Researchers at the University of California, Davis, and in the Netherlands have discovered how three fungal diseases have evolved into a lethal threat to the world’s bananas.
The discovery, reported in the online journal PLOS Genetics, better equips researchers to develop hardier, disease-resistant banana plants and more effective disease-prevention treatments.
“We have demonstrated that two of the three most serious banana fungal diseases have become more virulent by increasing their ability to manipulate the banana’s metabolic pathways and make use of its nutrients,” said UC Davis plant pathologist Ioannis Stergiopoulos, who led the effort to sequence two of the fungal genomes.
“This parallel change in metabolism of the pathogen and the host plant has been overlooked until now and may represent a ‘molecular fingerprint’ of the adaption process,” he said. “It is really a wake-up call to the research community to look at similar mechanisms between pathogens and their plant hosts.”
Bananas and the disease threat
The banana is one of the world’s top five staple foods. About 100 million tons of bananas are produced annually in nearly 120 countries. But the fruit suffers from an “image problem,” giving consumers the appearance that it is and always will be readily available, said Stergiopoulos. It’s an image problem that he fears could prove fatal to the entire banana industry in the very near future.
In reality, the global banana industry could be wiped out in just five to 10 years by fast-advancing fungal diseases. And that would prove devastating to millions of small-scale farmers who depend on the fruit for food, fiber and income. Already, Sigatoka — a three-fungus disease complex — reduces banana yields by 40 percent.
Three diseases in one
The Sigatoka complex’s three fungal diseases — yellow Sigatoka (Pseudocercospora musae), eumusae leaf spot (Pseudocercospora eumusae) and black Sigatoka (Pseudocercospora figiensis) — emerged as destructive pathogens in just the last century. Eumusae leaf spot and black Sigatoka are now the most devastating, with black Sigatoka posing the greatest constraint to banana production worldwide. The constant threat of the disease requires farmers to make 50 fungicide applications to their banana crops each year to control the disease.
“Thirty to 35 percent of banana production cost is in fungicide applications,” Stergiopoulos said. “Because many farmers can’t afford the fungicide, they grow bananas of lesser quality, which bring them less income.”
And for those growers who can afford fungicide, the applications pose environmental and human-health risks.
To make matters worse, all commercial “dessert” bananas — those most commonly found in grocery stores — are of the Cavendish variety. And unlike a tomato or green bean, which are grown from seeds, bananas are grown from shoot cuttings.
“The Cavendish banana plants all originated from one plant and so as clones, they all have the same genotype — and that is a recipe for disaster,” Stergiopoulos said, noting that a disease capable of killing one plant could kill them all.
Probing the genomes for solutions
Stergiopoulos and colleagues sequenced the genomes of eumusae leaf spot and black Sigatoka, comparing their findings with the previously sequenced yellow Sigatoka genome sequence.
They discovered that this complex of diseases has become lethal to banana plants not just by shutting down the plant’s immune system but also by adapting the metabolism of the fungi to match that of the host plants. As a result, the attacking fungi can produce enzymes that break down the plant’s cell walls. This allows the fungi to feed on the plant’s sugars and other carbohydrates.
“Now, for the first time, we know the genomic basis of virulence in these fungal diseases and the pattern by which these pathogens have evolved,” Stergiopoulos said.
People with diabetes often suffer from wounds that are slow to heal and can lead to ulcers, gangrene and amputation. New research from an international group led by Min Zhao, professor of ophthalmology and of dermatology at the University of California, Davis, shows that, in animal models of diabetes, slow healing is associated with weaker electrical currents in wounds. The results could ultimately open up new approaches for managing diabetic patients.
“This is the first demonstration, in diabetic wounds or any chronic wounds, that the naturally occurring electrical signal is impaired and correlated with delayed healing,” Zhao said. “Correcting this defect offers a totally new approach for chronic and nonhealing wounds in diabetes.”
It has been estimated that as much as $25 billion a year is spent on treating chronic ulcers and wounds related to diabetes, Zhao said.
Electric fields and wound healing
Electric fields are associated with living tissue. Previous work by Zhao and Brian Reid, project scientist at the UC Davis Department of Dermatology, showed that electric fields are associated with healing damage to the cornea, the transparent outer layer of the eye.
