Blocking the “bursts of nitric oxide” produced by a fungus may hold the key to saving the world's most popular banana from extinction. Studying how the fungus causes Panama disease and how it protects itself from nitric oxide-induced stress could open new avenues for eradicating the devastating infection in banana plants.
To produce fruit with minimal seeds, bananas are propagated clonally, resulting in little genetic diversity. This, combined with the dense monoculture plantations in which bananas are primarily grown, makes them highly vulnerable to diseases and pests. One major threat is Fusarium wilt (also known as Panama disease), caused by Fusarium oxysporum (Foc). One strain of Foc, race 1 (R1), was responsible for devastating the Gros Michel banana in the 1950s. The Cavendish banana was selected as an alternative to the Gros Michel based on its resistance to R1 and became the most popular cultivated banana worldwide. However, in 1989, another strain of Foc, tropical race 4 (TR4), with the ability to infect the Cavendish banana, was reported. TR4 is suspected to have originated in Indonesia and Malaysia and has spread from Asia to the Middle East, Africa, and Oceania. Colombia was identified as the world's largest exporter of Cavendish bananas in 2019, and Peru in 2021. Panama disease has once again brought the main banana varieties to the brink of functional extinction.
To understand how TR4 invades Cavendish banana plants, the researchers compared the genomes of 36 Foc strains from around the world. While most Foc strains have horizontally acquired auxiliary chromosomes that increase their virulence, the researchers found that TR4 does not. Instead, its genome contains auxiliary genes attached to the ends of multiple core chromosomes. These genes are enriched for sequences with known mitochondrial function, particularly those involved in nitric oxide biosynthesis and those that code for proteins that protect against nitrosative stress.
The researchers hypothesize that nitric oxide plays a key role in the interaction between TR4 and Cavendish, with the banana plant first recognizing the signal of fungal invasion and activating defense mechanisms involving the jasmonate signaling pathway. However, plant-produced methyl jasmonate (below) stimulates fungal NO production in TR4 thanks to the acquired auxiliary genes. The resulting “NO burst” causes nitrosative stress in banana roots, but not in TR4 due to the upregulation of detoxification genes.
To test their theory, the team measured NO production in TR4 and R1 after exposure to methyl jasmonate. Only TR4 showed a sharp increase in NO production. Similarly, knocking out genes involved in the NO biosynthesis pathway in TR4 created a mutant with significantly reduced toxicity.
The research team believes that NO scavengers could be one potential treatment option to slow or stop the introduction of TR4 into Cavendish bananas.
