A family of proteins, called importins, which according to conventional wisdom are only found near the cell nucleus, were also discovered at the far ends of the longest cells - nerve cells. Now the researchers from the Weizmann Institute who discovered them also discovered how the infortins get from the cell nucleus to the axons at the far end
A few years ago, Prof. Mike Feinzylver and his group members, from the Department of Biological Chemistry at the Weizmann Institute of Science, made a surprising discovery: a family of proteins, called importins, which according to conventional wisdom are only found near the cell nucleus, were also discovered at the far ends of the longest cells: nerve cells of the peripheral nervous system. These cells form extensions - called axons - which can reach up to a meter in length in an adult.
The main role of the importins near the nucleus was known: these proteins transport various substances into and out of the cell nucleus, through the membrane that protects the nucleus. Prof. Feinzylver and his group members showed that the importins in the axons, which are far from the cell nucleus, also play a role in transport, albeit of a different kind: when the nerve cell is damaged at some point along the axon, the importins are mobilized to help and function as a kind of "warning system", which transports the distress signals to their destination - The cell nucleus.
This discovery raised an interesting question: how do the importins get to the axons? Preliminary evidence indicated the possibility that one of the important importins, called importin beta 1, is produced exactly when and where it is needed: after an injury to the nerve cell, it is produced in the axon itself, near the injury site. These evidences contradicted the belief that was established after many years of scientific research, according to which proteins are not produced in the axonal extensions of the nerve cells, but only in the cell body. This opinion was based, among other things, on the fact that it was difficult to discover ribosomes (protein factories) in axons using microscopic methods.
Resolving the contradiction is not a simple task: the conventional methods of silencing genes - in order to study their function - are not effective in this case, since the importins are essential proteins for the survival of the cell and the entire animal. In the research of Rotam Ben-Tov Perry, a joint research student in the group of Prof. Feinzylver and the group of Dr. Avraham Yaron, a possibility was discovered to distinguish between the importin beta 1 protein in the cell body and its brother in the exon: it turned out that the messenger RNA molecule that codes for the protein The axon contains another piece, which is responsible for sending the RNA to the axon, so it is longer. To specifically damage this protein, the scientists, together with Prof. Jeff Twiss from Drexel University in Philadelphia, used precise gene deletion technologies. Instead of deleting the gene entirely, they removed only the extra piece of RNA. In this way, importin beta 1 which is created in the cell body, and is essential for the survival of the embryo, is not damaged.
The transgenic mice created in this way did make normal amounts of importin beta 1 in the nerve cell bodies, but not in the axons. These mice required a longer period of time to recover from nerve injury, and the genes normally activated in response to such injury also showed relatively low activation. All the evidence indicated that the importin beta 1, which tells the nerve cell of injury, is indeed produced locally in the axon.
Prof. Feinzylver: "In these experiments, for the first time, we were able to show that a delay in the transport of a certain messenger RNA to the axon causes the encoded protein to disappear from the axon. The study unequivocally proves that importin beta 1 is produced in axons, and confirms the essential role played by these proteins in the restoration of nerve cells." The findings, recently published in the journal Neuron, may indicate ways to more effectively treat nerve injuries, and to speed up the restoration of damaged nerve cells.
One response
Maybe the importin is produced in the nucleus, and is slightly different (because the RNA is different) and only then is it transferred to the axon?
I did not understand the evidence.
"It turned out that the messenger RNA molecule that codes for the protein in the axon contains another piece, which is responsible for sending the RNA to the axon" If the RNA itself is sent to the axon, then of course the protein is produced there, but what?