SA is a vital signaling molecule responsible for activation of plant defenses against various pathogen infections. Pathogen detection activates salicylic acid (SA) biosynthesis which is paramount to local and systemic acquired resistance in addition to pathogenesis-related (PR) protein accumulation. Recently, NPR1, NPR3 and NPR4 were identified as SA binding proteins and signal transducers; however, conflicting results have been obtained concerning the nature of NPR1 as a SA receptor. These, and other, SA signaling pathways are often heavily influenced by phytohormone crosstalk, whether by inhibiting or potentiating effects. Pathogenic infection can additionally activate defense responses that require increased protein synthesis and folding demands to be facilitated by the endoplasmic reticulum (ER). These increased demands may result in an overload of unfolded or misfolded proteins, which cause ER stress and activate signal transduction pathways. Collectively, these responses compose the unfolded protein response (UPR) and are responsible for restoring cellular homeostasis. In Arabidopsis, two homologs of Inositol-requiring enzyme 1, basic leucine zipper 17 and 28 (bZIP17, bZIP28) and GCN2 (general control nonrepressed 2) appear to be key components of UPR stress-sensing pathways. Many metazoan disorders have been linked to chronic ER stress; however, the plant immune functions regulated by Inositol-requiring enzyme 1 (IRE1) and GCN2 are not well understood. The role of UPR in the regulation of Arabidopsis hormone signaling pathways is also not well understood. SA signaling has been linked to UPR in both Arabidopsis and rice. However, Arabidopsis does not possess a known functional homologue to the intermediary rice protein responsible for SA-UPR crosstalk. Thus, the integrated nature of pathogen infection, ER stress, phytohormone signaling and cell death will be studied in light of current research. We demonstrate that Arabidopsis UPR can be activated by exogenous application of SA, indicating crosstalk between UPR and the plant hormone SA. In rice, UPR has recently been shown to regulate cell death control via caspase activation. Here, I demonstrate that Arabidopsis cell death control mechanisms may be executed by Arabidopsis IRE1 and GCN2 as indicated by deficient ion leakage and caspase-like activity after a virulent pathogen infection.
|Author||J. Lucas Boatwright|
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