, 2010). The disease symptoms include white or grey patches of filamentous mycelium on the body or the fins of freshwater fish. The cellular and molecular mechanisms underlying Saprolegnia

infection have not been studied extensively (Kamoun, 2003). Instead, considerably more is known about MK-2206 in vivo how plant pathogenic oomycetes infect their hosts. Most oomycetes generate asexual zoospores for dispersal, which encyst and germinate when they have reached a potential host. Saprolegnia parasitica is also able to generate both primary and secondary zoospores, whereby the latter type is infectious (Phillips et al., 2008; Bruno et al., 2010). Upon finding a host, some oomycetes form a swelling at the tip of a germ tube, called an appressorium, which forms a penetration peg to enter the host cell (Grenville-Briggs et al., 2008). These appressoria-like structures have not been described so far for S. parasitica. Biotrophic and hemibiotrophic plant pathogenic oomycetes can also generate specialized hyphal branches called haustoria. These are structures that invaginate Trametinib the plant cell and induce the formation of a plant-derived

extrahaustorial membrane with a gel-like layer between the extrahaustorial membrane and the haustorial wall, called the extrahaustorial matrix (Bushnell, 1972; Szabo & Bushnell, 2001). Within this extrahaustorial matrix, water and nutrients are exchanged between the pathogen and the host (Voegele & Mendgen, 2003). The extracellular space is also considered important for the trafficking of secreted proteins from the pathogen, including effector proteins (Ellis et al., 2006). Effector proteins are required to establish a successful infection, but if recognized, they can also trigger a host resistance response (Birch et al., 2006, 2009; Jones & Dangl, Selleckchem Decitabine 2006; Hogenhout et al., 2009). Some plant and animal pathogens have evolved intriguing molecular

mechanisms to inject or translocate potential effector proteins into their host cells (Coombes et al., 2004; Navarro et al., 2005; Birch et al., 2006; Jones & Dangl, 2006; Whisson et al., 2007). For example, bacterial pathogens can inject effector proteins into the host cytosol using a type-III secretion system, where these effectors can suppress basal/innate immunity, inhibit inflammatory responses, inhibit phagocytosis and induce apoptosis in macrophages (Hueck, 1998; Navarro et al., 2005; Galán & Wolf-Watz, 2006; Lewis et al., 2009). The eukaryotic parasite Plasmodium falciparum, the causative agent of malaria, is also able to translocate secreted proteins that contain a so-called PEXEL motif [amino acid motif RxLx (E, Q or D)] into the cytosol of red blood cells (Hiller et al., 2004; Marti et al., 2004; Hiss et al., 2008). During the blood stages of infection, the parasite invades mature human erythrocytes and develops within a parasitophorous vacuolar membrane.