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Stress response regulator FoSkn7 participates in the pathogenicity of Fusariumoxysporum f. sp. cubense race 4 by conferring resistance to exogenous oxidative stress

文献类型: 外文期刊

作者: Qi, Xingzhu 1 ; Liu, Lei 3 ; Wang, Jun 3 ;

作者机构: 1.Hainan Univ, Key Lab Trop Biol Resources, Minist Educ, Haikou 570228, Hainan, Peoples R China

2.Hainan Univ, Coll Ocean, Haikou 570228, Hainan, Peoples R China

3.Chinese Acad Trop Agr Sci, Inst Environm & Plant Protect, Haikou 571101, Hainan, Peoples R China

关键词: Fusariumoxysporum f; sp; cubense race 4; Stress response regulator FoSkn7; RNA-seq; Oxidative stress

期刊名称:JOURNAL OF GENERAL PLANT PATHOLOGY ( 影响因子:1.449; 五年影响因子:1.416 )

ISSN: 1345-2630

年卷期: 2019 年 85 卷 5 期

页码:

收录情况: SCI

摘要: An ortholog of the response regulator protein Skn7 in Fusariumoxysporum f. sp. cubense race 4 (Foc4) was identified here and named FoSkn7. Mutants lacking FoSkn7 displayed higher sensitivity than the wild-type strain to oxidative stress. In addition, the FoSkn7-deletion mutant caused an oxidative burst in banana seedlings at early stages of infection and had reduced virulence on Giant Cavendish bananas (Musa spp.). These results showed that FoSkn7 confers resistance to exogenous oxidative stress. To understand the underlying mechanism of this resistance to exogenous oxidative stress, we used RNA-seq to identify genes that are differentially regulated between the FoSkn7-deletion mutant and the wild-type strain. Among 104 upregulated and 566 downregulated genes with a two-fold change cutoff, 26 downregulated genes were related to stimulus response and antioxidant activity. KEGG enrichment analysis showed that 150 differentially expressed genes were enriched in 67 metabolic pathways, mainly including ribosomes, ribosome biogenesis in eukaryotes, RNA polymerase, peroxisome, glutamate metabolism, fatty acid degradation, and protein processing in the endoplasmic reticulum. These results suggest that FoSkn7, as an important stress response regulator of Foc4, confers resistance to exogenous oxidative stress by regulating the expression of several stress-response- and antioxidant-related genes and metabolic pathways to promote the virulence of Foc4.

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