Home • Cladosporium fulvum v1.0
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Photos: Bilal Okmen, Jerome Collemare and Pierre de Wit, Wageningen University

The fungal pathogen Cladosporium fulvum causes leaf mould of tomato, a disease first described by Cooke in 1883. The fungus presumably originates from South America, the centre of origin of cultivated tomato (Solanum lycopersicum) and related wild species. C. fulvum has been proposed to belong to the Mycosphaerellaceae, within the class of Dothideomycetes, which contain taxa with anamorphs and teleomorphs. Although C. fulvum is considered an asexual fungus, its mating type loci are very homologous to those of Mycosphaerella pini (anamorph, Dothistroma septosporum), M. fijiensis and M. graminicola (Stergiopoulos et al. 2007). All members of the Mycosphaerellaceae  show a similar infection strategy as they all penetrate open stomata and proliferate in the extracellular space between mesophyll cells without producing haustoria. However C. fulvum  differs from most other members by being a biotroph, while others are hemi-biotrophs or even necrotrophs.

The C. fulvum-tomato interaction is a model for pathosystems that comply with the gene-for-gene concept meaning that for every fungal avirulence gene (Avr ) there is a corresponding C. fulvum (Cf) tomato resistance gene that mediates recognition of the fungal pathogen by the host. As a consequence of this recognition, defence responses are activated culminating in a hypersensitive response (a type of programmed cell death) that limits further growth of this biotrophic pathogen. Many Avr genes from C. fulvum, presently also called effector genes, have been identified, and for some of them the intrinsic function of the encoded protein has been assigned and studied in detail (Avr2, Avr4, Ecp2, Ecp6). Some of these effectors are species-specific, whereas some are core effectors that do occur in many other fungi (Stergiopoulos and De Wit, 2009; Stergiopoulos et al., 2010).

Based on sequence information C. fulvum is most related to D. septosporum (a pathogen of pine) (De Wit et al. in preparation). Present research focuses on the molecular communication between these two pathogens with their two, taxonomically unrelated, host plants with a focus on the role of effectors in effector-triggered susceptibility (ETS) and in R gene-mediated effector-triggered immunity (ETI).

Apart from effectors, C. fulvum and D. septosporum produce secondary metabolites that can be toxic to microbes, plants and mammals (Collemare and Lebrun, 2012). Exploitation of the both genome sequences will help to decipher their biosynthesis, regulation, biological activities and molecular evolution in Dothideomycete fungi.


Stergiopoulos I, Groenewald M, Staats M, Lindhout P, Crous PW, De Wit PJGM (2007). Mating-type genes and the genetic structure of a world-wide collection of the tomato pathogen Cladosporium fulvum. Fung Gen Biol 44:415-429.
Stergiopoulos I, de Wit PJGM (2009). Fungal Effector Proteins. Annu Rev Phytopathol 47:233-263.
Stergiopoulos I, van den Burg HA, Okmen B, Beenen HG, van Liere S, Kema GHJ, de Wit PJGM (2010). Tomato Cf resistance proteins mediate recognition of cognate homologous effectors from fungi pathogenic on dicots and monocots. Proc Natll Acad Sci USA 107:7610-7615.
Collemare J, Lebrun M-H (2012). Fungal secondary metabolites: ancient toxins and novel effectors in plant-microbe interactions. In Effectors in Plant–Microbe Interaction (Eds F Martin and S Kamoun  John Wiley & Sons Inc.)

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