Molecular Mechanism of miR160d in Regulating Kiwifruit Resistance to Botrytis cinerea

Molecular Mechanism of miR160d in Regulating Kiwifruit Resistance to Botrytis cinerea
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DOI:
10.1021/acs.jafc.3c02741
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发表时间:
2023-06-29
影响因子:
6.1
通讯作者:
Jiang, Yusong
Jiang, Yusong
中科院分区:
农林科学1区
文献类型:
--
作者:
Li, Zhexin;Yang, Shuai;Jiang, Yusong

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灰霉病给猕猴桃产业带来巨大的经济损失。阐明了B的分子机制。灰霉病是猕猴桃抗病分子育种的理论基础。已有研究表明miR160通过吲哚-3-乙酸(IAA)信号通路调控植物抗病性。本研究以"红阳"猕猴桃为试材,对Ac-miR160d及其靶基因进行了鉴定和克隆。采用过表达和病毒诱导基因沉默(VIGS)技术结合RNA-seq分析Ac-miR160 d在猕猴桃抗B抗性中的调控作用。灰叶AcMIR160 d-KN基因沉默提高了猕猴桃对B的敏感性。而过表达Ac-miR160 d-OE则增强了猕猴桃对B的抗性。cinerea,证实Ac-miR160 d正调控猕猴桃对B的抗性。灰叶此外,Ac-miR160在猕猴桃中的过表达提高了过氧化氢酶(CAT)和超氧化物歧化酶(SOD)等抗氧化酶的活性以及内源植物生长素(IAA)和水杨酸(SA)的含量,以响应B的胁迫。电影引起的压力。RNA-seq在AcMIR160 d-KN与CK和AcMIR160 d-OE与CK组中分别鉴定出480和858个独特的差异表达基因,其倍数变化为GE; 2和假发现率
Gray mold caused by Botrytis cinerea leads to huge economic losses tothe kiwifruit (Actinidiachinensis) industry. Elucidating the molecular mechanismresponding to B. cinerea is the theoreticalbasis for the resistance to molecular breeding of kiwifruit. Previousstudies have shown that miR160 regulates plant disease resistancethrough the indole-3-acetic acid (IAA) signaling pathway. In thisstudy, kiwifruit "Hongyang" was used as the material,and Ac-miR160d and its target genes were identified and cloned. Overexpressionand virus-induced gene silencing (VIGS) technology combined with RNA-seqwere adopted to analyze the regulatory role of Ac-miR160d in kiwifruitresistance to B. cinerea. SilencingAc-miR160d (AcMIR160d-KN) increased kiwifruit sensitivityto B. cinerea, whereas overexpressionof Ac-miR160d (AcMIR160d-OE) increased kiwifruitresistance to B. cinerea, suggestingthat Ac-miR160d positively regulates kiwifruit resistance to B. cinerea. In addition, overexpression of Ac-miR160din kiwifruit increased antioxidant enzyme activities, such as catalase(CAT) and superoxide dismutase (SOD), and endogenous phytohormoneIAA and salicylic acid (SA) content, in response to B. cinerea-induced stress. RNA-seq identified 480and 858 unique differentially expressed genes in the AcMIR160d-KN vs CK and AcMIR160d-OE vs CK groups, respectively,with fold change & GE;2 and false discovery rate