The role of apoplastic peroxidases in the Arabidopsis thaliana defense response

Plants possess a multi-layered defense response in order to fend off pathogen attack. MAMP-triggered immunity (MTI) forms a first line of defense that is responsive to a wide variety of microbes. Virulent microbial species are those that have evolved mechanisms of suppressing MTI. In turn, the plant has a second defense system, effector-triggered immunity (ETI), which detects the proteins which microbes use to suppress MTI. ETI is a significantly stronger response typified by localized cell death known as the hypersensitive response (HR). Production of reactive oxygen species (ROS) such as superoxide and hydrogen peroxide has been associated with both layers of defense. In recent years, enzymatic sources of these ROS have been identified. While NADPH oxidases have received much attention, they have not been shown to be necessary for pathogen resistance in Arabidopsis. In contrast, the Ausubel and Bolwell laboratories have shown that two apoplastic peroxidases are critical for a full defense response. The work detailed in this thesis shows that when these two peroxidases, prx33 and prx34, are silenced, the plants are more susceptible to virulent bacterial and fungal pathogens. Furthermore, silencing of prx33 and prx34 disrupts defense hormone signaling, specifically the pathways controlled by salicylic acid and jasmonic acid. However, these two peroxidases do not appear necessary for MTI or resistance to non-host microbes and bacteria that are detected by the ETI defense response. Additionally, the HR associated with ETI is intact in prx33 and prx34 silenced transgenic plants. Finally, three independent methods of knocking-down prx33 and prx34 transcription have been employed to confirm the results obtained with the original transgenic line and have demonstrated that prx33 and prx34 are both required for an intact defense response and operate in a non-redundant manner