Genetic Regulation of Cell Death and Disease Resistance in Arabidopsis Public Deposited

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  • March 20, 2019
  • Roberts, Melinda Margaret
    • Affiliation: College of Arts and Sciences, Department of Biology
  • Plants are constantly identifying and responding to cues and threats from their surroundings, such as changes in light, temperature, and humidity, mechanical damage from herbivores and insect, and pathogen attack. Resistance to plant pathogens involves both passive barriers and active, inducible disease resistance responses. Induction of immune responses in plants leads to, for example, cellular redox changes, activation of MAP kinase cascades, massive transcriptional reprogramming, and frequently culminates in a form of programmed cell death known as the hypersensitive response. In my dissertation work, I characterized proteins involved in the regulation of cell death and disease resistance in the model plant Arabidopsis thaliana. My first project involved the zinc finger protein LSD1, a cytosolic scaffolding protein which is a negative regulator of cell death and disease resistance. lsd1 mutant plants exhibit inappropriately triggered cell death and increased resistance to multiple pathogens. LSD1 was used in a Y2H screen which identified the LSD1 interactor NF-YC3, a CAAT-binding transcription factor. nf-yc3 mutants have moderately increased susceptibility to the oomycete pathogen Hyaloperonospora arabidopsidis, and overexpression of NF-YC3 increases resistance to this pathogen, demonstrating that NF-YC3 is a positive regulator of disease resistance, likely via transcriptional regulation. This activity could be partially controlled by LSD1 sequestering NF-YC3 in the cytosol, thereby preventing its nuclear relocalization and subsequent disease resistance function. The latter half of my work involved the characterization of a positive regulator of lsd1 rcd, ADR1-L2. ADR1-L2 belongs to a small family of NB-LRRs, the main class of resistance proteins that are required to recognize specific pathogen effector proteins, leading to pathogen recognition and defense responses. I created an autoactive mutant of ADR1-L2, which required P-loop dependent ATPase activity for function and exhibited increased resistance to infection with virulent pathogens. I then used this autoactive mutant to try to understand the genetic requirements of the signaling pathway involved in this resistance response, finding that ADR1-L2 functions in a feedback loop involving the defense-related hormone salicylic acid, LSD1, and the lsd1 regulator EDS1. Together, my results refined the model of pathogen-triggered immunity in Arabidopsis.
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  • In Copyright
  • Dangl, Jeffery L.
  • Doctor of Philosophy
Graduation year
  • 2012

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