Xinyi Chen, Xingchen Jia, Ruizhou Fu, Maoli Wang, Hang Rong, Jinyi Wei, Zishu Wang, Mingyuan Wang
{"title":"香蕉Skp1-Cullin1-F-box (SCF) E3泛素连接酶介导的hos15依赖性应答的负调控免疫机制","authors":"Xinyi Chen, Xingchen Jia, Ruizhou Fu, Maoli Wang, Hang Rong, Jinyi Wei, Zishu Wang, Mingyuan Wang","doi":"10.1007/s00299-025-03614-7","DOIUrl":null,"url":null,"abstract":"<p><strong>Key message: </strong>Under Foc TR4 stress, MaSKP1-1, MaCULI1, and MaHOS15 form SCF<sup>HOS15</sup>-type E3 ubiquitin ligase, which inhibits the expression level of SA signal-related factors to regulate the immune process of bananas. Banana wilt disease, caused by Fusarium oxysporum f. sp. cubense, tropical race 4 (Foc TR4), poses a significant threat to global banana production. In Musa spp., HOS15 is believed to play a role in enhancing the response to Foc TR4 stress by the salicylic acid signaling pathway. Previous studies have indicated that HOS15 functions as an F-box protein within the SCF ubiquitin ligase complex, contributing to plant biotic stress responses. However, the regulatory mechanisms of SCF in bananas remain poorly understood. In this study, we identified MaSkp1-1 and MaCUL1 as key components in bananas. Under Foc TR4 stress conditions, expression levels of MaSkp1-1 and MaCUL1 increased in the roots of the susceptible variety Williams, whereas their expression decreased in the resistant variety 'Nantianhuang'. The involvement of the MaSkp1-1-MaCUL1-HOS15 module in banana wilt disease was confirmed through yeast two-hybrid assays and bimolecular fluorescence complementation experiments. Arabidopsis thaliana lines overexpressing MaSkp1-1 (MaSkp1 OE) and MaCUL1 (MaCUL1 OE) exhibited reduced resistance to Foc TR4 infection. Furthermore, both MaSkp1-1 and MaCUL1 were found to mediate Arabidopsis's response to Foc TR4 stress by influencing the expression of salicylic acid-related genes. In conclusion, these findings provide new insights into the molecular mechanisms underlying the function of the MaSkp1-1-MaCUL1-HOS15 module in plant responses to Foc TR4 stress.</p>","PeriodicalId":20204,"journal":{"name":"Plant Cell Reports","volume":"44 10","pages":"222"},"PeriodicalIF":4.5000,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The negative regulated immune mechanism of Skp1-Cullin1-F-box (SCF) E3 ubiquitin ligase-mediated HOS15-dependent responses in banana.\",\"authors\":\"Xinyi Chen, Xingchen Jia, Ruizhou Fu, Maoli Wang, Hang Rong, Jinyi Wei, Zishu Wang, Mingyuan Wang\",\"doi\":\"10.1007/s00299-025-03614-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Key message: </strong>Under Foc TR4 stress, MaSKP1-1, MaCULI1, and MaHOS15 form SCF<sup>HOS15</sup>-type E3 ubiquitin ligase, which inhibits the expression level of SA signal-related factors to regulate the immune process of bananas. Banana wilt disease, caused by Fusarium oxysporum f. sp. cubense, tropical race 4 (Foc TR4), poses a significant threat to global banana production. In Musa spp., HOS15 is believed to play a role in enhancing the response to Foc TR4 stress by the salicylic acid signaling pathway. Previous studies have indicated that HOS15 functions as an F-box protein within the SCF ubiquitin ligase complex, contributing to plant biotic stress responses. However, the regulatory mechanisms of SCF in bananas remain poorly understood. In this study, we identified MaSkp1-1 and MaCUL1 as key components in bananas. Under Foc TR4 stress conditions, expression levels of MaSkp1-1 and MaCUL1 increased in the roots of the susceptible variety Williams, whereas their expression decreased in the resistant variety 'Nantianhuang'. The involvement of the MaSkp1-1-MaCUL1-HOS15 module in banana wilt disease was confirmed through yeast two-hybrid assays and bimolecular fluorescence complementation experiments. Arabidopsis thaliana lines overexpressing MaSkp1-1 (MaSkp1 OE) and MaCUL1 (MaCUL1 OE) exhibited reduced resistance to Foc TR4 infection. Furthermore, both MaSkp1-1 and MaCUL1 were found to mediate Arabidopsis's response to Foc TR4 stress by influencing the expression of salicylic acid-related genes. In conclusion, these findings provide new insights into the molecular mechanisms underlying the function of the MaSkp1-1-MaCUL1-HOS15 module in plant responses to Foc TR4 stress.