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Published 28 August 2006. doi:10.1083/jcb.200605006
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 174, Number 5, 701-713
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Article

 Autoinhibition regulates cellular localization and actin assembly activity of the diaphanous-related formins FRL{alpha} and mDia1

Abhinav Seth, Chinatsu Otomo, and Michael K. Rosen

Department of Biochemistry, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390

Correspondence to Michael K. Rosen: Michael.Rosen{at}UTSouthwestern.edu

Diaphanous-related formins (DRFs) are key regulators of actin cytoskeletal dynamics whose in vitro actin assembly activities are thought to be regulated by autoinhibition. However, the in vivo consequences of autoinhibition and the involvement of DRFs in specific biological processes are not well understood. In this study, we show that in the DRFs FRL{alpha} (formin-related gene in leukocytes {alpha}) and mouse diaphanous 1, autoinhibition regulates a novel membrane localization activity in vivo as well as actin assembly activity in vitro. In FRL{alpha}, the Rho family guanosine triphosphatase Cdc42 relieves the autoinhibition of both membrane localization and biochemical actin assembly activities. FRL{alpha} is required for efficient Fc-{gamma} receptor–mediated phagocytosis and is recruited to the phagocytic cup by Cdc42. These results suggest that mutual autoinhibition of biochemical activity and cellular localization may be a general regulatory principle for DRFs and demonstrate a novel role for formins in immune function.

Abbreviations used in this paper: Arp2/3, actin-related protein 2/3; CC, coiled coil; DAD, diaphanous autoregulatory domain; DD, dimerization domain; DIC, differential interference contrast; DID, diaphanous inhibitory domain; DRF, diaphanous-related formin; FH, formin homology; FRL, formin-related gene in leukocytes; GBD, GTPase-binding domain; GMPPNP, ß,{gamma}-imidoguanosine 5'-triphosphate; MBP, maltose-binding protein; mDia1, mouse diaphanous 1; WASP, Wiskott-Aldrich syndrome protein.


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