Regulation of the stability of plant disease resistance proteins

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  • March 22, 2019
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  • Hubert, David Anthony
    • Affiliation: College of Arts and Sciences, Department of Biology
Abstract
  • Plants, like animals, can recognize specific pathogens by virtue of a highly-evolved immune system. Recognition of pathogens by plants leads to a well-defined series of outputs, including production of reactive oxygen species, cell wall thickening, and a form of programmed cell death called the Hypersensitive Response (HR). At the forefront of this recognition process are the disease Resistance (R) genes. The proteins encoded by R genes are positive regulators of cell death and thus their accumulation is tightly regulated. Here I present evidence implicating cytosolic HSP90 as a central figure in the maintenance of appropriate R protein levels. Cytosolic HSP90 is encoded by four genes in our model plant system, Arabidopsis thaliana. I present data for genetic interactions between two of these HSP90 paralogs. I also demonstrate a physical interaction between HSP90 and RAR1 and SGT1, two proteins previously identified as playing a role in R protein accumulation. Consistent with the physical interaction, double mutant analyses uncovered a genetic interaction between HSP90 and SGT1. Furthermore mutant forms of HSP90 and RAR1 reveal that changes in their ability to physically interact with each other and with SGT1 can explain the phenotypes of the mutants in planta. I also describe a genetic screen to identify new additional loci required for the function of the Arabidopsis R gene, RPM1. The phenotype of one mutant identified in this screen suggests that transcriptional regulation of R genes may play a more significant role in maintaining R protein levels than previously expected.
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  • In Copyright
Advisor
  • Dangl, Jeffery L.
Degree granting institution
  • University of North Carolina at Chapel Hill
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  • Open access
Date uploaded
  • October 19, 2010

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