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解析[具体物种或对象]中温度依赖性唑啉草酯抗性的转录基础

Unraveling the Transcriptional Basis of Temperature-Dependent Pinoxaden Resistance in .

作者信息

Matzrafi Maor, Shaar-Moshe Lidor, Rubin Baruch, Peleg Zvi

机构信息

The Robert H. Smith Institute of Plant Sciences and Genetics in Agriculture, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of JerusalemRehovot, Israel.

出版信息

Front Plant Sci. 2017 Jun 21;8:1064. doi: 10.3389/fpls.2017.01064. eCollection 2017.

DOI:10.3389/fpls.2017.01064
PMID:28680434
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5478685/
Abstract

Climate change endangers food security and our ability to feed the ever-increasing human population. Weeds are the most important biotic stress, reducing crop-plant productivity worldwide. Chemical control, the main approach for weed management, can be strongly affected by temperature. Previously, we have shown that temperature-dependent non-target site (NTS) resistance of is due to enhanced detoxification of acetyl-CoA carboxylase inhibitors. Here, we explored the transcriptional basis of this phenomenon. Plants were characterized for the transcriptional response to herbicide application, high-temperature and their combination, in an attempt to uncover the genetic basis of temperature-dependent pinoxaden resistance. Even though most of the variance among treatments was due to pinoxaden application (61%), plants were able to survive pinoxaden application only when grown under high-temperatures. Biological pathways and expression patterns of members of specific gene families, previously shown to be involved in NTS metabolic resistance to different herbicides, were examined. Cytochrome P450, glucosyl transferase and glutathione--transferase genes were found to be up-regulated in response to pinoxaden application under both control and high-temperature conditions. However, biological pathways related to oxidation and glucose conjugation were found to be significantly enriched only under the combination of pinoxaden application and high-temperature. Analysis of reactive oxygen species (ROS) was conducted at several time points after treatment using a probe detecting HO/peroxides. Comparison of ROS accumulation among treatments revealed a significant reduction in ROS quantities 24 h after pinoxaden application only under high-temperature conditions. These results may indicate significant activity of enzymatic ROS scavengers that can be correlated with the activation of herbicide-resistance mechanisms. This study shows that up-regulation of genes related to metabolic resistance is not sufficient to explain temperature-dependent pinoxaden resistance. We suggest that elevated activity of enzymatic processes at high-temperature may induce rapid and efficient pinoxaden metabolism leading to temperature-dependent herbicide resistance.

摘要

气候变化危及粮食安全以及我们养活不断增长的人口的能力。杂草是最重要的生物胁迫因素,降低了全球农作物的生产力。化学防治作为杂草管理的主要方法,会受到温度的强烈影响。此前,我们已经表明,[某种植物]的温度依赖性非靶标位点(NTS)抗性是由于乙酰辅酶A羧化酶抑制剂的解毒作用增强。在此,我们探究了这一现象的转录基础。对植物进行了表征,以研究其对除草剂施用、高温及其组合的转录反应,试图揭示温度依赖性抗丙酯草醚的遗传基础。尽管处理之间的大部分差异是由于丙酯草醚的施用(61%),但植物只有在高温下生长时才能在施用丙酯草醚后存活。研究了先前显示参与对不同除草剂的NTS代谢抗性的特定基因家族成员的生物学途径和表达模式。发现细胞色素P450、糖基转移酶和谷胱甘肽 - S - 转移酶基因在对照和高温条件下对丙酯草醚施用均有上调。然而,仅在丙酯草醚施用和高温组合的情况下,与氧化和葡萄糖结合相关的生物学途径才被发现显著富集。在处理后的几个时间点,使用检测羟基自由基/过氧化物的探针进行了活性氧(ROS)分析。处理之间ROS积累的比较显示,仅在高温条件下,丙酯草醚施用后24小时ROS数量显著减少。这些结果可能表明酶促ROS清除剂具有显著活性,这可能与抗除草剂机制的激活相关。这项研究表明,与代谢抗性相关的基因上调不足以解释温度依赖性抗丙酯草醚现象。我们认为,高温下酶促过程活性的提高可能诱导丙酯草醚的快速有效代谢,从而导致温度依赖性除草剂抗性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/e4e1f2cf5c0b/fpls-08-01064-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/d5c022eabf9b/fpls-08-01064-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/3d13d1ef38a7/fpls-08-01064-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/088abf0b760d/fpls-08-01064-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/e4e1f2cf5c0b/fpls-08-01064-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/d5c022eabf9b/fpls-08-01064-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/3d13d1ef38a7/fpls-08-01064-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/088abf0b760d/fpls-08-01064-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1367/5478685/e4e1f2cf5c0b/fpls-08-01064-g004.jpg

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