ATR and infection: Assuming that DNases and other factors during infection or herbivore attack generate fragments of DNA that accumulate in the extracellular space (arrow H1) and assuming further, that these fragments can enter the cell and activate ATM via the MRN complex (H2), exogenously applied fragments of self- and nonself-DNA could activate ATM and thereby induce the synthesis of SA, which triggers DNA damage (H3) and thereby activates ATR (arrow 7) to close the circle by connecting ATM-based and NPR1-dependent PR1 expression to the ATR-dependent and NPR1-independent Dong-pathway (4–6).