Achieving durable resistance against tomato leaf mold

Tomato leaf mold is a foliar disease caused by the hemi-biotrophic fungus Fulvia fulva (better known by its old name; Cladosporium fulvum), that can cause significant yield losses. It is mostly a problem in a temperate and humid climate, such as we have in the Netherlands and Japan, for example. Resistant tomato varieties are available, but new strains of the fungus have evolved to break this resistance. To achieve a more durable and longer lasting resistance, we are employing an integrative approach in which we combine both our expertise on phytopathology and plant breeding to select and introgress (combinations of) novel resistance genes from wild tomato species.


The interaction between F. fulva (syn. Cladosporium fulvum) and tomato has been studied extensively at Wageningen University for almost 50 years. It has become a well-known model system for studying a “gene-for-gene” interaction between plants and pathogens, in which a single effector on the pathogen side is recognized by a single resistance gene product on the host side.

This unfortunately also means that the fungus has so far shown its capability to easily circumvent recognition by single resistance genes, by mutation or even complete loss of the effectors that are recognized. Currently, the disease is re-emerging and is causing increased problems for growers in the field again. Therefore, we are applying our extensive knowledge and resources to find ways of generating more durable genetic resistance in tomato against this pathogen.

Project description

Resistant tomato recognizes F. fulva avirulence (Avr) effectors by means of Cf receptor proteins, resulting in hypersensitive response-based resistance. So far, several Cf genes have been characterized and deployed, however the durability of these genes has proven to be limited. Durable resistance remains elusive, since F. fulva readily overcomes Cf resistance by loss or mutation of the corresponding Avr effector, after which the deployed Cf gene becomes ineffective.

To achieve a more durable form of genetic resistance, we are introgressing, mapping and characterizing a significant number of novel Cf genes from wild Solanum germplasm at the Department of Plant Breeding. In parallel, at the Laboratory of Phytopathology, we are using CRISPR-Cas9 technology to generate knockouts of the corresponding effectors in F. fulva to determine their contribution to fungal virulence on susceptible tomato plants. We hypothesize that (combinations of) Cf genes corresponding to effectors that strongly contribute to virulence will result in more durable resistance.


So far, we have taken steps towards the mapping of several novel Cf genes, and we have generated knockouts of the corresponding effectors in F. fulva. Additionally, we collaborate with Massey University in New Zealand on the identification of the F. fulva effector Avr9B, which matches the Cf-9 homolog Cf-9B. This work explains the sequential breakdown of the widely used Cf-9 resistance locus and serves as a great example of how a plant pathogen is able to overcome a resistance locus harboring multiple functional resistance genes. In addition, we are currently working on identifying Avr6, which matches the most recently deployed Cf resistance locus Cf-6. The identification of the gene encoding this effector will help breeders to easily identify plants harboring the Cf-6 locus during breeding programs, and will accelerate the cloning and characterization of this new resistance locus.


Beyond the genomes of Fulvia fulva (syn. Cladosporium fulvum) and Dothistroma septosporum: New insights into how these fungal pathogens interact with their host plants

Molecular Plant Pathology

Specific Hypersensitive Response-Associated Recognition of New Apoplastic Effectors from Cladosporium fulvum in Wild Tomato

Molecular Plant-Microbe Interactions