Research
Klaus Willecke, Dr. rer. nat.Senior Professor of Geneticsphone: +49 (0)2 28 / 73 - 6 27 43 |
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| 1960-1964 | Undergraduate education in Chemistry (Dipl.), Universities of Kiel and Munich, Germany |
| 1964-1968 | Doctorate (Dr. rer. nat.) in Biochemistry (Advisor: F. Lynen) Ludwig-Maximilians-University of Munich, Germany |
| 1968-1971 | Postdoctoral fellow with A.B. Pardee, Princeton University |
| 1971-1976 | Group leader, Institute of Genetics, University of Cologne, Germany |
| 1972 | Habilitation in Genetics at the University of Cologne |
| 3/73-6/74 | Postdoctoral training with F.H. Ruddle, Yale University, USA |
| 1977-1986 | Associate Professor, Institute of Cell Biology, University of Essen, Germany |
| 10/82-5/83 | Visiting Scientist with R. Schimke, Stanford University, USA |
| 1986-2008 | Professor of Genetics and Director of the Institute of Genetics,University of Bonn |
| 10/93-3/94 | Visiting Scientist with R. Jaenisch, Massachusetts Institute of Technology, Whitehead Institute, Cambridge, USA |
| 1/93-3/93 | Visiting Scientist with B. Sutor, University of Munich |
| since 10/2008 | Senior Professor at the University of Bonn |
Research Interests
The research in our group has been focused on the biological function of connexin genes which code for 20 different proteins in the mouse genome and are cell type specifically expressed with partial overlaps. Connexin proteins can form hemichannels in plasma membranes. In apposing cells, hemichannels can dock to each other and form intercellular gap junction channels. Using the full repertoire of transgenic genetics,
we have generated and characterized many targeted
mouse mutants carrying defects in connexin genes.
The phenotypic abnormalities of these mouse mutants vary from embryonic lethality to more or less severe genetic disorders, some of which (for example deafness, epidermal skin disorders and bone abnormalities) are very similar to the corresponding human genetic disorders. More recently we have introduced connexin point mutations from human patients into the mouse genome to search for protein interactions of connexins and provide mouse models for studying the mechanism of the corresponding human genetic disorder. Very recently
we have inactivated certain key steps in sphingolipid
biosynthesis in transgenic mice which we are analyzing, in order to understand the
biological functions of this still enigmatic class of lipids.
Key publications
Torres A, Wang F, Xu Q, Fujita T, Dobrowolski R, Willecke K, Takano T, Nedergaard M. Extracellular Ca²? acts as a mediator of communication from neurons to glia. Sci Signal. 2012 Jan 24;5(208):ra8.
Tress O, Maglione M, Zlomuzica A, May D, Dicke N, Degen J, Dere E, Kettenmann H, Hartmann D, Willecke K. Pathologic and phenotypic alterations in a mouse expressing a connexin47 missense mutation that causes Pelizaeus-Merzbacher-like disease in humans. PLoS Genet. 2011 Jul;7(7):e1002146. Epub 2011 Jul 7.
Dicke N, Pielensticker N, Degen J, Hecker J, Tress O, Bald T, Gellhaus A, Winterhager E, Willecke K. Peripheral lymphangiogenesis in mice depends on ectodermal connexin-26 (Gjb2). J Cell Sci. 2011;124(Pt 16):2806-15.
Schütz M, Auth T, Gehrt A, Bosen F, Körber I, Strenzke N, Moser T, Willecke K. The connexin26 S17F mouse mutant represents a model for the human hereditary keratitis-ichthyosis-deafness syndrome. Hum Mol Genet. 2011 Jan 1;20(1):28-39. Epub 2010 Oct 6.
Frank M, Eiberger B, Janssen-Bienhold U, de Sevilla Müller LP, Tjarks A, Kim JS, Maschke S, Dobrowolski R, Sasse P, Weiler R, Fleischmann BK, Willecke K. Neuronal connexin-36 can functionally replace connexin-45 in mouse retina but not in the developing heart. J Cell Sci. 2010 Oct 15;123(Pt 20):3605-15.
Imgrund S, Hartmann D, Farwanah H, Eckhardt M, Sandhoff R, Degen J, Gieselmann V, Sandhoff K, Willecke K. Adult ceramide synthase 2 (CERS2)-deficient mice exhibit myelin sheath defects, cerebellar degeneration, and hepatocarcinomas. J Biol Chem. 2009 Nov 27;284(48):33549-60. Epub 2009 Sep 30.