Further, the superoxide radical can act as a reducing agent towards metal ions in the Fenton reaction, leading to the production of hydroxide radicals (OH˙−, GDC-0449 in vitro Imlay & Linn, 1988). The hydroxide radical is a strong oxidizing agent and can cause lipid peroxidation and damage to proteins and other cell components (Mehdy, 1994). In plant defences, ROS not only act as toxins, able to directly kill or slow the

growth of the pathogen, but also as part of a signalling cascade which may lead to multifarious defences including the hypersensitive response (Tenhanken et al., 1995; Torres et al., 2005), cell wall modifications (e.g. Bradley et al., 1992) and changes in gene expression (Alvarez et al., 1998). The importance of oxidative signalling in defence is illustrated by a recent study showing that induction of the oxidative signal-inducible1 (OXI1) serine/threonine protein kinase correlates both spatially and temporally with the oxidative burst in Arabidopsis and that OXI1 null mutants

and overexpressor lines are more susceptible to Pseudomonas syringae (Petersen et al., 2009). A large literature is dedicated to the study of the methods used by plant pathogens to avoid detection by the plant immune system and thus escape the oxidative burst. In the case of plant pathogenic bacteria, such as P. syringae, the type three secretion system (T3SS), encoded by hrp genes, is used for this purpose. The T3SS allows C59 wnt the bacteria to deliver effector proteins [type III secreted effector proteins (T3SE)], some of which delay or inhibit the plant’s defence responses, including the production of ROS (Grant et al., 2006). Some T3SE localize to the chloroplasts and mitochondria (Bretz & Hutcheson, 2004), locations at which ROS may be generated. Further evidence that the T3SS may be

used in manipulating plant ROS-based defences has been provided by Navarro et al. (2004), who found that five genes involved in ROS production in Arabidopsis may be targeted by T3SE secreted by P. syringae pv. tomato and P. syringae pv. maculicola, both of which are able to cause disease on Arabidopsis. However, it is important to note that the production of ROS also occurs in compatible Ribociclib supplier reactions between plant and pathogen, in which T3SE are successfully deployed and disease develops (Kim et al., 1999; Santos et al., 2001), albeit to a lesser extent than during an incompatible, nonhost reaction. Moreover, a recent study by Block et al. (2010) indicates that the effector HopG1a of P. syringae targets mitochondrial function, leading to increased ROS production, rather than suppression of ROS. An additional and relatively unexplored role for ROS tolerance in plant–pathogen interactions is suggested by studies of bacterial cell death mechanisms in response to bactericidal antibiotics. Kohanski et al.