How Nitric Oxide and Extra Genes Make a Banana-Killing Fungus More Dangerous

Jenn Hoskins
17th August, 2024

How Nitric Oxide and Extra Genes Make a Banana-Killing Fungus More Dangerous

Image Source: Natural Science News, 2024

Key Findings

  • The study from the University of Massachusetts Amherst found that all TR4 strains infecting Cavendish bananas have a distinct evolutionary origin separate from R1 strains
  • Unlike other Fusarium species, TR4 lacks accessory chromosomes but has virulence genes at the ends of core chromosomes
  • The study discovered that TR4 uniquely induces a nitric oxide (NO) biosynthesis pathway during infection, which is crucial for its virulence
Fusarium wilt of banana, caused by Fusarium oxysporum f. sp. cubense (Foc), is a major threat to global banana production. The disease has two significant races: Foc race 1 (R1), which decimated the Gros Michel banana trade, and Foc tropical race 4 (TR4), which now endangers the Cavendish banana. Recent research from the University of Massachusetts Amherst[1] sheds new light on the genetic and molecular mechanisms behind TR4's virulence, offering potential pathways for developing effective disease management strategies. The study revealed that all Cavendish-infecting TR4 strains share a distinct evolutionary origin separate from R1 strains. Unlike other Fusarium species that possess accessory chromosomes rich in virulence genes[2][3], TR4 lacks these chromosomes. Instead, TR4 has accessory genes located at the ends of some core chromosomes, which are enriched for virulence and mitochondria-related functions. This finding aligns with previous studies that highlight the importance of accessory genes in Fusarium pathogenicity[2][4]. A key discovery of the study was the unique induction of the entire mitochondrion-localized nitric oxide (NO) biosynthesis pathway during TR4 infection. Nitric oxide is a reactive molecule that can cause nitrosative stress, potentially contributing to the pathogen's virulence. The researchers confirmed the unique induction of a NO burst in TR4, suggesting that nitrosative pressure plays a role in the fungus's ability to infect banana plants. To further understand the functional importance of fungal NO production, the researchers performed targeted mutagenesis on TR4 strains. They demonstrated that disrupting NO production reduced the virulence of TR4, highlighting NO as a critical factor in the pathogenicity of this strain. Additionally, the study identified the accessory gene SIX4 as another virulence factor, which is consistent with previous findings that emphasize the role of accessory genes in Fusarium pathogenicity[3][5]. This study provides a deeper understanding of the molecular mechanisms behind TR4's virulence and offers new targets for disease management strategies. By focusing on the unique aspects of TR4's genome and its reliance on NO production, researchers can develop targeted approaches to mitigate the impact of Fusarium wilt on banana production.

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References

Main Study

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

Published 16th August, 2024

https://doi.org/10.1038/s41564-024-01779-7

Related Studies

2) Comparative genomics reveals mobile pathogenicity chromosomes in Fusarium.

https://doi.org/10.1038/nature08850

3) Deciphering Pathogenicity of Fusarium oxysporum From a Phylogenomics Perspective.

https://doi.org/10.1016/bs.adgen.2017.09.010

4) Accessory Chromosomes in Fusarium oxysporum.

https://doi.org/10.1094/PHYTO-03-20-0069-IA


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