Guangdong Province Key Laboratory of Microbial Signals and Disease Control, South China Agricultural University, Guangzhou 510642, China.
Guangdong Province Key Laboratory of Microbial Signals and Disease Control, South China Agricultural University, Guangzhou 510642, China; Institute of Plant Protection, Guangdong Academy of Agricultural Sciences, Guangzhou 510640, China.
Fungal Genet Biol. 2014 Apr;65:1-13. doi: 10.1016/j.fgb.2014.01.005. Epub 2014 Feb 4.
Fusarium oxysporum f. sp. cubense (FOC) is the causal agent of banana Fusarium wilt and has become one of the most destructive pathogens threatening the banana production worldwide. However, few genes related to morphogenesis and pathogenicity of this fungal pathogen have been functionally characterized. In this study, we identified and characterized the disrupted gene in a T-DNA insertional mutant (L953) of FOC with significantly reduced virulence on banana plants. The gene disrupted by T-DNA insertion in L953 harbors an open reading frame, which encodes a protein with homology to α-1,6-mannosyltransferase (OCH1) in fungi. The deletion mutants (ΔFoOCH1) of the OCH1 orthologue (FoOCH1) in FOC were impaired in fungal growth, exhibited brighter staining with fluorescein isothiocyanate (FITC)-Concanavalin A, had less cell wall proteins and secreted more proteins into liquid media than the wild type. Furthermore, the mutation or deletion of FoOCH1 led to loss of ability to penetrate cellophane membrane and decline in hyphal attachment and colonization as well as virulence to the banana host. The mutant phenotypes were fully restored by complementation with the wild type FoOCH1 gene. Our data provide a first evidence for the critical role of FoOCH1 in maintenance of cell wall integrity and virulence of F. oxysporum f. sp. cubense.
尖孢镰刀菌古巴专化型(FOC)是香蕉枯萎病的病原菌,已成为全球范围内威胁香蕉生产的最具破坏性的病原体之一。然而,该真菌病原体的形态发生和致病性相关的少数基因尚未得到功能表征。在本研究中,我们鉴定并表征了 T-DNA 插入突变体(L953)中一个基因的功能缺失,该突变体在香蕉植株上的毒力显著降低。L953 中 T-DNA 插入破坏的基因包含一个开放阅读框,该框编码与真菌中的α-1,6-甘露糖基转移酶(OCH1)具有同源性的蛋白质。FOC 中 OCH1 直系同源物(FoOCH1)的缺失突变体(ΔFoOCH1)在真菌生长、异硫氰酸荧光素(FITC)-伴刀豆球蛋白 A 染色更亮、细胞壁蛋白更少和分泌到液体培养基中的蛋白质更多方面表现出缺陷,与野生型相比。此外,FoOCH1 的突变或缺失导致穿透玻璃纸膜的能力丧失、菌丝附着和定殖能力下降以及对香蕉宿主的毒力下降。野生型 FoOCH1 基因的互补完全恢复了突变体的表型。我们的数据首次提供了证据,证明 FoOCH1 在维持尖孢镰刀菌古巴专化型细胞壁完整性和毒力方面的关键作用。