Exogenous applications of SA agonists, such as benzo thiadiazol-7-carothioic acid, confer enhanced disease resistance in plants. Oxidative bursts are also induced during PTI, ETS, and ETI, leading to production of reactive oxygen species. ROS can signal defense responses, cause crosslinking to strengthen cell wall, and at high concentrations Atractylenolide-III directly kill pathogens as well as host cells. Host cell death is commonly induced during an infection process. The hypersensitive response, a typical ETI during which host R proteins recognize cognate pathogen effectors, is characterized by massive cell death in the local infected region to quickly deprive pathogens of water and nutrients and thereby to kill the pathogens. Although many prior studies have tested accumulation of SA and ROS and the induction of cell death as part of defense phenotype assays of pathogen-challenged plants, how these signaling molecules and cell death formation change at different time points during PTI, ETS, and ETI, has not been compared under the same experimental condition. Similar to global gene expression profiling, a detailed analysis of the behavior of these defense signaling molecules and cell death formation in plants upon pathogen attack should contribute to a better understanding of PTI, ETS, and ETI, thereby host defense mechanisms. In this report, we carefully examined several defense related phenotypes in a time course during PTI, ETS, and ETI, using Arabidopsis-P. syringae as a model system. We found that there are dynamic differences between PTI, ETS, and ETI in SA accumulation, expression of the defense marker gene PR1, and cell death formation. Such differences are dependent on the doses of the strains used. In addition, our data LOUREIRIN-B provide precise temporal and spatial information on H2O2 during PTI, ETS, and ETI. Together these data support that the differences between PTI, ETS, and ETI are both quantitative and qualitative. Interestingly, we observed abnormal growths in the leaves at late infection stages, most obviously during PTI. The abnormal growths contain enlarged cells that have increased nuclear DNA content, suggesting a possible activation of endoreplication in host cells by P. syringae infection. Such hypertrophy of host cells induced by pathogen infection has been reported in several other plant pathosystems but has never been shown during Arabidopsis-P. syringae interactions. Thus, our study has demonstrated a comprehensive picture of dynamic changes of defense phenotypes and cell fate determination during Arabidopsis-P. syringae interactions, contributing to a better understanding of plant defense mechanisms. Oxidative burst is a key signature during host-pathogen interactions. However, where and when ROS are produced during PTI, ETS, and ETI have not been well understood. To provide a better understanding of ROS accumulation and localization during PTI, ETS, and ETI, we infected Arabidopsis leaves with the three strains at OD600 0.01 and collected the leaves in a time course for fixation in the presence of cerium chloride. Cerium ion reacts with H2O2 to produce electron-dense insoluble precipitates of cerium perhydroxides. The fixed tissue was further embedded and sectioned for transmission electron microscope analysis for the presence of electron-dense cerium deposits, an indicative of H2O2 accumulation. Mock-treated leaves did not show cerium deposits. With DG34 infection, we observed strong cerium deposits initially on the cell wall at 6 hpi. As infection progressed, cerium deposits were additionally found on the plasma membrane and the outer membranes of the chloroplast and mitochondrion from 24 to 48 hpi. Compared to DG34, DG3 did not induce detectable cerium deposits in the host cells until 18 hpi.