Regulation of Cell Death During Arabidopsis Effector Triggered Immunity
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In the plant innate immune system, diverse signals from a wide range of pathogens converge on the same output, effector triggered immunity (ETI) and the associated programmed cell death (PCD). Past genetic studies have succeeded in uncovering the role of R-genes in recognizing the presence of pathogen effectors, and in identifying a number of downstream executors of the immune response. However, the gap between effector recognition and phenotype regulation remains poorly understood, with each signaling component only contributing a minor quantitative effect to the phenotype of ETI-PCD. In this dissertation, my goal is to fill in a portion of that gap.
I demonstrate that there is a prolonged nuclear increase of calcium ions during ETI, and that that nuclear calcium signal is essential for PCD. I also utilize cpr5, a point mutant identified for its constitutive defense response and programmed cell death lesions, to identify a new role for cell cycle regulators in regulating ETI-PCD. I show that phosphorylation of the cell cycle regulator Retinoblastoma-Related 1 (RBR1) is responsive to ETI. The RBR1 target transcription factors E2Fa, E2Fb, and E2Fc have an additive role regulating ETI, and a triple e2fabc mutant is susceptible to pathogens. Using a reverse genetics approach in e2fabc, I identify repression of nonphotochemical quenching in the chloroplasts as a key step in ETI-PCD regulation.
Together, these studies emphasize the role of organelles in PCD regulation, with the nucleus serving as a hub of second messenger signaling and transcription and the chloroplasts responding to ETI by remodeling to serve a new role as a platform for ROS production. In addition, they define a new pathway of ETI regulation that contributes quantitatively to ETI-PCD.
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Rights for Collection: Duke Dissertations