The BOS loci of Arabidopsis are required for resistance to Botrytis cinerea infection

Abstract

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.

The Membrane-Anchored BOTRYTIS-INDUCED KINASE1 Plays Distinct Roles in Arabidopsis Resistance to Necrotrophic and Biotrophic Pathogens

“…After Botrytis infection, patches of dead cells were visible in both wild-type and mutant plants. This is consistent with previously described Arabidopsis mutants that have increased Botrytis susceptibility in the absence of a lesion-mimic phenotype (Thomma et al, 1999;Mengiste et al, 2003;Veronese et al, 2004).…”

“…The previously described bos1 mutant showed increased susceptibility to Botrytis and sensitivity to oxidative stress (Mengiste et al, 2003;Veronese et al, 2004). In the case of bik1, sensitivity to oxidative stress generated by paraquat (methyl viologen) was comparable to that in wild-type plants, suggesting that susceptibility to Botrytis is not linked to altered plant sensitivity to oxidative stress (data not shown).…”

“…PR-1 expression positively correlates with resistance to biotrophic pathogens but negatively correlates with resistance to Botrytis in some mutants, including bos3 and ssi2, and provides a clear distinction between host responses to the two classes of pathogens (Kachroo et al, 2001;Veronese et al, 2004). In the bos mutants described previously, expression of PR-1 and camalexin accumulation varied, with no consistent correlations to enhanced Botrytis susceptibility (Mengiste et al, 2003;Veronese et al, 2004). This lack of consistent correlation in different mutants may indicate that the roles of the pathways represented by the defense markers are not clear and may vary in the different mutants, because there may be cross-regulation of the different pathways.…”

“…The T-DNA inserted into the last exon of the BIK1 gene and resulted in the loss of detectable BIK1 transcript, indicating that bik1 is a loss-offunction mutant (Figures 1A and 1B). To determine the role of BIK1 in resistance to Botrytis, homozygous bik1 plants were inoculated by spraying a suspension containing 2 3 10 5 Botrytis spores per milliliter, as described previously (Mengiste et al, 2003;Veronese et al, 2004). In wild-type (ecotype Columbia) plants, Botrytis infection caused restricted disease symptoms, with no significant damage to the plant ( Figure 1C).…”

Arabidopsis Cell Death in Compatible and Incompatible Interactions with Alternaria brassicicola

“…Interactions between Arabidopsis thaliana and Alternaria brassicicola have been frequently employed to investigate the functions of plant genes in necrotrophic interactions (Cramer and Lawrence, 2004;Mengiste et al, 2003;Mukherjee et al, 2009;Oh et al, 2005;Veronese et al, 2004;Zheng et al, 2006). Based on the enigmatic innate immunity of Col-0 against MUCL20297, which is virulent on Brassica oleracea (Cramer et al, 2006), and the completion of the genome projects for both pathogen and host, a wealth of information has now accumulated on the roles of several plant genes and defense signaling pathways that are related with jasmonic acid and camalexin in the incompatible interactions.…”