Brassinosteroids regulate stomatal development through inhibition of BIN2- mediated phosphorylation of SPEECHLESS

GUSTAVO E. GUDESBLAT; JOANNA SCHNEIDER-PIZON; CAMILLA BETTI; JULIANE MAYERHOFER; ISABELLE VANHOUTTE; WALTER VAN DONGEN; SJEF BOEREN; MIROSLAVA ZHIPONOVA; SACCO DE VRIES; CLAUDIA JONAK; EUGENIA RUSSINOVA

Manchester

Congreso; 29th New Phytologist Symposium Stomata 2012; 2012

New Phytologist

Stomatal formation is regulated by multiple developmental and environmental signals, but how these signals are integrated to control this process is not fully understood. The activity and stability of the transcription factor SPEECHLESS, essential for stomatal development, is negatively by ERECTA family and TMM receptors through MAP kinase (MAPK)-mediated phosphorylation. We have found that SPCH activity is also modulated by the GSK3/SHAGGY-like kinase BIN2, which functions as a negative regulator of brassinosteroid signaling. BIN2 phosphorylates SPEECHLESS in residues overlapping those targeted by MAPKs, as well as in four residues in the N-terminal region of the protein outside the MAPK target domain. These phosphorylation events antagonise SPCH activity and limit epidermal cell proliferation. Conversely, brassinosteroid-mediated inhibition of BIN2 activity stabilizes SPCH and triggers excessive stomata and nonstomatal cell formation. Thus, SPEECHLESS serves as an integration node for the ERECTA/TMM and BR signalling pathways to control stomatal and epidermal development.