【摘 要】
：
BRI1-ASSOCIATED RECEPTOR KINASE 1(BAK1)and its closest paralog,BAK1-LIKE 1(BKK1),two leucine-rich repeat receptor-like protein kinases(LRR-RLKs),regulate a BR-independent cell-death pathway.Double nul
【机 构】
：
Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations,School of Life Scienc
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BRI1-ASSOCIATED RECEPTOR KINASE 1(BAK1)and its closest paralog,BAK1-LIKE 1(BKK1),two leucine-rich repeat receptor-like protein kinases(LRR-RLKs),regulate a BR-independent cell-death pathway.Double null mutant bak1-4 bkk1-1 displays a salicylic acid(SA)and light-dependent cell-death phenotype even without pathogen induction.Molecular mechanisms of the cell death controlled by BAK1 and BKK1 remain elusive.Here we report our identification of a suppressor of bak1-3 bkk1-1(sbb1-1).Genetic analyses indicated that the cell-death symptom in weak double mutant,bak1-3 bkk1-1,was completely suppressed by the loss-of-function mutant of SBB1,which encodes a nucleoporin(NUP)85-like protein.SBB1/NUP85 belongs to the NUP107-160 nucleoporin subcomplex consisting of eight different subunits.Genetic analyses demonstrated that three other NUPs in the NUP107-160 sub-complex were also able to rescue the cell death phenotype of bak1-3 bkk1-1when knocked-out individually.Further analyses indicated that the export of poly(A)+RNA is greatly blocked,resulting in significant RNA retention,in the nuclei of the nup mutants.Our results suggest that nucleocytoplasmic trafficking is critical in BAK1/BKK1-regulated cell-death control.
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