Identification and validation of immune signalling components in Cladosporium fulvum-resistant tomato

Leaf mould is caused by Cladosporium fulvum, a non-obligate biotrophic ascomycete, that serves as a model organism to study plant-fungus interactions. It is not only a model organism but also a fungal disease that has a destructive effect on tomato plants (Solanum lycopersicum). Various Cf resistance genes have been identified against C. fulvum. The mechanism by which Cf-4 provides resistance against C. fulvum is one of the most studied resistance mechanisms of plants against fungal pathogens. The Cf-4 protein is a receptor-like protein (RLP) that does not have an intracellular kinase domain to initiate downstream signalling. Thus, Cf proteins form a complex with the receptor-like kinase (RLK) SOBIR1 for the initiation of downstream signalling. Upon Cf-4 activation by the Avr4 effector of C. fulvum, the RLK BAK1 is recruited to the constitutive Cf-4/SOBIR1 complex, thereby combining two kinase domains that phosphorylate each other and it is proposed that this activated complex phosphorylates downstream receptor-like cytoplasmic kinases (RLCKs). These activated RLCKs in their turn provide a connection with downstream signalling partners to eventually trigger the hypersensitive response (HR). However, it is unclear which RLCKs are needed to be phosphorylated for the initiation of downstream immune signalling. Although there is considerable effort on dissecting the Cf-4-triggered immune signalling mechanism to reveal unknown components and functions, most of the work is done in the model Solanaceous plant Nicotiana benthamiana, instead of the actual only host of C. fulvum, which is tomato. We aim to both validate previous findings resulting from our work on N. benthamiana, in tomato and to find new signalling components, and then further transfer our knowledge to practical applications by working more on the host crop plant, tomato.