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光敏色素B介导的脂氧合酶激活调节拟南芥中过量红光诱导的防御反应。

Phytochrome B-mediated activation of lipoxygenase modulates an excess red light-induced defence response in Arabidopsis.

作者信息

Zhao Yuanyuan, Zhou Jun, Xing Da

机构信息

MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, PR China.

MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, PR China

出版信息

J Exp Bot. 2014 Sep;65(17):4907-18. doi: 10.1093/jxb/eru247. Epub 2014 Jun 10.

DOI:10.1093/jxb/eru247
PMID:24916071
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4144769/
Abstract

Lipoxygenase (LOX), a non-haem-iron-containing dioxygenase, is activated under various biotic or abiotic stresses to trigger a series resistance response, but the molecular mechanism of LOX activation remains unclear. This work investigated the activation of LOX during the plant defence response induced by excess red light (RL). In conditions of RL-induced defence, Arabidopsis LOX activity and transcription levels of LOX2, LOX3, and LOX4 were both upregulated. Under RL, phytochrome B promoted the degradation of phytochrome-interacting factor 3 (PIF3), a factor that inhibited the expression levels of LOXs, and thus the transcription levels of LOX2, LOX3, and LOX4 were increased. Upon pathogen infection, the activity of mitogen-activated protein kinase 3 (MPK3) and MPK6 was increased in plants pre-treated with RL. Moreover, experiments with the inhibitor PD98059 and mutants mpk3 and mpk6-2 demonstrated that MPK3 and MPK6 were both responsible for LOX activation. Further results showed that, in response to RL, an increase in cytoplasmic calcium concentration and upregulation of calmodulin 3 (CaM3) transcript level occurred upstream of MPK3 and MPK6 activation. Collectively, these results suggested that activation of LOX both at the transcript level and in terms of activity modulates the defence response induced by RL, providing a new insight into the mechanistic study of LOX during plant defences.

摘要

脂氧合酶(LOX)是一种不含血红素铁的双加氧酶,在各种生物或非生物胁迫下被激活,以触发一系列抗性反应,但LOX激活的分子机制仍不清楚。这项工作研究了在过量红光(RL)诱导的植物防御反应中LOX的激活情况。在RL诱导防御的条件下,拟南芥的LOX活性以及LOX2、LOX3和LOX4的转录水平均上调。在RL条件下,光敏色素B促进了抑制LOX表达水平的光敏色素互作因子3(PIF3)的降解,从而使LOX2、LOX3和LOX4的转录水平增加。在病原体感染时,用RL预处理的植物中丝裂原活化蛋白激酶3(MPK3)和MPK6的活性增加。此外,用抑制剂PD98059以及突变体mpk3和mpk6 - 2进行的实验表明,MPK3和MPK6都参与了LOX的激活。进一步的结果表明,响应RL时,细胞质钙浓度的增加和钙调蛋白3(CaM3)转录水平的上调发生在MPK3和MPK6激活的上游。总的来说,这些结果表明,LOX在转录水平和活性方面的激活调节了RL诱导的防御反应,为植物防御过程中LOX的机制研究提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/c5754a212560/exbotj_eru247_f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/fdf19e71e09c/exbotj_eru247_f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/2fe525403f28/exbotj_eru247_f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/c5754a212560/exbotj_eru247_f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/fdf19e71e09c/exbotj_eru247_f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/1763fb059a31/exbotj_eru247_f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/39b2058ce5fc/exbotj_eru247_f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/9da073182f6a/exbotj_eru247_f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/eb14dcad1731/exbotj_eru247_f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/11d6de4e25dc/exbotj_eru247_f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/2fe525403f28/exbotj_eru247_f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db8b/4144769/c5754a212560/exbotj_eru247_f0008.jpg

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