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基于RNA干扰(RNAi)抑制拟南芥促分裂原活化蛋白激酶AtMPK6,会导致对臭氧超敏以及AtMPK3调控异常。

RNA interference-based (RNAi) suppression of AtMPK6, an Arabidopsis mitogen-activated protein kinase, results in hypersensitivity to ozone and misregulation of AtMPK3.

作者信息

Miles Godfrey P, Samuel Marcus A, Zhang Yuelin, Ellis Brian E

机构信息

Michael Smith Laboratories, University of British Columbia, 2185 East Mall, Vancouver, British Columbia, Canada, V6T 1Z4.

出版信息

Environ Pollut. 2005 Nov;138(2):230-7. doi: 10.1016/j.envpol.2005.04.017.

DOI:10.1016/j.envpol.2005.04.017
PMID:15964670
Abstract

The recent increase in tropospheric ozone (O(3)) concentrations promotes additional oxidative stress through the production of reactive oxygen species (ROS) in plant tissues, resulting in the activation of genes whose products enable the stressed cells to retain their integrity and function. This response is made possible by an integration of highly regulated signaling networks that mediate the perception of, and response to, this oxidative assault. In Arabidopsis thaliana, ROS-induced signaling has been shown to flow through a protein phosphorylation cascade involving the mitogen-activated protein kinases (MAPKs) AtMPK3 (MPK3) and AtMPK6 (MPK6). We found that RNAi-mediated silencing of MPK6 renders the plant more sensitive to ozone, as determined by visible leaf damage. The MPK6-RNAi genotype also displayed a more intense and prolonged activation of MPK3 compared to that of WT plants. An MPK3 loss-of-function genotype is similarly very sensitive to ozone, and displays an abnormally prolonged MPK6 activation profile, suggesting reciprocity in regulation between these two MAPKs.

摘要

近期对流层臭氧(O₃)浓度的增加,通过在植物组织中产生活性氧(ROS)促进了额外的氧化应激,导致一些基因被激活,这些基因的产物能使受胁迫的细胞保持其完整性和功能。这种反应通过高度调控的信号网络整合得以实现,这些信号网络介导对这种氧化攻击的感知和反应。在拟南芥中,ROS诱导的信号传导已被证明通过涉及丝裂原活化蛋白激酶(MAPK)AtMPK3(MPK3)和AtMPK6(MPK6)的蛋白质磷酸化级联反应进行。我们发现,通过RNA干扰介导的MPK6沉默使植物对臭氧更敏感,这由可见的叶片损伤确定。与野生型植物相比,MPK6-RNAi基因型还显示出MPK3更强烈和持久的激活。MPK3功能缺失基因型对臭氧同样非常敏感,并显示出异常延长的MPK6激活谱,表明这两个MAPK之间存在调控的相互作用。

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