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 445909
Title A mathematical model for the co-receptors SERK1 and SERK3 in BRI1 mediated signaling
Author(s) Esse, G.W. van; Mourik, S. van; Albrecht, C.; Leeuwen, J.; Vries, S.C. de
Source Plant Physiology 163 (2013)3. - ISSN 0032-0889 - p. 1472 - 1481.
Department(s) Biochemistry
Mathematical and Statistical Methods - Biometris
Publication type Refereed Article in a scientific journal
Publication year 2013
Keyword(s) innate immunity - arabidopsis-thaliana - tyrosine kinases - plant-growth - bri1 - bak1 - pathways - autophosphorylation - transduction - endocytosis
Abstract Brassinosteroids (BRs) are key regulators in plant growth and development. The main BR perceiving receptor in Arabidopsis is Brassinosteroid Insensitive 1 (BRI1). Seedling root growth and hypocotyl elongation can be accurately predicted using a model for BRI1 receptor activity. Genetic evidence shows that non ligand-binding co-receptors of the Somatic Embryogenesis Receptor-like Kinase (SERK) family are essential for BRI1 signal transduction. A relatively simple biochemical model based on the properties of SERK loss-of-function alleles explains complex physiological responses of the BRI1 mediated BR pathway. The model uses BRI1-BR occupancy as the central estimated parameter and includes BRI1-SERK interaction based on mass action kinetics and accurately describes wild type root growth and hypocotyl elongation. Simulation studies suggest that the SERK co-receptors primarily act to increase the magnitude of the BRI1 signal. The model predicts that only a small number of active BRI1-SERK complexes are required to carry out BR signaling at physiological ligand concentration. Finally, when calibrated with single mutants, the model predicts that roots of the serk1serk3 double mutant are almost completely BL-insensitive, while the double mutant hypocotyls remain sensitive. This points to residual BRI1 signaling or to a different co-receptor requirement in shoots.
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