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Transcriptome Changes Induced by Botrytis cinerea Stress and Weighted Gene Co-expression Network Analysis (WGCNA) in Actinidia chinensis

Kiwifruit ( Actinidia chinensis ) is rich in dietary fiber and vitamin C and has high commercial value. However, it is susceptible to Botrytis cinerea pathogenesis . This fungus causes gray mold rot which negatively impacts kiwifruit quality. It also induces changes in superoxide dismutase, peroxida...

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Published in:Plant molecular biology reporter 2022-06, Vol.40 (2), p.389-401
Main Authors: Li, Zhe-Xin, Zhang, Wen-Lin, Jue, Deng-Wei, Liu, Xia, Jiang, Yu-Song, Tang, Jian-Min
Format: Article
Language:English
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Summary:Kiwifruit ( Actinidia chinensis ) is rich in dietary fiber and vitamin C and has high commercial value. However, it is susceptible to Botrytis cinerea pathogenesis . This fungus causes gray mold rot which negatively impacts kiwifruit quality. It also induces changes in superoxide dismutase, peroxidase, and catalase activity. Peroxidase and superoxide dismutase activities were detected at 1 dpi, increased till 4 dpi, and decreased by 5 dpi. Catalase was activated at 2 dpi, increased thereafter, and declined by 5 dpi. RNA-seq identified 2726 unique differentially expressed genes. The fold change was at least two, and the false discovery rate was less than 0.01. The 233 genes relevant to B. cinerea response were modulated in the first three infection stages. A weighted gene co-expression network analysis identified genes and modules in the transcriptome datasets that were responsive to B. cinerea . A network analysis disclosed the families “Plant-pathogen interactions”, “Lipid metabolism”, “Phytohormone signaling”, “Transcription factor”, “Cell wall biogenesis” and “Phenylpropanoid biosynthesis” possibly regulating B. cinerea response. The hub genes identified here are potential targets for breeding kiwifruit with improved biotic stress tolerance. This work lays an empirical foundation for investigating the proteins in kiwifruit that are modulated in response to B. cinerea pathogenesis.
ISSN:0735-9640
1572-9818
DOI:10.1007/s11105-021-01325-3