M35金属蛋白酶效应子FocM35_1是香蕉枯萎病菌4号生理小种完全致病力所必需的。

The M35 Metalloprotease Effector FocM35_1 Is Required for Full Virulence of f. sp. Tropical Race 4.

作者信息

Zhang Xiaoxia, Huang Huoqing, Wu Bangting, Xie Jianghui, Viljoen Altus, Wang Wei, Mostert Diane, Xie Yanling, Fu Gang, Xiang Dandan, Lyu Shuxia, Liu Siwen, Li Chunyu

机构信息

College of Bioscience and Biotechnology, Shenyang Agricultural University, Shenyang 110866, China.

Key Laboratory of South Subtropical Fruit Biology and Genetic Resource Utilization, Ministry of Agriculture, Key Laboratory of Tropical and Subtropical Fruit Tree Research of Guangdong Province, Institution of Fruit Tree Research, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China.

出版信息

Pathogens. 2021 May 29;10(6):670. doi: 10.3390/pathogens10060670.

f. sp. tropical race 4 ( TR4) causes Fusarium wilt of banana, the most devastating disease on a banana plant. The genome of TR4 encodes many candidate effector proteins. However, little is known about the functions of these effector proteins on their contributions to disease development and TR4 virulence. Here, we discovered a secreted metalloprotease, FocM35_1, which is an essential virulence effector of TR4. FocM35_1 was highly upregulated during the early stages of TR4 infection progress in bananas. The FocM35_1 knockout mutant compromised the virulence of TR4. FocM35_1 could interact with the banana chitinase MaChiA, and it decreased banana chitinase activity. FocM35_1 induced cell death in while suppressing the INF1-induced hypersensitive response (HR), and its predicted enzymatic site was required for lesion formation and the suppression to INF1-induced HR on leaves. Importantly, treatment of banana leaves with recombinant FocM35_1 accelerates TR4 infection. Collectively, our study provides evidence that metalloprotease effector FocM35 seems to contribute to pathogen virulence by inhibiting the host immunity.

尖孢镰刀菌古巴专化型热带4号生理小种（TR4）引发香蕉枯萎病，这是香蕉植株上最具毁灭性的病害。TR4的基因组编码许多候选效应蛋白。然而，关于这些效应蛋白在病害发展和TR4毒力方面的功能却知之甚少。在此，我们发现了一种分泌型金属蛋白酶FocM35_1，它是TR4的一种必需毒力效应因子。在香蕉中TR4感染进程的早期阶段，FocM35_1高度上调。FocM35_1基因敲除突变体削弱了TR4的毒力。FocM35_1能够与香蕉几丁质酶MaChiA相互作用，并降低香蕉几丁质酶的活性。FocM35_1在烟草中诱导细胞死亡，同时抑制INF1诱导的过敏反应（HR），并且其预测的酶切位点对于叶片上病斑的形成和对INF1诱导的HR的抑制是必需的。重要的是，用重组FocM35_1处理香蕉叶片会加速TR4的感染。总体而言，我们的研究提供了证据，表明金属蛋白酶效应因子FocM35似乎通过抑制宿主免疫来促进病原体的毒力。