Nieuws - 13 maart 2012

Fungus enters plant by stealing plant genes

The fungi Verticillium infects tomatoes with help from a gene which it has previously 'kidnapped' from a plant. At the same time, this gene exposes the fungus as a pathogen, report Wageningen phytopathologists in the Proceedings of the National Academy of Sciences (PNAS).

Verticillium wilt in a tomato plant
The soil fungus Verticillium causes the wilting disease in tomatoes and other crops. The tomato does in fact have a defence mechanism to keep the fungus at bay: the immune receptor Ve1. But researchers saw that tomatoes with Ve1 are not always able to avoid damage caused by the fungus. Therefore, they compared the genomes of fungal strains known to the plant with those of unknown strains. Their attention was caught by a gene which makes the fungus visible to the immune system of the tomato. Without this gene, Ave1, the fungus becomes invisible to the tomato plant and is able to sneak into it.
This gene has several surprises in store. Firstly, Ave1 is found almost exclusively in plants. The fungus has probably 'stolen' this gene from a plant previously, reason the phytopathologists. Secondly, this gene causes the fungus to become more aggressive. When the phytopathologists switched off the gene, the fungus was hardly able to cause tomato wilt. 'The fungus faces a dilemma,' says phytopathologist Ronnie de Jonge. 'While it succeeds in making plants sick with the Ave1 gene, the gene gives away its presence to the resistance gene of the plant.'
The researchers discovered that other pathogenic fungi also have this stolen gene, such as the soil fungus Fusarium. As such, the immune reactor Ve1 can also pick out Fusarium and subdue it. Breeders can therefore take a leaf from this study and build receptors into other useful crops, to protect these not only from Verticillium, but also from other fungi which have stolen the Ave1 gene from plants.
The article - written by the Wageningen phytopathologists Ronnie de Jonge, Peter van Esse and Bart Thomma, with colleagues in Belgium, Japan and the United States - is published in the 12 March issue of PNAS.