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BRI1-ASSOCIATED KINASE 1 (BAK1) was initially identified as a co-receptor of the brassinosteroid (BR) receptor BRI1. Genetic analyses also revealed that BAK1 and its closest homolog BAK1-LIKE 1 (BKK1) regulate a BR-independent cell-death control pathway. The double null mutantbak1 bkk1displays a salicylic acid- and light-dependent cell-death phenotype even without pathogen invasion. Molecular mechanisms of the spontaneous cell death mediated by BAK1 and BKK1 remain unknown. Here we report our identification of asuppressor of bak1 bkk1(sbb1–1). Genetic analyses indicated that cell-death symptoms in a weak double mutant,bak1–3 bkk1–1, were completely suppressed by the loss-of-function mutation inSBB1, which encodes a nucleoporin (NUP) 85-like protein. Genetic analyses also demonstrated that individually knocking out three other nucleoporin genes from the SBB1-located sub-complex was also able to rescue the cell-death phenotype ofbak1–3 bkk1–1. In addition, a DEAD-box RNA helicase, DRH1, was identified in the same protein complex as SBB1 via a proteomic approach. Thedrh1mutation also rescues the cell-death symptoms ofbak1–3 bkk1–1. Further analyses indicated that export of poly(A)+ RNA was greatly blocked in thenupanddrh1mutants, resulting in accumulation of significant levels of mRNAs in the nuclei. Over-expression of a bacterialNahGgene to inactivate salicylic acid also rescues the cell-death phenotype ofbak1–3 bkk1–1. Mutants suppressing cell-death symptoms always showed greatly reduced salicylic acid contents. These results suggest that nucleocytoplasmic trafficking, especially of molecules directly or indirectly involved in endogenous salicylic acid accumulation, is critical in BAK1- and BKK1-mediated cell-death control.The receptor-like kinases BAK1 and BKK1 were known tomediate celldeath, but the molecular mechanisms have not been elucidated. Here we characterized a suppressor of a bak1;bkk1 mutant and showed that nucleocytoplasmic trafficking, especially for molecules directly or indirectly involved in salicylic acid accumulation, plays critical roles BAK1 and BKK1-mediated cell death.