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Published 31 January 2005. doi:10.1083/jcb.200409078
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 168, Number 3, 453-463
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Receptor tyrosine phosphatase–dependent cytoskeletal remodeling by the hedgehog-responsive gene MIM/BEG4



Rosa Gonzalez-Quevedo, Marina Shoffer, Lily Horng, and Anthony E. Oro

Program in Epithelial Biology, School of Medicine, Stanford University, Stanford, CA 94305

Correspondence to A.E. Oro: oro{at}cmgm.stanford.edu

During development, dynamic remodeling of the actin cytoskeleton allows the precise placement and morphology of tissues. Morphogens such as Sonic hedgehog (Shh) and local cues such as receptor protein tyrosine phosphatases (RPTPs) mediate this process, but how they regulate the cytoskeleton is poorly understood. We previously identified Basal cell carcinoma–enriched gene 4 (BEG4)/Missing in Metastasis (MIM), a Shh-inducible, Wiskott-Aldrich homology 2 domain–containing protein that potentiates Gli transcription (Callahan, C.A., T. Ofstad, L. Horng, J.K. Wang, H.H. Zhen, P.A. Coulombe, and A.E. Oro. 2004. Genes Dev. 18:2724–2729). Here, we show that endogenous MIM is induced in a patched1-dependent manner and regulates the actin cytoskeleton. MIM functions by bundling F-actin, a process that requires self-association but is independent of G-actin binding. Cytoskeletal remodeling requires an activation domain distinct from sequences required for bundling in vitro. This domain associates with RPTP{delta} and, in turn, enhances RPTP{delta} membrane localization. MIM-dependent cytoskeletal changes can be inhibited using a soluble RPTP{delta}-D2 domain. Our data suggest that the hedgehog-responsive gene MIM cooperates with RPTP to induce cytoskeletal changes.

Abbreviations used in this paper: MEF, mouse embryonic fibroblast; PIP2, phosphoinositol diphosphate; RPTP, receptor protein tyrosine phosphatase; Shh, Sonic hedgehog; TEM, transmission electron microscopy; WH2, Wiskott-Aldrich homology 2.


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