The mekk2 and summ2 mutants suppress the cell death mediated by silencing of MEKK1. A, Silencing of MEKK1 by VIGS triggers cell death phenotype resembling the mekk1 mutant. Col-0 wild-type (WT) and mekk1 were grown on soil for 3 weeks (left two). Plant phenotypes of Col-0 wild-type plants are shown 2 weeks after VIGS of a vector control (Ctrl) or MEKK1. Bars = 1 cm. B, The let4/mekk2 mutant suppresses growth defects triggered by RNAi-MEKK1. Plant phenotypes of wild-type and mekk2 after VIGS of MEKK1. CLA1 is a visible marker for VIGS efficiency. Plant pictures were digitally extracted and placed on a black background in (A) and (B). Bars = 1 cm. C, The mekk2 mutant suppresses cell death and H2O2 accumulation triggered by RNAi-MEKK1. Plant true leaves after VIGS of MEKK1 were stained with trypan blue for cell death (left) and 3,3′-diaminobenzidine (DAB) for H2O2 accumulation (right). Bars = 0.5 cm. D, The mekk2 mutant suppresses PR1 and PR2 expression triggered by RNAi-MEKK1. The expression of PR1 and PR2 was normalized to the expression of UBQ10. The data are shown as mean ± se from three independent repeats. The different letters denote statistically significant difference according to one-way ANOVA followed by Tukey test (P < 0.05). E, The let5/summ2-9 mutant suppresses growth defects triggered by RNAi-MEKK1. Plant phenotypes of wild-type and let5/summ2-9 after VIGS of MEKK1 or CLA1. Bars = 1 cm. F, PCR analysis of SUMM2 in let5. At top, SUMM2 was not amplified in the let5 mutant with primers amplifying full length genomic DNA. At bottom, ACTIN2 control is shown. G, The mekk2, summ2, and crck3 mutants specifically suppressed RNAi MEKK1, but not BAK1/SERK4 or BIR1 cell death. Plant phenotypes of Col-0 plants and mutants are shown 2 weeks after VIGS of a vector control, MEKK1, BAK1/SERK4, BIR1, or CLA1. Bars = 1 cm.