Figure 9. A model for the regulation of ADR1-L2_D484V activity.

ETI activates both an AtRbohD-dependent ROI burst and SID2-dependent SA accumulation via ADR1-L2. Activated ADR1-L2 initiates cell death and disease resistance via SA-dependent and -independent pathways. EDS1 functions downstream of activated ADR1-L2 as a positive regulator of both SA accumulation and of the SA-independent pathway. ADR1-L2 also triggers SA via a pathway that is controlled by LSD1 and antagonized by EDS1. Therefore, the spread of this SA accumulation is spatially down-regulated through a combined action of EDS1 and LSD1. Due to its position in these feedback loops, SA functions both up- and down-stream of ADR1-L2.