Poster: Plant Pathogen/Symbiont Interactions

Abs # 764: PMR5, a plant-specific protein for cell wall-mediated disease resistance in Arabidopsis – interactions with PMR6, a pectate lyase-like gene

Presenter:	Raab, Theodore K, tkraab@Andrew2.Stanford.edu
Authors	Raab, Theodore K (A)   Vogel, John P (B)   Somerville, Shauna C (A)
Affiliations:	(A): Carnegie Institution of Washington (B): US Dept. of Agriculture Western Regional Center

PMR5 is a recently described Arabidopsis locus identified in a search for plant genes mediating resistance to powder mildew. Cloning of PMR5 demonstrated that it codes for a membrane-associated 402 aa-protein, unique to plants. Its coding sequence has very few recognizable protein structural motifs; however, the first 22 aa's of the protein are predicted to serve as an N-terminal target sequence for the ER. Compared to wild type plants, the visual phenotype of pmr5 mutant plants is similar to the previously described pmr6 mutation: (1) reduced plant size, (2) upward-cupping leaves, and most importantly, (3) quantitative resistance to the powdery mildew fungus, Erysiphe cichoracearum. As well, the mutants depend on activation of neither the salicylic acid- nor the jasmonic acid/ethylene-dependent pathways for defense. We undertook a synchrotron FT-IR spectromicroscopic study of cleared leaves from plants homozygous for mutations in pmr5, a double mutant pmr5pmr6, and plants that had been complemented with DNA for the PMR6 gene. Mid-infrared light from synchrotrons is 2 - 3 orders of magnitude brighter than conventional sources, providing contrast based on the spectral signature of the reflected signal at a spatial resolution of 3-10 microns. Direct biochemical extractions of the cell walls from plants used for the IR studies demonstrated alterations in pectin modification, and IR confirmed the spectral similarity of pmr5 mutants compared to pmr6. We suggest that the two genes affect the same pectin component of the cell wall, and serve as susceptibility genes for the powdery mildew pathogen.