RAR1 and its interacting partner SGT1 play a central role in plant disease resistance triggered by a number of resistance (R) proteins. We identified cytosolic heat shock protein 90 (HSP90), a molecular chaperone, as another RAR1 interacting protein by yeast twohybrid screening. RAR1 interacts with the N-terminal half of HSP90 that contains the ATPase domain. HSP90 also specifically interacts with SGT1 that contains a tetratricopeptide repeat motif and a domain with similarity to the cochaperone p23. In Arabidopsis, the HSP90 inhibitor geldanamycin reduces the hypersensitive response and abolishes resistance triggered by the R protein RPS2 against Pseudomonas syringae pv. tomato DC3000 (avrRpt2). One of four Arabidopsis cytosolic HSP90 isoforms, AtHSP90.1 is required for full RPS2 resistance and is rapidly induced upon pathogen challenge. We propose that RAR1 and SGT1 function closely with HSP90 in chaperoning roles that are essential for disease resistance.

Lack of the barley (Hordeum vulgare) seven-transmembrane domain MLO protein confers resistance against the fungal pathogen Blumeria graminis f. sp. hordei (Bgh). To broaden the basis for MLO structure/function studies, we sequenced additional mlo resistance alleles, two of which confer only partial resistance. Wild-type MLO dampens the cell wall-restricted hydrogen peroxide burst at points of attempted fungal penetration of the epidermal cell wall, and in subtending mesophyll cells, it suppresses a second oxidative burst and cell death. Although the Bgh-induced cell death in mlo plants is spatially and temporally separated from resistance, we show that the two processes are linked. Uninoculated mutant mlo plants exhibit spontaneous mesophyll cell death that appears to be part of accelerated leaf senescence. Mlo transcript abundance increases in response to Bgh, rice (Oryza sativa) blast, wounding, paraquat treatment, a wheat powdery mildew-derived carbohydrate elicitor, and during leaf senescence. This suggests a broad involvement of Mlo in cell death protection and in responses to biotic and abiotic stresses.Homozygous mutant (mlo) alleles of the Mlo gene confer broad spectrum disease resistance to the biotrophic powdery mildew fungus, Blumeria graminis f. sp. hordei (Bgh; Jørgensen, 1992). The resistance is manifested in the failure of the fungus to penetrate the epidermal cell wall, and at these sites, cell wall remodeling and oxidative cross-linking processes fortify the cell wall (Thordal-Christensen et al., 1997; von Rö penack et al., 1998; Hü ckelhoven et al., 1999). Although cell wall reinforcement is likely to contribute to the resistant phenotype, other yet unknown molecular events may lead to abortion of fungal attack. Although the wild-type Mlo gene in effect acts as a negative regulator of a defense response, wildtype Ror1 and Ror2 are two genes that are required for full expression of mlo resistance to Bgh, but not race-specific resistance (Freialdenhoven et al., 1996; Peterhänsel et al., 1997). It is curious that powdery mildew-resistant mlo plants exhibit enhanced susceptibility to the fungal pathogens Magnaporthe grisea and Bipolaris sorokiniana (Jarosch et al., 1999; Kumar et al., 2001).Mutant mlo plants exhibit a spontaneous mesophyll cell death phenotype that is compromised by ror1 and ror2 mutations (Wolter et al., 1993; Peterhänsel et al., 1997). In this respect, mlo mutations resemble other mutations known to enhance host cell death processes along with disease resistance (Shirasu and SchulzeLefert, 2000). Many of these mutants constitutively express pathogen-related (PR) genes, but in barley (Hordeum vulgare) mlo, maize (Zea mays) lls1, and Arabidopsis lsd1 and edr1 plants, pathogen inoculation is required to trigger an enhanced defense response (Jabs et al., 1996; Frye and Innes, 1998; Simmons et al., 1998). These four genes have been isolated (Bü schges et al., 1997; Dietrich et al., 1997; Gray et al., 1997; Frye et al., 2001), and encode dissimilar proteins.Barley MLO is the pro...

Innate immunity signaling pathways in both animals and plants are regulated by mitogen-activated protein kinase (MAPK) cascades. An Arabidopsis MAPK cascade (MEKK1, MKK4/MKK5, and MPK3/MPK6) has been proposed to function downstream of the flagellin receptor FLS2 based on biochemical assays using transient overexpression of candidate components. To genetically test this model, we characterized two mekk1 mutants. We show here that MEKK1 is not required for flagellin-triggered activation of MPK3 and MPK6. Instead, MEKK1 is essential for activation of MPK4, a MAPK that negatively regulates systemic acquired resistance. We also showed that MEKK1 negatively regulates temperature-sensitive and tissue-specific cell death and H 2 O 2 accumulation that are partly dependent on both RAR1, a key component in resistance protein function, and SID2, an isochorismate synthase required for salicylic acid production upon pathogen infection.