Protein farnesylation negatively regulatesbrassinosteroid signaling via reducing BES1 stabilityinArabidopsis thaliana^(∞)

摘要

Brassinosteroids(BRs)are a group of steroidal phytohormones,playing critical roles in almost all physiological aspects during the life span of a plant.In Arabidopsis,BRs are perceived at the cell surface,triggering a reversible phosphorylation-based signaling cascade that leads to the activation and nuclear accumulation of a family of transcription factors,represented by BES1 and BZR1.Protein famesylation is a type of post-translational modification,functioning in many important cellular processes.Previous studies demonstrated a role of famesylation in BR biosynthesis via regulating the endoplasmic reticulum localization of a key bassino-lide(BL)biosynthetic enzyme BR6ox2.Whether such a process is also involved in BR signaling is not un­derstood.Here,we demonstrate that protein fame­sylation is involved in mediating BR signaling in Arabidopsis.A loss-of-function mutant of EN HANCED RESPONSE TO ABA 1(iERA1).encoding a(3 subunit of the protein famesyl transferase hoi oenzyme,can alter the BL sensitivity of bak1~4 from a reduced to a hypersensitive level,era 7 can partially rescue the BR defective phenotype of a hetero zygous mutant of bin2-1,a gain-of function mutant of BIN2 which encodes a negative regulator in the BR signaling.Our genetic and biochemical analyses re­vealed that ERA1 plays a significant role in regulating the protein stability of BES1.