Cladophialophora guangxiense sp. nov., a New Species of Dark Septate Endophyte, Mitigates Tomato Bacterial Wilt and Growth Promotion Activities
文献类型: 外文期刊
第一作者: Wei, Xihong
作者: Wei, Xihong;Mataka, Stanley Nyenje;Jiang, Xue;Zhou, Yi;Sun, Zhengxiang;Long, Yanyan;Xie, Ling;Long, Yanyan;Xie, Ling;Long, Yanyan;Xie, Ling;Chen, Yanlu
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期刊名称:AGRONOMY-BASEL ( 影响因子:3.4; 五年影响因子:3.8 )
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年卷期: 2024 年 14 卷 12 期
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收录情况: SCI
摘要: Bacterial wilt of tomatoes, caused by Ralstonia solanacearum, is a significant soilborne disease that often causes significant reductions in the yield of tomatoes. Dark septate endophytic fungi (DSE) represent potential biocontrol agents against plant pathogens that can also enhance plant growth. To collect DSE fungi with potential for biocontrol, the fungus Cladophialophora guangxiense HX2 was isolated from the rhizosphere soil of sugarcane in Hengzhou Guangxi Province, China, and a novel species of Cladophialophora was identified based on morphological properties and DNA sequence analysis. C. guangxiense HX2 demonstrated a controlling effect of 76.7% on tomato bacterial wilt and promoted a 0.5-fold increase in tomato seedling height. It colonized tomato seedling roots, enhancing the activity of antioxidant and defensive enzyme systems. Transcriptomic and qPCR approaches were used to study the induction response of the strain HX2 infection by comparing the gene expression profiles. Gene ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway enrichment revealed that tomatoes can produce salicylic acid metabolism, ethylene-activated signaling, photosynthesis, and phenylpropanoid biosynthesis to the strain HX2 infection. The expression of IAA4 (3.5-fold change), ERF1 (3.5-fold change), and Hqt (1.5-fold change) was substantially enhanced and Hsc 70 (0.5-fold change) was significantly reduced in the treatment group. This study provides a theoretical foundation for further investigation into the potential of C. guangxiense HX2 as a biological agent for the prevention and control of tomato bacterial wilt.
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