Mining Effector Proteins in Phytopathogenic Fungi

“Pathogen effector” has been increasingly used in the past decades in the plant-pathogen interactions (Hogenhout et al., 2009).Presently, the definition of pathogen effector commonly adopted the definition given by Sophien Kamoun, that is, effectors are ‘molecules that manipulate host cell structure and function, thereby facilitating infection (virulence factors or toxins) and/or triggering defense responses (avirulence factors or elicitors)’ (Kamoun, 2006). Plant and their related pathogen have coevolved for many millions of years, which resulted in evolving some resistance genes in plants to prevent or limit pathogen infection, and simultaneously pathogen also evolved some effector proteins to overcome plant defense as well as cause disease. Many plant pathogens secreted effector proteins into host cells to repress plant defense and contribute to pathogen colonization and breach (Birch et al., 2006;Chisholm et al., 2006; Grant et al., 2006; Huang et al., 2006 a, 2006 b; Jones and Dangl, 2006; Kamoun, 2006; O’Connell and Panstruga, 2006). Oomycetes could cause many destructive plant diseases, like potato late blight that caused the Irish potato famine in the nineteenth century (Tyler, 2007). Oomycete effector proteins could be translocated into host cells with the help of RXLR and dEER motifs in the absence of the pathogen (Dou et al., 2008; Whisson et al., 2007).Oomycetes secreted effector proteins into the infection site. The effector proteins were categorized into two classes based on action site of effectors, and one was extracellular effectors acted in the apoplastic space where they interact with extracellular molecules of hosts. The other was cytoplasmic effectors that acted within the boundary of plant cell wall. Plant fungal pathogen also secreted effector proteins into host cells where they incompatibly interacted with plants receptors encoded by major resistance genes, which rapidly triggered host defense response (Ellis et al., 2006; Tyler, 2002). Oomycete effectors play dual role in disease and plant defense, fungal effector proteins were no exception. For example, victorin of Cochliobolus victoriae, NIP1 of R.secalis, and AAL toxin of Alternaria alternate played the role in toxin(Lorang et al., 2007; Navarre and Wolpert, 1999; Rohe et al., 1995; Spassieva et al., 2002; van’t Slot and Knogge, 2002; Wang et al., 1996, Wolpert et al., 2002), but some studies showed NIP1 and ToxA also interacted with corresponding host-resistance or toxinsensitivity genes, which resulted in NIP1 and ToxA acted in the same way as the Avr genes (Schürch et al., 2004; Stukenbrock and McDonald, 2007). So, it is necessary to clarify fungal effector proteins incompatibly or compatibly interact with host receptors when they were