All ETDs from UAB

Advisory Committee Chair

Karolina Mukhtar

Advisory Committee Members

Shahid Mukhtar

Denise Monti

Zsuzsanna Bebok

Document Type


Date of Award


Degree Name by School

Master of Science (MS) College of Arts and Sciences


In eukaryotic cells, the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) results in ER stress that induces a cascade of reactions termed the unfolded protein response (UPR). The most conserved UPR sensor amongst eukaryotes, Inositol-Requiring Enzyme 1 (IRE1), responds to ER stress by activating a pathway that, under normal conditions, would up-regulate the cellular pro-survival pathway. However, under extreme conditions the infected portion of the plant will ultimately “switch” from pro-survival to pro-death in order to avoid further unfavorable circumstances for the plant as a whole. Arabidopsis possesses two homologs of the major UPR sensor, IRE1a and IRE1b. In this study, I focused on the IRE1a response pathway and the essential role it plays in the immune response of the plant. Unlike mammals, the molecular mechanisms for turning off the pro-survival branch of IRE1a in plants remain largely undefined. In Arabidopsis, IRE1a directly cleaves bZIP60 (basic leucine zipper 60 transcription factor) mRNA in response to both physiological stresses and pathological perturbations, leading to the production of an active transcription factor that promotes the expression of multiple ER stress-responsive genes. Throughout this study, the plant bacterial pathogen Pseudomonas syringae pv. maculicola ES4326 (Psm ES4326) was used as a biotic inducer for ER stress in an attempt to uncover regulatory mechanisms governing bZIP60 expression. We suggest that novel Arabidopsis thaliana microRNA (miR5658; At4g39838) that can potentially target bZIP60, is specifically up-regulated upon acute ER stress. Moreover, quantification of miR5658 reveals its induction coincides with bZIP60 mRNA suppression suggesting that miR5658 might participate in the exquisite regulation of bZIP60 in a manner reminiscent of the mammalian X-box binding protein 1-miR-30c-2* regulatory mechanism. We also propose that the central plant immune regulator NPR1 (Non-Expressor of PR genes 1) plays an important role in regulating miR5658. Taken together, these results suggest that upon cell death-triggering stimuli, NPR1, via miR5658, may target bZIP60 mRNA to turn off the IRE1a-mediated pro-survival pathway.



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