How *Fusarium oxysporum* threatens Cavendish bananas

Have you ever considered that the bananas eaten today differ from those people ate only a few generations ago?

The banana you may have eaten at breakfast is probably the Cavendish variety. Until the 1950s, however, supermarket shelves stocked Gros Michel bananas, a variety devastated by a disease known as Fusarium wilt of banana, or FWB.

In Gros Michel, FWB resulted from Fusarium oxysporum race 1, a banana-infecting fungal pathogen. The fungus kills plants by colonising their vascular system and obstructing the movement of water and minerals.

Plant biologists bred the Fusarium-resistant Cavendish variety as a replacement for Gros Michel. But during the past several decades, FWB has re-emerged in the form of tropical race 4, or TR4, a different strain of the same fungus that is again endangering banana production worldwide.

How did Fusarium oxysporum acquire the capacity to bypass resistance and infect such a wide range of plants?

The two-part genome of F. oxysporum

As a genomicist, I have investigated the genetic evolution of Fusarium oxysporum for the past 10 years. This species complex causes wilt and root-rot diseases in more than 120 plant species, while some strains are also able to infect humans.

In 2010, my laboratory found that every F. oxysporum genome has two components. Its core genome, shared by every strain, encodes essential housekeeping functions. Its accessory genome differs between strains and encodes specialised traits, including the ability to infect a particular plant host.

Every plant species has a complex immune system that protects it from microbial invasion. To successfully infect a host, each F. oxysporum strain relies on its accessory genome to overcome that plant's particular defences. This division of functions enables F. oxysporum to expand its host range considerably.

TR4 and Cavendish banana infection

In newly published research, my team and collaborators in China and South Africa showed that TR4, the strain responsible for killing Cavendish bananas, has a distinct evolutionary origin from the strain that destroyed Gros Michel bananas. The two strains also have different accessory-genome sequences.

By examining the point at which TR4 confronts its Cavendish banana host, we found that certain activated accessory genes produce nitric oxide, a gas that harms Cavendish bananas.

This abrupt release of toxic gas assists infection by disabling the plant's defence system. Meanwhile, the fungus shields itself by stepping up the production of chemicals that neutralise nitric oxide.

Increasing banana diversity

When tracing the worldwide spread of this new form of Fusarium oxysporum, we found that the international banana industry's reliance on one banana clone is a major reason for the recent return of this fungal disease.

Cultivating a wider selection of banana varieties could make farming more sustainable and lessen disease pressure on any one crop. Farmers and researchers can manage Fusarium wilt of banana by finding or developing banana varieties that tolerate or resist TR4.

Our results indicate that Cavendish bananas might also be protected by creating effective nitric oxide scavengers, which would lessen the toxic effects of the gas surge.

It may be difficult to see how consumers who simply enjoy bananas can contribute to combating a disease that is ruining banana crops. Yet consumers shape the market, and growers must produce what that market wants.

How shoppers can support banana diversity

You can encourage greater banana diversity at your supermarket by deliberately buying one or more of the hundreds of other banana varieties when they are available. Purchasing locally grown varieties of other fruit and agricultural produce can likewise help conserve plant diversity while supporting local growers.

Co-operation between scientists, farmers, industry and consumers worldwide can help prevent future shortages of bananas and other crops.

Li-Jun Ma, Professor of Biochemistry and Molecular Biology, UMass Amherst

This article is republished from The Conversation under a Creative Commons licence. Read the original article.