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First published online 31 January 2007
doi: 10.1242/dev.02792
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1 University of Köln, Botanical Institute III, Gyrhofstr. 15, 50931
Köln, Germany.
2 The Integrative Cell Biology Laboratory, School of Biological and Biomedical
Sciences, University of Durham, South Road, Durham DH1 3LE, UK.
3 School of Biosciences, Division of Molecular Cell Biology, University of
Birmingham, Birmingham B15 2TT, UK.
Author for correspondence (e-mail:
martin.huelskamp{at}uni-koeln.de)
Accepted 19 December 2006
The actin-nucleating ARP2-ARP3 complex controls cell shape in plants in many different cell types. Its activity is controlled by a multimeric complex containing BRK1 (also known as HSPC300), NAP1, SRA1, ABI and SCAR/WAVE. In this study, we focus on the function of the five putative SCAR homologues in Arabidopsis and we provide biochemical evidence that AtSCAR2 can activate the ARP2-ARP3 complex in vitro. Among the single mutants, mutations in only AtSCAR2 result in a subtle or weak phenotype similar to ARP2, ARP3 and other `distorted' mutants. Double-mutant analysis revealed a redundancy with AtSCAR4. Systematic application of the yeast two-hybrid system and Bimolecular Fluorescence Complementation (BiFC) revealed a complex protein-interaction network between the ARP2-ARP3 complex and its genetically defined regulators. In addition to protein interactions known in other systems, we identified several new interactions, suggesting that SPIKE1 may be an integral component of the SCAR/WAVE complex and that SCAR proteins in plants might act as direct effectors of ROP GTPases.
Key words: ARP2-ARP3, Actin, SCAR/WAVE, Trichomes, Arabidopsis
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