Figure 5. Combinatory stress induced by tunicamycin and BTH leads to early senescence and uncontrolled cell death in autophagy-deficient mutants. (A) 4-wk-old Col-0 WT, npr1, atg2, and atg2 npr1 plants grown on MS plates supplemented with 0.00005% DMSO (Mock), 5 ng mL⁻¹ TM, 50 μM BTH or 5 ng mL⁻¹ TM and 50 μM BTH. Double treatment with BTH and TM decreases germination and induces early senescence in atg2 mutants but these features are rescued by NPR1 loss of function. (B) 4-wk-old WT, npr1, atg2 npr1, and atg2 leaves injected in one side with 100 ng mL⁻¹ TM (“Tunicamycin” and “AvrRpm1/Tunicamycin”) or 0.00005% DMSO (“AvrRpm1”), and then injected 5 d later with Pst DC3000 (AvrRpm1) at 2 x 10⁷ CFU mL⁻¹ (“AvrRpm1” and “AvrRpm1/Tunicamycin”) or 10 mM MgCl₂ (“Tunicamycin”), in the opposite side of the leaves. Priming of atg2 mutants with TM before infection leads to unrestricted HR cell death. Loss of NPR function in the atg2 background is sufficient to permit survival under combinatory stress and restrict HR cell death to the infection site. Pictures taken 4 d after Pst DC3000 (AvrRpm1) or MgCl₂ injections.