Fungi can also catch viruses, and this can have amazing consequences, researchers report: a notorious harmful fungus on canola plants mutates when infected with a virus from a pathogen to a benefactor of the plants, the study shows. The infected fungus lives peacefully in the plants and strengthens their immune system, making them healthier and more resistant to pathogens. According to the scientists, there is considerable potential in this effect for the development of processes for biological crop protection.
Sclerotinia infestation! For oilseed rape farmers this is a terrifying diagnosis. The harmful fungus also known as rapeseed cancer Sclerotinia sclerotiorum can literally cause the yield to collapse: the pathogen leads to the collapse of the plants by primarily destroying tissue in the stem area.
As a result, Sclerotinia causes considerable losses in oilseed rape cultivation worldwide, because control with fungicides and other measures is problematic or not very effective. Against this background, the researchers led by Daohong Jiang from the Huazhong Agricultural University in China have now explored the potential of a special control approach: Could you fight the pathogen by making it sick yourself?
A wolf becomes a sheep
The so-called mycoviruses were the focus of the researchers. Just as coronaviruses and the like affect us, these special viruses can cause problems for various types of fungus. Often, however, they also exist in their hosts without causing any significant harmful effects. As part of their study, Jiang and his colleagues have now examined how the harmful fungus Sclerotinia changes when infected with the mycovirus SsHADV-1.
It turned out that the infection does not lead to the death of the fungus, but it disarms Sclerotinia: The researchers’ experiments showed that infected fungal strains colonize oilseed rape plants, but no longer damage them. “The virus can transform the fungus from a deadly pathogen into what is known as an endophytic fungus. Sclerotinia then treats the plant like home instead of killing it, ”says the Jiang. There are numerous examples of such endophytic organisms that live in plant tissues without causing disease. Sometimes they even use their hosts – they become symbiotic partners.
And that is exactly the case with the virus-infected Sclerotinia fungi, as further studies by the researchers have shown: The colonization with the virally tamed fungi stimulates the immune system of the plants, making them healthier and more resistant to diseases. This effect is also clearly noticeable: In test fields, the scientists were able to achieve a yield increase of 6.9 to 14.9 percent by treating the plants with the virus-infected Sclerotinia fungi. “The virus can turn the enemy into a friend,” says Jiang.
Vaccination against plant diseases in sight?
The scientists were also able to show the processes on which the effect is based. Their genetic studies show that the virus slows down the activity of genes in the fungus that play a role in its harmful effects. The colonization of plants with these virally disarmed fungi led to the activation of genetic makeup in oilseed rape, which play a role in natural disease resistance, the researchers report. With the virus-infected Sclerotinia fungi, a kind of vaccination effect can be achieved: “If you treat the seeds with these fungi, they will grow with the plant for the entire life cycle. As with some human vaccinations, this creates lifelong protection, ”says Jiang.
He and his colleagues now want to further explore the potential of mycoviruses for plant protection. As they explain, it seems possible that these pathogens also cause a similar effect in other harmful fungi. As you emphasize, the importance of these pathogens is enormous: the stubborn fungal pathogens cause more than 80 percent of all plant diseases and annually destroy a third of all food crops. “Our approach to disease prevention can now benefit research in crop protection and, ultimately, hopefully agricultural production too,” says Jiang.
Source: Cell Press, article: Molecular Plant, doi: Molecular Plant, doi: 10.1016 / j.molp.2020.08.016