Weizmann Institute scientists have recently revealed part of the mechanism that enables the regeneration of cells in the peripheral nervous system
Nerve cells are wondrous creatures. From the cell body they grow several tree-like extensions (dendrites) and one special extension, called an axon, whose length may reach about one meter. The axon is the main tool that allows the cell to transmit messages. Thus, in fact, the axons serve as the body's neural communication lines. Unfortunately, the neural communication lines can be torn, disconnected, and become inoperable as a result of an injury, just like the electrical wires and telephone lines that can be severed on a stormy night. Weizmann Institute scientists recently revealed part of the mechanism that allows cells in the peripheral nervous system to regenerate after an injury, and to repair and return to normal operation the damaged axons (the peripheral nervous system includes all the nerves in the body, except for the brain and spinal cord, which together constitute the central nervous system). The discovered mechanism can contribute, for example, to the body's ability to renew the sense of touch after an injury.
Dr. Michael Fainzilber and research students Shlomit Hantz and Eran Perelson, from the Department of Biological Chemistry at the Weizmann Institute of Science, recently reported, in an article published in the scientific journal Neuron, that they discovered that a special protein, called importin-beta, which is usually found near the nucleus of the cell, and helps various proteins penetrate into The cell nucleus is also produced in damaged axons, in "suspicious" proximity to the injury site. Normally, importin-beta resides away from the axon, near the nucleus of the neuron. There it is a kind of "key" that allows different molecules to enter the nucleus. The institute's scientists hypothesized that a damaged axon should, in some way, inform the cell nucleus of the damage, so that the appropriate genes start working and produce the proteins essential for the healing process. This hypothesis led them to another hypothesis, according to which the importin-beta protein, which is the essential "key" for introducing the reporter molecules into the cell nucleus, may be produced - along with the reporter molecules themselves - in damaged axons. They discovered that importin-beta's sister protein, called importin-alpha, is normally found in axons. In the search process, they discovered that importin-beta is not found in axons at normal times, but immediately after an injury it is produced in them in large quantities.
Further observations showed that after its formation in the damaged axon, importin-beta binds to its sister protein, importin-alpha, and both bind to other proteins that constitute the message of the damage to the axon (the exact identity of these reporter proteins is still unknown). The entire gang connects to a protein "train" called dynein, which travels on the "rails" of the cytoskeleton fibers leading from the axon to the cell nucleus.
At this stage, thanks to the "key", importin-beta, the entire group manages to penetrate through the nuclear membrane and reach the place where the genetic material is stored.
The next step in the research will, of course, be an attempt to reveal the exact identity of the proteins that report to the nucleus about the damage caused to the axon, and the identification of the genes whose expression directs the process of nerve cell regeneration. The scientists hope that the disclosure of these proteins and genes will also help advance research designed to find a way to bring about the recovery of damaged nerve fibers in the central nervous system.
