Chen Xinyi, Jia Xingchen, Fu Ruizhou, Wang Maoli, Rong Hang, Wei Jinyi, Wang Zishu, Wang Mingyuan
Institute of Horticulture Science and Engineering, Huaqiao University, Xiamen, 361021, China.
Fujian General Station of Cropland Construction and Soil and Fertilizer Technology, Fuzhou, 350003, China.
Plant Cell Rep. 2025 Sep 25;44(10):222. doi: 10.1007/s00299-025-03614-7.
Under Foc TR4 stress, MaSKP1-1, MaCULI1, and MaHOS15 form SCF-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.
在尖孢镰刀菌古巴专化型热带4号小种(Foc TR4)胁迫下,MaSKP1-1、MaCULI1和MaHOS15形成SCF型E3泛素连接酶,抑制SA信号相关因子的表达水平,从而调控香蕉的免疫过程。由尖孢镰刀菌古巴专化型热带4号小种(Foc TR4)引起的香蕉枯萎病对全球香蕉生产构成重大威胁。在芭蕉属植物中,HOS15被认为通过水杨酸信号通路在增强对Foc TR4胁迫的反应中发挥作用。先前的研究表明,HOS15在SCF泛素连接酶复合物中作为F-box蛋白发挥作用,参与植物对生物胁迫的反应。然而,香蕉中SCF的调控机制仍知之甚少。在本研究中,我们鉴定出MaSkp1-1和MaCUL1是香蕉中的关键成分。在Foc TR4胁迫条件下,感病品种威廉姆斯根部MaSkp1-1和MaCUL1的表达水平升高,而抗病品种‘南天黄’中它们的表达则下降。通过酵母双杂交试验和双分子荧光互补实验证实了MaSkp1-1-MaCUL1-HOS15模块参与香蕉枯萎病。过表达MaSkp1-1(MaSkp1 OE)和MaCUL1(MaCUL1 OE)的拟南芥品系对Foc TR4感染的抗性降低。此外,发现MaSkp1-1和MaCUL1均通过影响水杨酸相关基因的表达来介导拟南芥对Foc TR4胁迫的反应。总之,这些发现为MaSkp1-1-MaCUL1-HOS15模块在植物对Foc TR4胁迫反应中的功能分子机制提供了新的见解。