Date Available

12-7-2018

Year of Publication

2016

Degree Name

Doctor of Philosophy (PhD)

Document Type

Doctoral Dissertation

College

Agriculture, Food and Environment

Department/School/Program

Plant Pathology

First Advisor

Dr. Pradeep Kachroo

Abstract

The various modes of defense induced upon the recognition of pathogen-derived molecules provide species level resistance to non-host pathogens, local and systemic resistance to race-specific pathogens, and basal resistance to virulent pathogens. Resistance (R) gene-mediated or species-specific immunity is induced when a strain-specific avirulence (avr) effector from the pathogen associates directly/indirectly with a cognate plant R protein. Plant viruses often encode suppressors of host RNA silencing machinery. In turn, plants recognize such suppressors via R proteins. Recognition of the Turnip Crinkle Virus (TCV) coat-protein (CP, RNA silencing suppressor) induces HRT-mediated resistance in Arabidopsis thaliana. This requires the RNA silencing component, double-stranded RNA-binding protein (DRB)4, even though HRT-mediated resistance neither requires the RNA silencing suppressor function of CP, nor is it associated with the accumulation of TCV-specific small-RNA. The drb4 mutant plants contain reduced HRT protein and induce spreading hypersensitive-response to TCV. HRT interacts with DRB4, but only its cytosolic fraction. TCV infection increases the cytosolic DRB4 pool, but also inhibits the HRT-DRB4 interaction. The virulence inducing R8A CP mutation also disrupts this interaction, but alters DRB4 localization partially. This suggests that subcellular compartmentalization of DRB4 may contribute to HRT-derived resistance signaling. DRB4 is likely a universal defense regulator because it also regulates R-mediated defense to bacteria. Consequently, drb4 plants are compromised in systemic acquired resistance (SAR). SAR involves symplastic intracellular transport between adjacent cells occurs via channels known as plasmodesmata (PD). I show that proteins that regulate PD gating, such as the PD localizing proteins (PDLP) 1 and 5 are essential for SAR. Furthermore, while phloem loading of the SAR-inducing azelaic acid (AzA) and glycerol-3-phosphate (G3P) occurs via the symplast, that of salicylic acid (SA) occurs via the apoplast. Plants overexpressing PDLP5 have constitutively closed PD and are impaired for SAR because their PD closure impaired the transport of AzA and G3P, but not SA. Together, these results identify the transport routes of SAR signals and highlight an important regulatory role for DRB and PDLP proteins in plant defense and systemic immunity. Notably, the pdlp1/5 mutants with constitutively open PD, are also compromised for SAR. PDLP1 interacts with a protein (AZI1) that is required for AzA/G3P-induced SAR and contributes to the partitioning of AZI1 between the plastids and cytoplasm.

Digital Object Identifier (DOI)

https://doi.org/10.13023/ETD.2016.448

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