Molecular characterization of PR and WRKY genes during SA- and MeJA-induced resistance against Colletotrichum musae in banana fruit
文献类型: 外文期刊
作者: Tang, Yang 1 ; Kuang, Jian-fei 1 ; Wang, Feng-yan 1 ; Chen, Lei 1 ; Hong, Ke-qian; Xiao, Yun-yi 1 ; Xie, Hui 1 ; Lu, W 1 ;
作者机构: 1.South China Agr Univ, Coll Hort Sci, Guangdong Key Lab Postharvest Sci, State Key Lab Conservat & Utilizat Subtrop Agrobi, Guangzhou 510642, Guangdong, Peoples R China
2.South Chin
关键词: Banana fruit;Induced pathogen resistance;PR proteins;Transcriptional regulation;WRKY
期刊名称:POSTHARVEST BIOLOGY AND TECHNOLOGY ( 影响因子:5.537; 五年影响因子:5.821 )
ISSN: 0925-5214
年卷期: 2013 年 79 卷
页码:
收录情况: SCI
摘要: In order to further elucidate the molecular mechanisms underlying induced resistance of banana fruit against Colletotrichum musae, causing anthracnose disease, the expression patterns of fifteen genes encoding for pathogenesis-related proteins (PRs), including three PR1, one PR2, three PR5, one PR10c, four chitinase and three chitinase-like genes, and two WRKY transcription factors (TFs) in banana fruit in relation to salicylic acid (SA) and methyl jasmonate (MeJA) induced resistance, was investigated. Application of SA and MeJA significantly reduced the anthracnose disease index and lesion diameter of banana fruit, along with enhanced accumulation of endogenous SA or JA contents, and higher expression levels of MaWRKYs, MaPR1-1, MaPR2, MaPR10c, MaCHI3, MaCHI4 and MaCHIL1. Moreover, yeast one-hybrid analysis showed that MaWRKYs could bind to the promoters of four SA and MeJA-inducible PR genes, MaPR1-1, MaPR2, MaPR10c and MaCHIL1. Taken together, our results suggest that the activation of banana PRs and WRKYs genes by SA and MeJA treatments, and WRKY TFs binding to PRs promoters, may be attributed at least or partially to SA- and MeJA-induced pathogen resistance. Our study expands our understanding of PR proteins and their transcriptional regulation in economic fruit crops in relation to induced pathogen resistance. (c) 2013 Elsevier B.V. All rights reserved.
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