PHYTOALEXIN-DEFICIENT MUTANTS OF ARABIDOPSIS REVEAL THAT PAD4 ENCODESA REGULATORY FACTOR AND THAT 4 PAD GENES CONTRIBUTE TO DOWNY MILDEW RESISTANCE

We are working to determine the role of the Arabidopsis phytoalexin, c amalexin, in protecting the plant from pathogen attack by isolating ph ytoalexin-deficient (pad) mutants in the accession Columbia (Col-0) an d examining their response to pathogens. Mutations in PAD1, PAD2, and PAD4 caused enhanced susceptibility to the bacterial pathogen Pseudomo nas syringae pv. maculicola strain ES4326 (PsmES4326), while mutations in PAD3 or PAD5 did not. Camalexin was not detected in any of the dou ble mutants pad1-1 pad2-1, pad1-1 pad3-1 or pad2-1 pad3-1. Growth of P smES4326 in pad1-1 pad2-1 was greater than that in pad1-1 or pad2-1 pl ants, while growth in pad1-1 pad3-1 and pad2-1 pad3-1 plants was simil ar to that in pad1-1 and pad2-1 plants, respectively. The pad4-1 mutat ion caused reduced camalexin synthesis in response to PsmES4326 infect ion, but not in response to Cochliobolus carbonum infection, indicatin g that PAD4 has a regulatory function. PAD1, PAD2, PAD3 and PAD4 are a ll required for resistance to the eukaryotic biotroph Peronospora para sitica. The pad4-1 mutation caused the most dramatic change, exhibitin g full susceptibility to four of six Col-incompatible parasite isolate s. Interestingly, each combination of double mutants between pad1-1, p ad2-1 and pad3-1 exhibited additive shifts to moderate or full suscept ibility to most of the isolates.