scholarly journals BSKs Mediate Signal Transduction from the Receptor Kinase BRI1 in Arabidopsis

Science ◽  
2008 ◽  
Vol 321 (5888) ◽  
pp. 557-560 ◽  
Author(s):  
W. Tang ◽  
T.-W. Kim ◽  
J. A. Oses-Prieto ◽  
Y. Sun ◽  
Z. Deng ◽  
...  
1994 ◽  
Vol 14 (10) ◽  
pp. 6715-6726 ◽  
Author(s):  
A K Arvidsson ◽  
E Rupp ◽  
E Nånberg ◽  
J Downward ◽  
L Rönnstrand ◽  
...  

Ligand stimulation of the platelet-derived growth factor (PDGF) beta-receptor leads to activation of its intrinsic tyrosine kinase and autophosphorylation of the intracellular part of the receptor. The autophosphorylated tyrosine residues mediate interactions with downstream signal transduction molecules and thereby initiate different signalling pathways. A pathway leading to activation of the GTP-binding protein Ras involves the adaptor molecule GRB2. Here we show that Tyr-716, a novel autophosphorylation site in the PDGF beta-receptor kinase insert, mediates direct binding of GRB2 in vitro and in vivo. In a panel of mutant PDGF beta-receptors, in which Tyr-716 and the previously known autophosphorylation sites were individually mutated, only PDGFR beta Y716F failed to bind GRB2. Furthermore, a synthetic phosphorylated peptide containing Tyr-716 bound GRB2, and this peptide specifically interrupted the interaction between GRB2 and the wild-type receptor. In addition, the Y716(P) peptide significantly decreased the amount of GTP bound to Ras in response to PDGF in permeabilized fibroblasts as well as in porcine aortic endothelial cells expressing transfected PDGF beta-receptors. The mutant PDGFR beta Y716F still mediated activation of mitogen-activated protein kinases and an increased DNA synthesis in response to PDGF, indicating that multiple signal transduction pathways transduce mitogenic signals from the activated PDGF beta-receptor.


2006 ◽  
Vol 26 (20) ◽  
pp. 7550-7560 ◽  
Author(s):  
Alison R. Meloni ◽  
Gregory B. Fralish ◽  
Patrick Kelly ◽  
Ali Salahpour ◽  
James K. Chen ◽  
...  

ABSTRACT Deregulation of the Sonic hedgehog pathway has been implicated in an increasing number of human cancers. In this pathway, the seven-transmembrane (7TM) signaling protein Smoothened regulates cellular proliferation and differentiation through activation of the transcription factor Gli. The activity of mammalian Smoothened is controlled by three different hedgehog proteins, Indian, Desert, and Sonic hedgehog, through their interaction with the Smoothened inhibitor Patched. However, the mechanisms of signal transduction from Smoothened are poorly understood. We show that a kinase which regulates signaling by many “conventional” 7TM G-protein-coupled receptors, G protein-coupled receptor kinase 2 (GRK2), participates in Smoothened signaling. Expression of GRK2, but not catalytically inactive GRK2, synergizes with active Smoothened to mediate Gli-dependent transcription. Moreover, knockdown of endogenous GRK2 by short hairpin RNA (shRNA) significantly reduces signaling in response to the Smoothened agonist SAG and also inhibits signaling induced by an oncogenic Smoothened mutant, Smo M2. We find that GRK2 promotes the association between active Smoothened and β-arrestin 2. Indeed, Gli-dependent signaling, mediated by coexpression of Smoothened and GRK2, is diminished by β-arrestin 2 knockdown with shRNA. Together, these data suggest that GRK2 plays a positive role in Smoothened signaling, at least in part, through the promotion of an association between β-arrestin 2 and Smoothened.


2010 ◽  
Author(s):  
Fabiola Cecchi ◽  
Deborah Pajalunga ◽  
Brian McNeil ◽  
Daniel Rabe ◽  
Andrew Fowler ◽  
...  

