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ABA信号通路的三种转录激活因子通过激活猕猴桃中的细胞色素P450正向调控木栓质单体合成。

Three Transcription Activators of ABA Signaling Positively Regulate Suberin Monomer Synthesis by Activating Cytochrome P450 in Kiwifruit.

作者信息

Wei Xiaopeng, Mao Linchun, Lu Wenjing, Wei Xiaobo, Han Xueyuan, Guan Weiliang, Yang Yajie, Zha Meng, Xu Changjie, Luo Zisheng

机构信息

College of Biosystems Engineering and Food Science, Zhejiang Key Laboratory of Agro-Food Processing, Key Laboratory of Agro-Products Postharvest Handling of Ministry of Agriculture and Rural Affairs, Zhejiang University, Hangzhou, China.

Ningbo Research Institute, Zhejiang University, Ningbo, China.

出版信息

Front Plant Sci. 2020 Jan 10;10:1650. doi: 10.3389/fpls.2019.01650. eCollection 2019.

DOI:10.3389/fpls.2019.01650
PMID:31998339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6967411/
Abstract

Wound attack stimulates accumulation of abscisic acid (ABA) that activates a number of genes associated with wound suberization of plants. Cytochrome P450 fatty acid ω-hydroxylase CYP86A1 catalyzes ω-hydroxylation of fatty acids to form the ω-functionalized monomers that play a pivotal role in suberin synthesis. However, the transcriptional regulation of ABA signaling on has not been characterized in kiwifruit. In this study, , a kiwifruit homolog of , was isolated. -overexpressed leaves displayed that the AchnCYP86A1 functioned as a fatty acid ω-hydroxylase associated with synthesis of suberin monomer. The regulatory function of three transcription factors (TFs, including AchnMYC2, AchnMYB41 and AchnMYB107) on was identified. All the three TFs were localized in nucleus and could individually interact with promoter to activate gene expression in yeast one-hybrid and dual-luciferase assays. The findings were further demonstrated in transient overexpressed , in which all TFs notably elevated the expression of aliphatic synthesis genes including and the accumulation of ω-hydroxyacids, α, ω-diacids, fatty acids and primary alcohols. Moreover, exogenous ABA induced the expression of , and that promoted involving in suberin monomer formation. Contrary to the inductive effects of ABA, however, fluridone (an inhibitor of ABA biosynthesis) inhibited the three TFs expression and suberin monomer formation. These results indicate that AchnMYC2, AchnMYB41 and AchnMYB107 positively regulate suberin monomer synthesis by activating promoter in response to ABA.

摘要

伤口刺激会促使脱落酸(ABA)积累,从而激活许多与植物伤口栓质化相关的基因。细胞色素P450脂肪酸ω-羟化酶CYP86A1催化脂肪酸的ω-羟化反应,形成在栓质合成中起关键作用的ω-官能化单体。然而,ABA信号在猕猴桃中对[具体基因,原文未明确写出]的转录调控尚未得到表征。在本研究中,分离出了猕猴桃中[具体基因,原文未明确写出]的同源基因AchnCYP86A1。过表达AchnCYP86A1的叶片显示,AchnCYP86A1作为一种与栓质单体合成相关的脂肪酸ω-羟化酶发挥作用。鉴定了三种转录因子(TFs,包括AchnMYC2、AchnMYB41和AchnMYB107)对[具体基因,原文未明确写出]的调控功能。这三种TFs均定位于细胞核,并且在酵母单杂交和双荧光素酶测定中能够分别与[具体基因,原文未明确写出]启动子相互作用以激活基因表达。在瞬时过表达[具体基因,原文未明确写出]中进一步证明了这些发现,其中所有TFs均显著提高了包括[具体基因,原文未明确写出]在内的脂肪族合成基因的表达以及ω-羟基酸、α,ω-二酸、脂肪酸和伯醇的积累。此外,外源ABA诱导了[具体基因,原文未明确写出]、[具体基因,原文未明确写出]和[具体基因,原文未明确写出]的表达,这些基因促进了参与栓质单体形成的[具体基因,原文未明确写出]。然而,与ABA的诱导作用相反,氟啶酮(一种ABA生物合成抑制剂)抑制了这三种TFs的表达和栓质单体的形成。这些结果表明,AchnMYC2、AchnMYB41和AchnMYB107通过响应ABA激活[具体基因启动子,原文未明确写出]来正向调控栓质单体的合成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/9cb16bd977fe/fpls-10-01650-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/c3491374a3ac/fpls-10-01650-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/742a9d11106f/fpls-10-01650-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/1e3acd69bec0/fpls-10-01650-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/2ff77f4dee36/fpls-10-01650-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/844ced2da3c6/fpls-10-01650-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/c6cb0788627c/fpls-10-01650-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/6010dc993bc4/fpls-10-01650-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/4331b3365a84/fpls-10-01650-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/9eb218789a3a/fpls-10-01650-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/9cb16bd977fe/fpls-10-01650-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/c3491374a3ac/fpls-10-01650-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/742a9d11106f/fpls-10-01650-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/1e3acd69bec0/fpls-10-01650-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/2ff77f4dee36/fpls-10-01650-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/844ced2da3c6/fpls-10-01650-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/c6cb0788627c/fpls-10-01650-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/6010dc993bc4/fpls-10-01650-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/4331b3365a84/fpls-10-01650-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/9eb218789a3a/fpls-10-01650-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2218/6967411/9cb16bd977fe/fpls-10-01650-g010.jpg

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