No.7/August 15, 2002
E m b a r g o e d until: Thursday, August 15, 2002, 3 .00 pm
Diversin - MDC researchers discover a new gene
A regulator of a critical signal molecule in cells
A gene which plays a key role in the smooth “signal trafficking”
between cells and, hence, in the development of a healthy fully functional
organism, has been identified by Prof. Walter Birchmeier and his group at the
Max Delbrück Center for Molecular Medicine (MDC), Berlin-Buch, a National
Research Centre of the Helmholtz-Association. The gene is associated with a
highly complex signaling system, the so-called Wnt pathway. It extends from the
cell surface into the cell nucleus. If signal transmission via this information
channel is disrupted, this can lead to construction errors and tumors. Thomas
Schwarz-Romond and Prof. Birchmeier have been able to show that the gene
triggers the breakdown of beta-Catenin, an important member of this signal
chain, thereby preventing it from operating at the wrong time in the cell
nucleus and causing local damage. They have also been able to elucidate the
individual activation steps (phosphorylation) of this key breakdown process.
The researchers have named this gene “Diversin” since it most likely has a
number of diverse functions in the body. Their study has just been published in the research journal “Genes and
Development”* (Vol. 16, No. 16, August 15, 2002; http://www.genesdev.org).
In humans and animals, cells are linked to each other by what are called adhesion molecules. These molecules do not only confine cells to their cell groups but cells are also able to exchange information via these molecules. Other molecules which, for example, produce growth or differentiation factors, and hormones and their receptors, also exchange information between cells. Included in this group of adhesion and signaling molecules that researchers have discovered in recent years is beta-Catenin (Latin:catena - chain). Prof. Birchmeier and his colleagues have been carrying out detailed investigations of this molecule since 1992.
It has been shown that beta-Catenin is altered (mutated) if developmental errors occur as well as by a number of different tumors. Thus, for example, beta-Catenin undergoes mutation in half of all cases of liver cancer, and in ten percent of cases of colon cancer. Therefore, Prof. Birchmeier and his group want to investigate if the Diversin gene is also defective in tumor cells. It remains to be seen, if, in the future, it will be possible to predict whether a tumor will form metastases or not.
*The
ankyrin repeat protein Diversin recruits Casein kinase I to the
-catenin degradation complex and acts in both canonical Wnt and Wnt/JNK
signaling Thomas Schwarz-Romond, Christian Asbrand,
Jeroen Bakkers*, Michael Kühl†, Hans-Joerg Schaeffer, Jörg Huelsken, Jürgen
Behrens‡, Matthias Hammerschmidt*, and Walter Birchmeier Max Delbrueck Center for Molecular Medicine,
Robert-Roessle-Strasse 10, D-13092 Berlin, Germany, *Max Planck Institute for
Immunobiology, Stübeweg51, D-79108 Freiburg, Germany, †University of Ulm, Dep.
of Biochemistry, Albert-Einstein-Allee 11, D-89081 Ulm, Germany, and
‡University of Erlangen, Nikolaus-Fiebiger-Center, Glückstr.6, D-91054
Erlangen, Germany
Barbara Bachtler
Press and Public Affairs
Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch
Robert-Rössle-Straße 10; 13125 Berlin; Germany
Phone: +49 (0) 30 94 06 - 38 96
Fax: +49 (0) 30 94 06 - 38 33
e-mail: presse@mdc-berlin.de
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