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香蕉枯萎病致病真菌尖孢镰刀菌热带 4 号的毒力由一氧化氮生物合成和辅助基因介导。

Virulence of banana wilt-causing fungal pathogen Fusarium oxysporum tropical race 4 is mediated by nitric oxide biosynthesis and accessory genes.

机构信息

Department of Biochemistry and Molecular Biology, University of Massachusetts Amherst, Amherst, MA, USA.

NIH-National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.

出版信息

Nat Microbiol. 2024 Sep;9(9):2232-2243. doi: 10.1038/s41564-024-01779-7. Epub 2024 Aug 16.

DOI:10.1038/s41564-024-01779-7
PMID:39152292
Abstract

Fusarium wilt of banana, caused by Fusarium oxysporum f. sp. cubense (Foc), is one of the most damaging plant diseases known. Foc race 1 (R1) decimated the Gros Michel-based banana (Musa acuminata) trade, and now Foc tropical race 4 (TR4) threatens global production of its replacement, the Cavendish banana. Here population genomics revealed that all Cavendish banana-infecting Foc race 4 strains share an evolutionary origin distinct from that of R1 strains. Although TR4 lacks accessory chromosomes, it contains accessory genes at the ends of some core chromosomes that are enriched for virulence and mitochondria-related functions. Meta-transcriptomics revealed the unique induction of the entire mitochondrion-localized nitric oxide (NO) biosynthesis pathway upon TR4 infection. Empirically, we confirmed the unique induction of a NO burst in TR4, suggesting that nitrosative pressure may contribute to virulence. Targeted mutagenesis demonstrated the functional importance of fungal NO production and the accessory gene SIX4 as virulence factors.

摘要

香蕉枯萎病,由尖孢镰刀菌古巴专化型(Foc)引起,是已知最具破坏性的植物病害之一。Foc 小种 1(R1)使以大麦克香蕉(Musa acuminata)为基础的香蕉贸易遭受重创,而现在,Foc 热带小种 4(TR4)威胁着其替代品种卡文迪什香蕉的全球产量。本研究通过群体基因组学揭示了所有感染卡文迪什香蕉的 Foc 热带小种 4 菌株与 R1 菌株具有不同的进化起源。尽管 TR4 缺乏附加染色体,但它在一些核心染色体的末端包含辅助基因,这些基因富集了与毒力和线粒体相关的功能。宏转录组学揭示了 TR4 感染后整个定位于线粒体的一氧化氮(NO)生物合成途径的独特诱导。通过实验,我们证实了 TR4 中独特的一氧化氮爆发的诱导,表明硝化压力可能有助于毒力。靶向诱变证实了真菌 NO 产生和辅助基因 SIX4 作为毒力因子的功能重要性。

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