RhoA is dispensable for skin development, but crucial for contraction and directed migration of keratinocytes

RhoA is a small GTPase shown to be crucial for cytokinesis, stress fiber formation, and epithelial cell–cell contacts. Analyzing mice with a keratinocyte-restricted deletion of the RhoA gene, we find that RhoA is not required for skin development and maintenance but has specific functions in vitro.

[1]  R. Karlsson,et al.  Rho GTPase function in tumorigenesis. , 2009, Biochimica et biophysica acta.

[2]  S. Lim,et al.  A FAK-p120RasGAP-p190RhoGAP complex regulates polarity in migrating cells , 2009, Journal of Cell Science.

[3]  K. Rottner,et al.  Cortactin promotes migration and platelet-derived growth factor-induced actin reorganization by signaling to Rho-GTPases. , 2009, Molecular biology of the cell.

[4]  S. Lim,et al.  A FAK-p120RasGAP-p190RhoGAP complex regulates polarity in migrating cells , 2009, Journal of Cell Science.

[5]  R. Karlsson,et al.  Cdc42 is crucial for the maturation of primordial cell junctions in keratinocytes independent of Rac1. , 2009, Experimental cell research.

[6]  M. Glogauer,et al.  A common cofilin activity cycle in invasive tumor cells and inflammatory cells , 2009, Journal of Cell Science.

[7]  S. Narumiya,et al.  Rho signaling, ROCK and mDia1, in transformation, metastasis and invasion , 2009, Cancer and Metastasis Reviews.

[8]  Guojun Sheng,et al.  RhoA and microtubule dynamics control cell–basement membrane interaction in EMT during gastrulation , 2008, Nature Cell Biology.

[9]  K. Rottner,et al.  Differentially oriented populations of actin filaments generated in lamellipodia collaborate in pushing and pausing at the cell front , 2008, Nature Cell Biology.

[10]  Klemens Rottner,et al.  Arp2/3 complex interactions and actin network turnover in lamellipodia , 2008, The EMBO journal.

[11]  D. Soll,et al.  Cofilin determines the migration behavior and turning frequency of metastatic cancer cells , 2007, The Journal of cell biology.

[12]  H. Mellor,et al.  Actin stress fibres , 2007, Journal of Cell Science.

[13]  C. Brakebusch,et al.  Cdc42 is crucial for the establishment of epithelial polarity during early mammalian development , 2007, Developmental dynamics : an official publication of the American Association of Anatomists.

[14]  K. Eisenmann,et al.  Myeloproliferative defects following targeting of the Drf1 gene encoding the mammalian diaphanous related formin mDia1. , 2007, Cancer research.

[15]  W. Nelson,et al.  Localized zones of Rho and Rac activities drive initiation and expansion of epithelial cell–cell adhesion , 2007, The Journal of cell biology.

[16]  X. Bustelo,et al.  GTP‐binding proteins of the Rho/Rac family: regulation, effectors and functions in vivo , 2007, BioEssays : news and reviews in molecular, cellular and developmental biology.

[17]  J. Iwasa,et al.  Spatial and Temporal Relationships between Actin-Filament Nucleation, Capping, and Disassembly , 2007, Current Biology.

[18]  D. Zillikens,et al.  Inhibition of Rho A activity causes pemphigus skin blistering , 2006, The Journal of cell biology.

[19]  F. Quondamatteo,et al.  Rac1 Is Crucial for Hair Follicle Integrity but Is Not Essential for Maintenance of the Epidermis , 2006, Molecular and Cellular Biology.

[20]  K. Nozaki,et al.  The Rho-mDia1 Pathway Regulates Cell Polarity and Focal Adhesion Turnover in Migrating Cells through Mobilizing Apc and c-Src , 2006, Molecular and Cellular Biology.

[21]  F. Quondamatteo,et al.  Cdc42 controls progenitor cell differentiation and beta-catenin turnover in skin. , 2006, Genes & development.

[22]  S. Offermanns,et al.  Gα12/13 Is Essential for Directed Cell Migration and Localized Rho-Dia1 Function* , 2005, Journal of Biological Chemistry.

[23]  M. Glotzer,et al.  Cytokinesis: welcome to the Rho zone. , 2005, Trends in cell biology.

