Necrotrophic pathogens cause major pre-and post-harvest diseases in numerous agronomic and horticultural crops infl icting signifi cant economic losses. In contrast to biotrophs, obligate plant parasites that infect and feed on living cells, necrotrophs promote the destruction of host cells to feed on their contents. This difference underpins the divergent pathogenesis strategies and plant immune responses to biotrophic and necrotrophic infections. This chapter focuses on Arabidopsis immunity to necrotrophic pathogens. The strategies of infection, virulence and suppression of host defenses recruited by necrotrophs and the variation in host resistance mechanisms are highlighted. The multiplicity of intraspecifi c virulence factors and species diversity in necrotrophic organisms corresponds to variations in host resistance strategies. Resistance to host-specifi c necrotophs is monogenic whereas defense against broad host necrotrophs is complex, requiring the involvement of many genes and pathways for full resistance. Mechanisms and components of immunity such as the role of plant hormones, secondary metabolites, and pathogenesis-related proteins are presented. We will discuss the current state of knowledge of Arabidopsis immune responses to necrotrophic pathogens, the interactions of these responses with other defense pathways, and contemplate on the directions of future research.: e0136.
of 34The Arabidopsis Book Infection by fungal necrotrophs generally involves stages of conidial attachment, germination, host penetration, primary lesion formation, lesion expansion, and tissue maceration followed by sporulation (Prins et al., 2000). Following germination, penetration may be achieved by active mechanisms such as appressoria formation and enzymatic degradation or passively through prior infection or wound sites as well as stomates (Prins et al., 2000). After entry, tissue is decomposed through further cellular dismantling using many of the lytic enzymes employed for initial penetration as well as toxic levels of reactive oxygen species (ROS). Many necrotrophs produce various low-molecular weight phytotoxic metabolites, ranging from host-specifi c to those having adverse effects on many diverse species (van Kan, 2006). Others secrete phytotoxic proteins known to induce necrosis, with the vast majority of broad host necrotrophs producing multiples of both (Pemberton and Salmond, 2004;Gijzen and Nurnberger, 2006;Choquer et al., 2007). Throughout infection, these fungi also actively manipulate host cellular machinery in order to suppress defenses and/or aid in disease progression. Some necrotrophs infl uence host phytohormone levels or employ their own hormone biosynthesis thereby disrupting defense signaling (Prins et al., 2000;Sharon et al., 2004). Others have adapted mechanisms to detoxify host metabolites that interfere with virulence (Morrissey and Osbourn, 1999).Overall, bacterial necrotrophs follow a similar mode of pathogenesis to their fungal counterparts, secreting virulence factors into host tissue to induc...