Figure 7.

Working Model of the Interplay of ssi2, sfd1, sfd2, and sfd4 in Defense Signaling in Arabidopsis.

This model is a refinement of Figure 1. The sfd1, sfd2, and sfd4 mutant alleles suppress (−) the ssi2-conferred dwarfing, spontaneous development of lesions containing dead cells, NPR1-independent expression of PR1, and enhanced resistance to Psm. In addition, sfd1 and sfd4 also suppress the ssi2-conferred accumulation of high SA levels. However, SA application is ineffective in restoring PR1 expression in sfd1 ssi2 npr1, sfd2 ssi2 npr1, and sfd4 ssi2 npr1 plants, implicating the involvement of another ssi2-contributed factor in the activation of the NPR1-independent pathway leading to the expression of PR1 and enhanced resistance to Psm. The absence of SA accumulation in the ssi2 nahG and ssi2 eds5 plants does not ameliorate the ssi2-conferred cell death phenotype, suggesting that high levels of SA do not have a causal role in the cell death phenotype. The sfd2 ssi2 npr1 plants accumulate increased SA levels despite the lack of spontaneous cell death, suggesting that cell death is not the primary factor that promotes SA accumulation in the ssi2 mutant. Hence, ssi2-conferred cell death and SA accumulation are shown to be independent of each other. The sfd1 mutant alleles restore JA-inducible PDF1.2 expression in sfd1 ssi2 npr1 plants. sfd1 is shown to impinge on a step that is common to the activation of cell death, SA accumulation, the activation of the NPR1-independent defense pathway, and the repression of JA signaling in the ssi2 mutant. However, because sfd1 does not restore resistance to B. cinerea, despite restoring PDF1.2 expression in the sfd1 ssi2 npr1 plants, an additional ssi2-modulated mechanism is shown to suppress (−) the defense against B. cinerea. sfd4 does not restore JA-inducible PDF1.2 expression in sfd4 ssi2 npr1. Hence, sfd4 is shown to suppress (−) a step that is common to the activation of cell death and dwarfing, SA accumulation, and the activation of the NPR1-independent defense pathway. sfd2 is shown to interfere with (−) a step common to the activation of ssi2-conferred cell death and the activation of NPR1-independent signaling.