[24]  Klemens Rottner,et al.  Cdc42 is not essential for filopodium formation, directed migration, cell polarization, and mitosis in fibroblastoid cells. , 2005, Molecular biology of the cell.

[25]  T. Mak,et al.  RhoC is dispensable for embryogenesis and tumor initiation but essential for metastasis. , 2005, Genes & development.

[26]  Hiroko Oshima,et al.  ROCK-I regulates closure of the eyelids and ventral body wall by inducing assembly of actomyosin bundles , 2005, The Journal of cell biology.

[27]  P. Lappalainen,et al.  Actin-depolymerizing factor and cofilin-1 play overlapping roles in promoting rapid F-actin depolymerization in mammalian nonmuscle cells. , 2004, Molecular biology of the cell.

[28]  A. Ridley,et al.  Why three Rho proteins? RhoA, RhoB, RhoC, and cell motility. , 2004, Experimental cell research.

[29]  M. Vidal,et al.  A keratin K5Cre transgenic line appropriate for tissue‐specific or generalized cre‐mediated recombination , 2004, Genesis.

[30]  K. Aktories,et al.  The Yersinia pseudotuberculosis Cytotoxic Necrotizing Factor (CNFY) Selectively Activates RhoA* , 2004, Journal of Biological Chemistry.

[31]  Fumio Matsumura,et al.  Distinct roles of MLCK and ROCK in the regulation of membrane protrusions and focal adhesion dynamics during cell migration of fibroblasts , 2004, The Journal of cell biology.

[32]  J. Saras,et al.  Rho GTPases have diverse effects on the organization of the actin filament system. , 2004, The Biochemical journal.

[33]  Yue Zhang,et al.  Regulation of Cell Polarity and Protrusion Formation by Targeting RhoA for Degradation , 2003, Science.

[34]  G. Borisy,et al.  Cell Migration: Integrating Signals from Front to Back , 2003, Science.

[35]  S. Narumiya,et al.  Targeted Disruption of the Mouse Rho-Associated Kinase 2 Gene Results in Intrauterine Growth Retardation and Fetal Death , 2003, Molecular and Cellular Biology.

[36]  Anne J. Ridley,et al.  Shear stress–induced endothelial cell polarization is mediated by Rho and Rac but not Cdc42 or PI 3-kinases , 2003, The Journal of cell biology.

[37]  K. Burridge,et al.  RhoA and ROCK Promote Migration by Limiting Membrane Protrusions* , 2003, The Journal of Biological Chemistry.

[38]  L. Machesky,et al.  Microtubule involvement in NIH 3T3 Golgi and MTOC polarity establishment , 2003, Journal of Cell Science.

[39]  Benjamin Geiger,et al.  How do microtubules guide migrating cells? , 2002, Nature Reviews Molecular Cell Biology.

[40]  G. Prendergast,et al.  RhoB Is Dispensable for Mouse Development, but It Modifies Susceptibility to Tumor Formation as Well as Cell Adhesion and Growth Factor Signaling in Transformed Cells , 2001, Molecular and Cellular Biology.

[41]  W. Arthur,et al.  RhoA inactivation by p190RhoGAP regulates cell spreading and migration by promoting membrane protrusion and polarity. , 2001, Molecular biology of the cell.

[42]  John G. Collard,et al.  Oncogenic Ras Downregulates Rac Activity, Which Leads to Increased Rho Activity and Epithelial–Mesenchymal Transition , 2000, The Journal of cell biology.

[43]  K. Rottner,et al.  Interplay between Rac and Rho in the control of substrate contact dynamics , 1999, Current Biology.

[44]  Alan Hall,et al.  Rho GTPases Control Polarity, Protrusion, and Adhesion during Cell Movement , 1999, The Journal of cell biology.

[45]  R. Fässler,et al.  Integrin gene targeting. , 1999, Methods in molecular biology.

[46]  A. Hall,et al.  The Small GTPases Rho and Rac Are Required for the Establishment of Cadherin-dependent Cell–Cell Contacts , 1997, The Journal of cell biology.

[47]  W Singer,et al.  Neurophysiology: The changing face of inhibition , 1996, Current Biology.