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Necrotrophic pathogens kill host cells before colonizing them (van Kan, 2006). Unlike gene-for-gene resistance to biotrophic pathogens, plant resistance to necrotrophic pathogens is often polygenic, but so far only a few genes involved in plant resistance to necrotrophic pathogens have been identified (Mengiste et al., 2003; Nandi et al., 2005; Brodersen et al., 2006; Veronese et al., 2006). Although effective against biotrophic pathogens, the HR is actually promoted by necrotrophic pathogens and facilitates their infection (Govrin and Levine, 2000). In Arabidopsis, resistance to necrotrophic pathogens depends on jasmonate (JA) and ethylene (ET) signaling and synthesis of the phytoalexin camalexin (Penninckx et al., 1996, 1998; Thomma et al., 1998, 1999; Ferrari et al., 2003). However, susceptibility to necrotrophic pathogens under conditions of normal JA and ET signaling and camalexin synthesis has been documented (Ferrari et al., 2003; Mengiste et al., 2003; Veronese et al., 2004), suggesting that other unknown pathways may be equally or even more important.
In Arabidopsis WRKY33 transcription factor is important for plant resistance to necrotrophic pathogens (Zheng et al., 2006). Knockout wrky33 mutant plants are highly susceptible to the necrotrophic fungal pathogens Botrytis cinerea (hereafter Botrytis) and Alternaria brassicicola, but respond normally to hemi-biotrophic P. syringae (Zheng et al., 2006). Overexpression of WRKY33 increases resistance to Botrytis and A. brassicicola (Zheng et al., 2006). WRKY33 interacts with MKS1, an MPK4 substrate (Andreasson et al., 2005). An MPK4-release-WRKY33 model has been proposed for regulation of PAD3, a gene that is required for biosynthesis of the phytoalexin camalexin (Qiu et al., 2008b). However, mutations and over-expression of MKS1 affect only SA-dependent defense (Qiu et al., 2008a).
Thus, autophagy plays a complex role in the regulation of JA-regulated defense genes. Autophagy plays a negative role in basal expression of PDF1.2, probably by suppressing or delaying senescence. In Botrytis-infected plants, JA-mediated signaling, including induction of PDF1.2 expression, is induced as a defense response, in which autophagy apparently plays a positive role. The contrasting effects of autophagy on basal versus induced expression of PDF1.2 may reflect complex interaction of JA signaling with SA signaling. A previous study suggested that the outcomes of interactions between SA and JA signaling are concentration-specific (Mur et al., 2006). When both signals were applied at low concentrations, there was a transient synergistic enhancement in expression of genes associated with JA or SA. When the signals were used at higher concentrations or for prolonged times, their actions became antagonistic. Three- to four-week-old atg mutants contain significantly increased levels of SA and JA (Yoshimoto et al., 2009), which may interact positively or even synergistically in induction of the PR1 and PDF1.2 genes, respectively. After infection by a necrotrophic pathogen, a further increase in SA levels and signaling in the atg mutants may antagonize JA signaling, leading to reduced expression of JA-regulated defense genes (Yoshimoto et al., 2009).
Using several autophagy-deficient (atg) genotypes, we determined the function of autophagy in basal plant immunity. Arabidopsis mutants lacking ATG5, ATG10 and ATG18a develop spreading necrosis upon infection with the necrotrophic fungal pathogen, Alternaria brassicicola, which is accompanied by the production of reactive oxygen intermediates and by enhanced hyphal growth. Likewise, treatment with the fungal toxin fumonisin B1 causes spreading lesion formation in atg mutant genotypes. In contrast, atg plants do not show spreading necrosis, but exhibit marked resistance against the virulent biotrophic phytopathogen, Pseudomonas syringae pv. tomato. Inducible defenses associated with basal plant immunity, such as callose production or mitogen-activated protein kinase activation, were unaltered in atg genotypes. However, phytohormone analysis revealed that salicylic acid (SA) levels in non-infected and bacteria-infected atg plants were slightly higher than those in Col-0 plants, and were accompanied by elevated SA-dependent gene expression and camalexin production. This suggests that previously undetected moderate infection-induced rises in SA result in measurably enhanced bacterial resistance, and that autophagy negatively controls SA-dependent defenses and basal immunity to bacterial infection.
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