All ETDs from UAB

Advisory Committee Chair

Karolina Mukhtar

Advisory Committee Members

Marina Gorbatyuk

Shahid Mukhtar

Robert Palazzo

Stephen Watts

Document Type


Date of Award



Pathogens and plants are involved in a coevolutionary battle for dominance. As plants lack adaptive immune systems, they rely on their innate immunity to protect themselves from infectious agents. Upon pathogen attack, plant cells activate their pro-survival strategy by recognizing the pathogen and actively transcribing and translating proteins to effectively defend against the pathogen infection. As the intensity of infection increases, the heightened demand for proteins places an excessive burden on the ER machinery resulting in the accumulation of misfolded or unfolded proteins within the ER. To restore the protein homeostasis, a cellular relief signaling pathway called Unfolded Protein Response (UPR) is initiated. Endoplasmic Reticulum (ER)-resident protein AtIRE1 (Arabidopsis thaliana inositol requiring enzyme-1) is the most conserved UPR sensor that can reduce ER stress by sequentially activating pro-survival and pro-death signaling pathways. In the pro-survival pathway, upon the accumulation of misfolded or unfolded proteins, AtIRE1 via its endonuclease domain directly cleaves AtbZIP60 (Arabidopsis thaliana basic leucine zipper 60) mRNA, leading to the production of an active transcription factor that promotes the expression of multiple ER stress-responsive genes. In the case of acute or chronic ER stress, AtIRE1 can also contribute to pro-death signaling mechanisms that involve the degradation of specific classes of mRNAs in a process called Regulated IRE1-Dependent Decay (RIDD). AtIRE1, as an ER-resident protein, is likely to form complexes with another ER-resident molecule(s) to orchestrate the Pro survival and pro-death cellular mechanism. With our proteomic study, we identified that AtBI-1 (Arabidopsis thaliana Bax inhibitor- 1) known to be involved in cell survival and cell death roles, associates with AtIRE1 to trigger and/or modulate UPR. The underlying molecular mechanisms by which AtBI-1 executes its function, particularly in biotic stress-mediated UPR pathways, are largely unknown. In summary, this dissertation uncovers the crucial role of AtIRE1 and AtBI-1 in modulating the pro-survival to pro-death molecular switch. Furthermore, it reveals the downstream effects of the AtIRE1-AtBI1 interaction on bacterial disease resistance and suppression of plant pathogen-induced cell death.

Available for download on Thursday, June 27, 2024