In the new work, published June 10 in the journal Scientific Reports, Zhao, Reid and colleagues used a highly sensitive probe to measure electrical fields in the corneas of isolated eyes from three different lab mouse models with different types of diabetes: genetic, drug-induced and in mice fed a high-fat diet.
In a healthy eye, there is an electrical potential across the thickness of the cornea. Removing a small piece of cornea collapses this potential and creates electric currents, especially at the edges of the wound. Cells migrate along the electric currents, closing the scratch wound in about 48 hours.
The University of California, Davis (also referred to as UCD, UC Davis, or Davis) is a public teaching and research university located in Davis, California just west of Sacramento.
The campus covers 7,309 acres (2,958 ha), making it the largest within the 10 campus University of California system. UC Davis also has the third largest enrollment in the UC System after UCLA and UC Berkeley.
Howard and Matthew Greene named UC Davis a Public Ivy in 2001, a publicly funded university considered as providing a quality of education comparable to those of the Ivy League. In 2013, U.S. News and World Report ranked UC Davis as the 9th best public university in the United States, 39th nationally, and tied for 3rd best of the UC schools with UC San Diego, following UC Berkeley and UCLA. UC Davis is also one of 62 members in the Association of American Universities.
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Joint BioEnergy Institute Study Identifies Bacterial Protein that is Key to Protecting Rice against Bacterial Blight
A bacterial signal that when recognized by rice plants enables the plants to resist a devastating blight disease has been identified by a multi-national team of researchers led by scientists with the U.S. Department of Energy (DOE)’s Joint BioEnergy Institute (JBEI) and the University of California (UC) Davis.
The research team discovered that a tyrosine-sulfated bacterial protein called “RaxX,” activates the rice immune receptor protein called “XA21.” This activation triggers an immune response against Xanthomonas oryzaepv.oryzae (Xoo), a pathogen that causes bacterial blight, a serious disease of rice crops.
“Our results show that RaxX, a small, previously undescribed bacterial protein, is required for activation of XA21-mediated immunity to Xoo,” says Pamela Ronald, a plant geneticist for both JBEI and UC Davis who led this study. “XA21 can detect RaxX and quickly mobilize its defenses to mount a potent immune response against Xoo. Rice plants that do not carry the XA21 immune receptor or other related immune receptors are virtually defenseless against bacterial blight.”
Ronald, who directs JBEI’s grass genetics program and is a professor in the UC Davis Department of Plant Pathology, is one of two corresponding authors of a paper describing this research inScience Advances, along with Benjamin Schwessinger, a grass geneticist with JBEI’s Feedstocks Division at the time of this study and now with the Australian National University. The paper is titled “The rice immune receptor XA21 recognizes a tyrosine-sulfated protein from a Gram-negative bacterium.” (See end of story for a complete list of authors.)
Rice is a staple food for half the world’s population and a model plant for perennial grasses, such as Miscanthus and switchgrass, which are prime feedstock candidates for the production of clean, green and renewable cellulosic biofuels. Just as bacterial blight poses a major threat to rice crops, bacterial infections of grass-type fuel plants could present major problems for the future production of advanced biofuels. However, the mechanisms by which bacteria infect such grasses is poorly understood.
“Pathogens of grass-type biofuel crops that would reduce the yield of fuel-producing biomass likely use similar infection mechanisms to Xoo,” says Schwessinger. “Having identified the activator of XA21, we will be able to study the rice immune system in far greater detail than ever before. As rice is the model for grass-type biofuel feedstocks, this might help in the future engineering of more disease-resistant grass-type biofuel crops.”
Most plants and many animals can only defend themselves against a given disease if they carry specialized immune receptors that sense the invading pathogen behind the disease. In 2009, Ronald and her group identified a small bacterial protein they named “Ax21” as the molecular key that binds to the XA21 receptor to activate a rice plant’s immune response. Diligent follow-up research by her group led to Ronald retracting these results and continuing the search for the true key.
“We were ecstatic with our results in 2009 because identifying the molecule that XA21 recognizes provides an important piece to the puzzle of how the rice plant is able to respond to infection,” Ronald says, “but then it was back to the drawing board. Now we have the real XA21 activator.”
Read more: Unlocking the Rice Immune System