Three Botrytis-susceptible mutants
bos2,
bos3, and bos4 which define independent and novel genetic loci required for Arabidopsis resistance to Botrytis cinerea were isolated. The
bos2 mutant is susceptible to B. cinerea but retains wild-type levels of resistance to other pathogens tested, indicative of a defect in a response pathway more specific to B. cinerea. The
bos3 and bos4 mutants also show increased susceptibility to Alternaria brassicicola, another necrotrophic pathogen, suggesting a broader role for these loci in resistance. bos4 shows the broadest range of effects on resistance, being more susceptible to avirulent strain of Pseudomonas syringae pv. tomato. Interestingly,
bos3 is more resistant than wild-type plants to virulent strains of the biotrophic pathogen Peronospora parasitica and the bacterial pathogen P. syringae pv. tomato. The Pathogenesis Related gene 1 (PR-1), a molecular marker of the
salicylic acid (SA)-dependent resistance pathway, shows a wild-type pattern of expression in
bos2, while in
bos3 this gene was expressed at elevated levels, both constitutively and in response to pathogen challenge. In bos4 plants, PR-1 expression was reduced compared with wild type in response to B. cinerea and SA. In
bos3, the mutant most susceptible to B. cinerea and with the highest expression of PR-1, removal of SA resulted in reduced PR-1 expression but no change to the B. cinerea response. Expression of the plant
defensin gene PDF1-2 was generally lower in bos mutants compared with wild-type plants, with a particularly strong reduction in
bos3. Production of the phytoalexin
camalexin is another well-characterized plant defense response. The
bos2 and bos4 mutants accumulate reduced levels of
camalexin whereas
bos3 accumulates significantly higher levels of
camalexin than wild-type plants in response to B. cinerea. The
BOS2,
BOS3, and BOS4 loci may affect
camalexin levels and responsiveness to
ethylene and
jasmonate. The three new mutants appear to mediate disease responses through mechanisms independent of the previously described
BOS1 gene. Based on the differences in the phenotypes of the bos mutants, it appears that they affect different points in defense response pathways.