in which I warned against assuming that the HR is a single phenomenon with a single role [9]. Conceptually, not much has changed in the elapsing twenty-three years, and in a Commentary for this issue, Richael and Gilchrist [16] revisit the role of hypersensitive cell death in disease resistance and point out that there still is a gap between perception and reality in how we view this response. It has long been recognized that hypersensitive cell death can generate signals that cause local or systemic changes in the plant. Looking at this from a somewhat unusual angle, Graham and Graham [6] in this issue review data that suggests that hypersensitive cell death is necessary to trigger the competency of surrounding living cells to respond to elicitors of defence responses. They also present the interesting hypothesis that these ‘‘competent’’ surrounding cells enter a hypersensitive cell death programme that is ‘‘rescued’’ by scavengers of active oxygen species and this is necessary for the cell to perform the metabolic functions associated with localized tissue defence.