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核黄素诱导的抗病性需要拟南芥中的促分裂原活化蛋白激酶3和6 。

Riboflavin-Induced Disease Resistance Requires the Mitogen-Activated Protein Kinases 3 and 6 in Arabidopsis thaliana.

作者信息

Nie Shengjun, Xu Huilian

机构信息

International Nature Farming Research Center, Hata 5632, Matsumoto-city, Nagano 390-1401, Japan.

出版信息

PLoS One. 2016 Apr 7;11(4):e0153175. doi: 10.1371/journal.pone.0153175. eCollection 2016.

DOI:10.1371/journal.pone.0153175
PMID:27054585
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4824526/
Abstract

As a resistance elicitor, riboflavin (vitamin B2) protects plants against a wide range of pathogens. At molecular biological levels, it is important to elucidate the signaling pathways underlying the disease resistance induced by riboflavin. Here, riboflavin was tested to induce resistance against virulent Pseudomonas syringae pv. Tomato DC3000 (Pst DC3000) in Arabidopsis. Results showed that riboflavin induced disease resistance based on MAPK-dependent priming for the expression of PR1 gene. Riboflavin induced transient expression of PR1 gene. However, following Pst DC3000 inoculation, riboflavin potentiated stronger PR1 gene transcription. Further was suggested that the transcript levels of mitogen-activated protein kinases, MPK3 and MPK6, were primed under riboflavin. Upon infection by Pst DC3000, these two enzymes were more strongly activated. The elevated activation of both MPK3 and MPK6 was responsible for enhanced defense gene expression and resistance after riboflavin treatment. Moreover, riboflavin significantly reduced the transcript levels of MPK3 and MPK6 by application of AsA and BAPTA, an H2O2 scavenger and a calcium (Ca2+) scavenger, respectively. In conclusion, MPK3 and MPK6 were responsible for riboflavin-induced resistance, and played an important role in H2O2- and Ca2+-related signaling pathways, and this study could provide a new insight into the mechanistic study of riboflavin-induced defense responses.

摘要

作为一种抗性激发子,核黄素(维生素B2)可保护植物抵御多种病原体。在分子生物学水平上,阐明核黄素诱导抗病性的信号通路很重要。在此,对核黄素诱导拟南芥对强毒丁香假单胞菌番茄致病变种DC3000(Pst DC3000)的抗性进行了测试。结果表明,核黄素基于丝裂原活化蛋白激酶(MAPK)依赖的引发作用诱导抗病性,从而使PR1基因表达。核黄素诱导PR1基因瞬时表达。然而,接种Pst DC3000后,核黄素使PR1基因转录增强。进一步研究表明,在核黄素作用下,丝裂原活化蛋白激酶MPK3和MPK6的转录水平被引发。在被Pst DC3000感染后,这两种酶被更强地激活。MPK3和MPK6的激活增强是核黄素处理后防御基因表达增强和抗性提高的原因。此外,分别通过应用抗坏血酸(AsA)和BAPTA(一种H2O2清除剂和一种钙(Ca2+)清除剂),核黄素显著降低了MPK3和MPK6的转录水平。总之,MPK3和MPK6介导了核黄素诱导的抗性,并在与H2O2和Ca2+相关的信号通路中发挥重要作用,本研究可为核黄素诱导防御反应的机制研究提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1251/4824526/6e7a095a7426/pone.0153175.g008.jpg
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