</p>\",\"PeriodicalId\":20204,\"journal\":{\"name\":\"Plant Cell Reports\",\"volume\":\"44 10\",\"pages\":\"222\"},\"PeriodicalIF\":4.5000,\"publicationDate\":\"2025-09-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Plant Cell Reports\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1007/s00299-025-03614-7\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PLANT SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Plant Cell Reports","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s00299-025-03614-7","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PLANT SCIENCES","Score":null,"Total":0}
The negative regulated immune mechanism of Skp1-Cullin1-F-box (SCF) E3 ubiquitin ligase-mediated HOS15-dependent responses in banana.
Key message: Under Foc TR4 stress, MaSKP1-1, MaCULI1, and MaHOS15 form SCFHOS15-type E3 ubiquitin ligase, which inhibits the expression level of SA signal-related factors to regulate the immune process of bananas. Banana wilt disease, caused by Fusarium oxysporum f. sp. cubense, tropical race 4 (Foc TR4), poses a significant threat to global banana production. In Musa spp., HOS15 is believed to play a role in enhancing the response to Foc TR4 stress by the salicylic acid signaling pathway. Previous studies have indicated that HOS15 functions as an F-box protein within the SCF ubiquitin ligase complex, contributing to plant biotic stress responses. However, the regulatory mechanisms of SCF in bananas remain poorly understood. In this study, we identified MaSkp1-1 and MaCUL1 as key components in bananas. Under Foc TR4 stress conditions, expression levels of MaSkp1-1 and MaCUL1 increased in the roots of the susceptible variety Williams, whereas their expression decreased in the resistant variety 'Nantianhuang'. The involvement of the MaSkp1-1-MaCUL1-HOS15 module in banana wilt disease was confirmed through yeast two-hybrid assays and bimolecular fluorescence complementation experiments. Arabidopsis thaliana lines overexpressing MaSkp1-1 (MaSkp1 OE) and MaCUL1 (MaCUL1 OE) exhibited reduced resistance to Foc TR4 infection. Furthermore, both MaSkp1-1 and MaCUL1 were found to mediate Arabidopsis's response to Foc TR4 stress by influencing the expression of salicylic acid-related genes. In conclusion, these findings provide new insights into the molecular mechanisms underlying the function of the MaSkp1-1-MaCUL1-HOS15 module in plant responses to Foc TR4 stress.
期刊介绍:
Plant Cell Reports publishes original, peer-reviewed articles on new advances in all aspects of plant cell science, plant genetics and molecular biology. Papers selected for publication contribute significant new advances to clearly identified technological problems and/or biological questions. The articles will prove relevant beyond the narrow topic of interest to a readership with broad scientific background. The coverage includes such topics as:
- genomics and genetics
- metabolism
- cell biology
- abiotic and biotic stress
- phytopathology
- gene transfer and expression
- molecular pharming
- systems biology
- nanobiotechnology
- genome editing
- phenomics and synthetic biology
The journal also publishes opinion papers, review and focus articles on the latest developments and new advances in research and technology in plant molecular biology and biotechnology.