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Molecular and Cellular Biology, April 2009, p. 1735-1748, Vol. 29, No. 7
0270-7306/09/$08.00+0     doi:10.1128/MCB.01483-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Regulation of Cell-Cell Adhesion by Abi/Diaphanous Complexes{triangledown}

Jae Ryun Ryu, Asier Echarri,{dagger} Ran Li, and Ann Marie Pendergast*

Department of Pharmacology and Cancer Biology, Duke University Medical Center, Box 3813, Durham, North Carolina 27710

Received 22 September 2008/ Returned for modification 29 October 2008/ Accepted 6 January 2009

Actin polymerization provides the driving force for the formation of cell-cell junctions and is mediated by two types of actin nucleators, Arp2/3 and formins. Proteins required for coordinately linking cadherin-mediated adhesion to Arp2/3-dependent versus formin-dependent nucleation have yet to be defined. Here we show a role for Abi, the Abi-binding partner Nap1, and the Nap1-binding protein Sra1 in the regulation of cadherin-dependent adhesion. We found that Abi, which is known to interact with Wave, leading to activation of the Arp2/3 complex, is also capable of interacting with the Diaphanous (Dia)-related formins in the absence of Wave. Knockdown of Abi, Nap1, Sra1, or Dia markedly inhibited cell-cell junctions, whereas knockdown of Wave or Arp2/3 produced mild and transient phenotypes. Dia and Abi colocalized with β-catenin at cell-cell junctions. Further, Dia and Wave bound to overlapping sites on Abi1, and Wave competed with Dia for Abi1 binding. Notably, an active Dia1 C-terminal fragment that localizes to cell-cell junctions rescued the abnormal junctions induced by depletion of Abi or Nap1 in epithelial cells. These findings uncover a novel link between cadherin-mediated adhesion and the regulation of actin dynamics through the requirement for an Abi/Dia complex for the formation and stability of cell-cell junctions.

* Corresponding author. Mailing address: Department of Pharmacology and Cancer Biology, Duke University Medical Center, Box 3813, Durham, NC 27710. Phone: (919) 681-8086. Fax: (919) 681-7148. E-mail: pende014{at}mc.duke.edu

{triangledown} Published ahead of print on 21 January 2009.

{dagger} Present address: Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid 28029, Spain.

Molecular and Cellular Biology, April 2009, p. 1735-1748, Vol. 29, No. 7
0270-7306/09/$08.00+0     doi:10.1128/MCB.01483-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Nowak, S. J., Nahirney, P. C., Hadjantonakis, A.-K., Baylies, M. K. (2009). Nap1-mediated actin remodeling is essential for mammalian myoblast fusion. J. Cell Sci. 122: 3282-3293 [Abstract] [Full Text]  
  • Lin, T.-Y., Huang, C.-H., Kao, H.-H., Liou, G.-G., Yeh, S.-R., Cheng, C.-M., Chen, M.-H., Pan, R.-L., Juang, J.-L. (2009). Abi plays an opposing role to Abl in Drosophila axonogenesis and synaptogenesis. Development 136: 3099-3107 [Abstract] [Full Text]  


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