Poster: Plant Pathogen/Symbiont Interactions

Abs # 721: dnd1- and dnd2-mediated disease resistance

Presenter:	Jurkowski, Grace , gij@plantpath.wisc.edu
Authors	Jurkowski, Grace  (A)   Smith, Roger  (B)   Yu, I-Ching  (A)   Bent, Andrew  (A)
Affiliations:	(A): University of Wisconsin-Madison (B): The Institute for Genomic Research

The hypersensitive response (HR) in plants is a common characteristic of gene-for-gene resistance responses. We have identified and characterized two mutants, dnd1 and dnd2, that fail to elicit the HR in response to pathogens expressing a recognized avr gene, yet still block pathogen growth. These mutants also exhibit constitutive PR gene expression, high salicylic acid (SA) levels, and the ability to partially restrict virulent pathogen growth. The dnd1 and dnd2 mutants provide a genetic background for exploring how other defense genes contribute to the initiation and regulation of the HR and systemic resistance. Introduction of npr1 (which blocks SA-mediated defense responses) into dnd1 or dnd2 plants does not relieve the dwarf rosette phenotype. Interestingly, constitutive PR gene expression and ability to restrict pathogen growth is partially blocked in dnd1 npr1 plants, suggesting the existence of a SA-dependent but NPR1-independent defense pathway. In contrast to dnd1 npr1, dnd1 ndr1 plants show a partial relief of dwarfism that is correlated with a partial relief of constitutive PR gene expression. This suggests a role for NDR1 in general resistance pathways, and not just R gene pathways. We have also introduced eds16 and ein2 into a dnd1 background to assess the contribution of SA biosynthesis and ethylene response pathways to dnd1-mediated defense responses. The eds16 mutation completely relieves dnd1 of its constitutive PR gene expression. We are now examining the ability of this line to restrict pathogen growth. Initial characterization of dnd1 ein2 is in progress, and studies with analogous dnd2 double mutants are also in progress. Finally, we will report on map-based cloning of DND2.