Multiple mechanisms modulate brassinosteroid signaling

This review focuses on recent advances in our understanding of cellular dynamics of intracellular signaling components, function of BRI1-ASSOCIATED RECEPTOR KINASE 1 receptor kinase in disease resistance, and mechanisms of transcriptional regulation by phosphorylation

Joshua M Gendron; Zhi-Yong Wang

2007

Scholarcy highlights

  • About a decade ago, the discovery of brassinosteroid-deficient Arabidopsis mutants established brassinosteroids as an essential plant hormone and stimulated extensive studies of BR signal transduction
  • BR activation of the receptor kinases leads to dephosphorylation of BRASSINAZOLE-RESISTANT 1 and BRASSINZAZOLE RESISTANT 2/BES1, possibly by inhibiting BRASSINOSTEROID-INSENSITIVE 2 or activating bri1 SUPPRESSOR 1 through unknown mechanisms
  • This review focuses on recent advances in our understanding of cellular dynamics of intracellular signaling components, function of BRI1-ASSOCIATED RECEPTOR KINASE 1 receptor kinase in disease resistance, and mechanisms of transcriptional regulation by phosphorylation
  • In contrast to endosomal BRASSINOSTEROIDINSENSITIVE 1, a mutant BRI1 receptor retained in the endoplasmic reticulum cannot activate BR signaling, but it is functional when localized on the PM due to mutation of a component of the ER quality control system identified as the bri1-9 suppressor ebs1
  • The only major gap in the current BR signaling pathway is between the receptor kinases and BIN2 or BSU1
  • A link has been found between BR regulation of FLC expression and flowering, a role for BR in organ boundary formation has been revealed by studies of bzr1-1D, and cell type-specific actions of BR, such as epidermal control of plant growth, have been recognized
  • More exciting discoveries will be made in the decade

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