2011 ◽  
Vol 43 (4) ◽  
pp. 561-571 ◽  
Author(s):  
Tae-Wuk Kim ◽  
Shenheng Guan ◽  
Alma L. Burlingame ◽  
Zhi-Yong Wang

2008 ◽  
Vol 21 (10) ◽  
pp. 1337-1348 ◽  
Author(s):  
Mark Kinkema ◽  
Peter M. Gresshoff

The Glycine max nodule autoregulation receptor kinase (GmNARK) plays a central role in the systemic signal transduction pathway controlling nodulation in soybean. We used transcriptional profiling to identify potential downstream signals of this receptor kinase. These studies revealed that GmNARK-mediated signaling controls the expression of genes involved in the jasmonic acid (JA) pathway. Genes encoding the key enzymes controlling JA biosynthesis as well as JA-response genes were regulated systemically but not locally by root inoculation with Bradyrhizobium japonicum. This systemic regulation was abolished in Gmnark mutant plants, indicating that their expression was specifically controlled by signaling events associated with this receptor kinase. Foliar application of a JA biosynthesis inhibitor significantly reduced nodulation specifically in supernodulating mutant plants. These results indicate that the receptor-mediated regulation of JA signaling plays an important role in the AON signal transduction pathway. A second class of genes was identified that were controlled by GmNARK in a rhizobia-independent manner. These candidates provide insight on additional, nonsymbiotic signaling pathways that are likely regulated by GmNARK, such as those involved in root growth and defense. The discovery of downstream components of the GmNARK receptor kinase advances our understanding of the systemic control of nodule development and its association with other signaling networks.


2019 ◽  
Author(s):  
Ajeet Chaudhary ◽  
Xia Chen ◽  
Jin Gao ◽  
Barbara Leśniewska ◽  
Richard Hammerl ◽  
...  

AbstractPlant cells are encased in a semi-rigid cell wall of complex build. As a consequence, cell wall remodeling is essential for the control of growth and development as well as the regulation of abiotic and biotic stress responses. Plant cells actively sense physico-chemical changes in the cell wall and initiate corresponding cellular responses. However, the underlying cell wall monitoring mechanisms remain poorly understood. In Arabidopsis the atypical receptor kinase STRUBBELIG (SUB) mediates tissue morphogenesis. Here, we show that SUB-mediated signal transduction also regulates the cellular response to a reduction in the biosynthesis of cellulose, a central carbohydrate component of the cell wall. SUB signaling affects early increase of intracellular reactive oxygen species, stress gene induction as well as ectopic lignin and callose accumulation upon exogenous application of the cellulose biosynthesis inhibitor isoxaben. Moreover, our data reveal that SUB signaling is required for maintaining cell size and shape of root epidermal cells and the recovery of root growth after transient exposure to isoxaben. SUB is also required for root growth arrest in mutants with defective cellulose biosynthesis. Genetic data further indicate that SUB controls the isoxaben-induced cell wall stress response independently from other known receptor kinase genes mediating this response, such as THESEUS1 or MIK2. We propose that SUB functions in a least two distinct biological processes: the control of tissue morphogenesis and the response to cell wall damage. Taken together, our results reveal a novel signal transduction pathway that contributes to the molecular framework underlying cell wall integrity signaling.Author SummaryPlant cells are encapsulated by a semi-rigid and biochemically complex cell wall. This particular feature has consequences for multiple biologically important processes, such as cell and organ growth or various stress responses. For a plant cell to grow the cell wall has to be modified to allow cell expansion, which is driven by outward-directed turgor pressure generated inside the cell. In return, changes in cell wall architecture need to be monitored by individual cells, and to be coordinated across cells in a growing tissue, for an organ to attain its regular size and shape. Cell wall surveillance also comes also into play in the reaction against certain stresses, including for example infection by plant pathogens, many of which break through the cell wall during infection, thereby generating wall-derived factors that can induce defense responses. There is only limited knowledge regarding the molecular system that monitors the composition and status of the cell wall. Here we provide further insight into the mechanism. We show that the cell surface receptor STRUBBELIG, previously known to control organ development in Arabidopsis, also promotes the cell’s response to reduced amounts of cellulose, a main component of the cell wall.


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