Regulation of Cell Death During Arabidopsis Effector Triggered Immunity

dc.contributor.advisor

Dong, Xinnian

dc.contributor.author

Zebell, Sophia

dc.date.accessioned

2019-06-07T19:48:01Z

dc.date.available

2021-05-21T08:17:26Z

dc.date.issued

2019

dc.department

Biology

dc.description.abstract

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.

dc.identifier.uri

https://hdl.handle.net/10161/18653

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Plant sciences

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Arabidopsis

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Cell cycle

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Chloroplast

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Effector Triggered Immunity

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Plant

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ROS

dc.title

Regulation of Cell Death During Arabidopsis Effector Triggered Immunity

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Dissertation

duke.embargo.months

23

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