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
中科院分区:
文献类型:
--
作者:
Li, Zhexin;Yang, Shuai;Jiang, Yusong
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