Oxidative burst is critical for host-pathogen interactions. Many prior studies used methods involving dye staining, fluorescence, and/or chemiluminescence to detect ROS production. These methods are based on the activities of oxidase enzymes, such as peroxidase and NADPH oxidase, and therefore indirectly measure the levels of ROS in planta. Although providing relative 3,4,5-Trimethoxyphenylacetic acid quantitative information on ROS production, these methods do not offer precise subcellular localization of ROS, which could play a critical role in defense signal activation and transduction. The cerium chloride-based method, on the other hand, detects via TEM the electron dense precipitates resulting from the reaction of CeCl3 with H2O2, thus allowing a direct detection of H2O2 at the organelle levels. This method has been used in several plant-pathogen systems, such as Arabidopsis and lettuce-P. syringae, French bean�CXanthomonas, tomato/bean-Botrytis cinerea, legume-Rhizobia, tomato-nematode, and Solanum-Potato virus Y, and has provided spatial information of H2O2 accumulation in these plant pathosystems. We used this method for the first time to systematically examine when and where ROS is produced during PTI, ETS, and ETI. Our data have revealed temporal and spatial resolution of H2O2 localization during Arabidopsis-P. syringae interactions. We show that ETI is associated with much faster H2O2 accumulation than ETS, which is consistent with previous studies. Our data also show spatial difference in H2O2 accumulation, with ETI-induced H2O2 initially on the cell wall then inside of the cell and ETS-induced H2O2 beginning both inside and outside of the cell. H2O2 may contribute to cell death caused by DG34 and DG3 since the induction of H2O2 Mechlorethamine hydrochloride precedes the timing of massive cell death in the infected tissue. PTI-induced H2O2, on the other hand, accumulated much slowly and was only limited to the cell wall. Such temporal and spatial differences in H2O2 accumulation might reflect different mechanisms of plant resistance during PTI, ETS, and ETI. Pathogen-induced programmed cell death 
has been the focus in the studies of host-pathogen interactions. However, the change of host cell growth upon pathogen infection has been largely overlooked. Some animal pathogens are known to interfere with the host cell cycle machinery, activating cell growth and sometimes leading to tumorigenesis in animals. Pathogen-triggered cell growth has also been documented in some plants. For instance, nematodes induce host plants to form large cells, either resulting from fusion of the infected cells with its neighboring cells or from cell enlargement. The fungal pathogen powdery mildew was also shown to induce cell enlargement in Arabidopsis. These enlarged cells have increased nuclear DNA content, suggesting an activation of endoreplication. In addition, bacteria, such as Xanthomonas and Agrobacterium tumefaciens, can induce gall-like abnormal growths in their specific hosts, which could result from host cell enlargement and/or cell division. However, the mechanisms underlying host cell fate control upon pathogen infection have not been fully understood. Here we show that P. syringae also induces abnormal growths in Arabidopsis, which consist of enlarged mesophyll cells. The fact that the HrcC- strain induces more abnormal growths than both DG3 and DG34 strains suggests that PTI plays a major role in regulating cell growth. Consistent with this notion, our data further show that flg22- and perhaps also other PAMPs-induced PTI could act together to induce cell fate change in the host. Bacterial effectors were also reported to control host cell fate. Our data show that only the avirulent but not the virulent P. syringae strain induced minor abnormal.