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  • The EMBO Journal (2009) 28, 1157 - 1169
  • doi:10.1038/emboj.2009.58

Published online: 5 March 2009

Profilin 1 is required for abscission during late cytokinesis of chondrocytes

Ralph T Böttcher1, Sebastian Wiesner1, Attila Braun1, Reiner Wimmer1, Alejandro Berna2, Nadav Elad3, Ohad Medalia3, Alexander Pfeifer4, Attila Aszódi1, Mercedes Costell2 and Reinhard Fässler1

  1. Department of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany
  2. Department of Biochemistry and Molecular Biology, University of Valencia, Valencia, Spain
  3. Department of Life Sciences and The National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva, Israel
  4. Institute for Pharmacology and Toxicology, University of Bonn, Bonn, Germany

Correspondence to:

Reinhard Fässler, Department of Molecular Medicine, Max Planck Institute of Biochemistry, Am Klopferspitz 18, Martinsried 82152, Germany. Tel.: +49 89 8578 2424; Fax: +49 89 8578 2422; E-mail: faessler@biochem.mpg.de

Received 5 December 2008; Accepted 11 February 2009

Profilins are key factors for dynamic rearrangements of the actin cytoskeleton. However, the functions of profilins in differentiated mammalian cells are uncertain because profilin deficiency is early embryonic lethal for higher eukaryotes. To examine profilin function in chondrocytes, we disrupted the profilin 1 gene in cartilage (Col2pfn1). Homozygous Col2pfn1 mice develop progressive chondrodysplasia caused by disorganization of the growth plate and defective chondrocyte cytokinesis, indicated by the appearance of binucleated cells. Surprisingly, Col2pfn1 chondrocytes assemble and contract actomyosin rings normally during cell division; however, they display defects during late cytokinesis as they frequently fail to complete abscission due to their inability to develop strong traction forces. This reduced force generation results from an impaired formation of lamellipodia, focal adhesions and stress fibres, which in part could be linked to an impaired mDia1-mediated actin filament elongation. Neither an actin nor a poly-proline binding-deficient profilin 1 is able to rescue the defects. Taken together, our results demonstrate that profilin 1 is not required for actomyosin ring formation in dividing chondrocytes but necessary to generate sufficient force for abscission during late cytokinesis.

  • Keywords:

    • chondrocytes,
    • cytokinesis,
    • knockout mice,
    • profilin,
    • traction force