What causes cell movement
Hooked: This is how cells move their nucleus
Photo: Stefan Kutscheidt / Oliver Fackler
Researchers at Heidelberg University Hospital publish in Nature Cell Biology: Protein anchor connects cell nucleus with conveyor belt
When a cell moves, it must also transport its internal structures, including the cell nucleus, which contains and protects the genetic information, in the direction of movement. How she does this is almost unknown. Researchers from Heidelberg and New York have now identified a protein that plays an important role in this transport process. Together with another protein, it anchors the relatively bulky core to the so-called actin filaments, which function like a conveyor belt when cells move. They pull the nucleus with them. The knowledge of this movement mechanism could be useful for cancer medicine, e.g. to better understand how tumors form settlements or grow into healthy tissue. The research results have been published in the journal "Nature Cell Biology".
Mechanism of cell nucleus movement is still largely unknown
Mobility is important for most cells in the body: this is the only way for them to take the right place in the respective tissue - for example during the development of an organ in the embryo or during immune reactions to ward off infections. The white blood cells of the immune system are the performers of movement among the cells. When there is an inflammatory reaction, they meander between the cells of a tissue in order to fight off foreign bodies, viruses or bacteria. It is important to move the cell nucleus and other structures in an organized manner. Otherwise these would collect like a block at the rear end of the cell and significantly impede progress in the narrow spaces between the cells. "It has only been known for a few years that the cell nucleus actively moves during this process," says Professor Dr. Oliver T. Fackler, Head of the Integrative Virology Section of the Department of Infectious Diseases at Heidelberg University Hospital. "So far, very little is known about the machinery behind it."
The new results shed some light on the darkness: two proteins, the already known Nesprin-2 Giant and FHOD1, which has not been associated with these processes, hook the cell nucleus onto the moving actin filaments. These cable-like structures form the skeleton of the cells, stabilize their shape and shift in the sliding direction as they move. "The movement of the cell nucleus works like a cable car, in which the wagon is coupled to a circulating cable," explains Fackler. If FHOD1 is missing, the remaining gripper arm made of Nesprin-2 Giant is too weak, the cell nucleus remains lying and cell movement is impaired.
Defective protein could contribute to congenital heart disease
The scientist and his colleagues assume that congenital defects in this important mechanism can lead to organ disorders. In certain congenital heart diseases, for example, the function of the heart muscle is impaired because the nuclei are not correctly positioned within the muscle cell network. "This must first be examined more closely, but we suspect that changes in the FHOD1 protein could be the cause of the disease in some patients," says Fackler.
The protein may also play a role in the development of cancer, since the settlement of tumor cells in particular is directly dependent on the mobility of the cells. As a member of a group of very similar proteins, the formins, it is to a certain extent biased: All 15 human formins known to date are known to be involved in the development of cancer and a role of FHOD1 in tumor cell movement has already been described. "As a next step, we are therefore currently investigating whether the role of FHOD1 in tumor cell movement can be traced back to the mechanism we discovered for regulating nuclear movement. This may open up opportunities to hinder the mobility and aggressive spread of cancer cells," says the Molecular biologist.
FHOD1 interaction with nesprin-2G mediates TAN line formation and nuclear movement: Stefan Kutscheidt, Ruijun Zhu, Susumu Antoku, GantW. Luxton, Igor Stagljar, Oliver T. Fackler and Gregg G. Gundersen. Nature Cell Biology, Volume: 16, Pages: 708-715, Year published: (2014) DOI: doi: 10.1038 / ncb2981
Further information on the Internet:
Research group Fackler, Department of Infectious Diseases at Heidelberg University Hospital (page in English)
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