Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 427649
Title SPEECHLESS integrates brassinosteroid and stomata signalling pathways.
Author(s) Gudesblat, G.E.; Schneider-Pizon, J.; Betti, C.; Mayerhofer, J.; Vanhoutte, I.; Dongen, W.M.A.M. van; Boeren, J.A.; Zhiponova, M.; Vries, S.C. de; Jonak, C.; Russinova, E.T.
Source Nature Cell Biology 14 (2012)5. - ISSN 1465-7392 - p. 548 - 554.
Department(s) Biochemistry
Publication type Refereed Article in a scientific journal
Publication year 2012
Keyword(s) asymmetric cell-division - arabidopsis-thaliana - receptor kinases - phosphorylation sites - transcription factors - secretory peptide - gsk3-like kinases - differentiation - identification - biosynthesis
Abstract Stomatal formation is regulated by multiple developmental and environmental signals, but how these signals are integrated to control this process is not fully understood1. In Arabidopsis thaliana, the basic helix-loop-helix transcription factor SPEECHLESS (SPCH) regulates the entry, amplifying and spacing divisions that occur during stomatal lineage development. SPCH activity is negatively regulated by mitogen-activated protein kinase (MAPK)-mediated phosphorylation2. Here, we show that in addition to MAPKs, SPCH activity is also modulated by brassinosteroid (BR) signalling. The GSK3/SHAGGY-like kinase BIN2 (BR INSENSITIVE2) phosphorylates residues overlapping those targeted by the MAPKs, as well as four residues in the amino-terminal region of the protein outside the MAPK target domain. These phosphorylation events antagonize SPCH activity and limit epidermal cell proliferation. Conversely, inhibition of BIN2 activity in vivo stabilizes SPCH and triggers excessive stomatal and non-stomatal cell formation. We demonstrate that through phosphorylation inputs from both MAPKs and BIN2, SPCH serves as an integration node for stomata and BR signalling pathways to control stomatal development in Arabidopsis
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