Finding this evidence was far from simple: Importins are so crucial in the cell's nucleus that even the smallest embryo could not survive without them. But Rotem Ben-Tov Perry, a research student at the Weizmann Institute who was lead author of the new study, found a way to distinguish the importin beta1 in the cell body from that in the axon: The axonal protein was apparently made from a longer version of messenger RNA, the cell's working recipe for building a protein. To see if they could selectively affect just the axonal version of the protein, the Weizmann researchers worked with Drexel's Twiss to take advantage of high precision knock-out technology. Rather than knocking a whole gene out of the system, they managed to remove one little piece of the messenger RNA's recipe for manufacturing importins -just the longer bit that sends the RNA to the axon.
Now they observed plenty of importin beta1 in the cell body, but none in the axons. With the axonal segment of RNA knocked out of the recipe for importin beta1, a mouse embryo still had the importin it needed near the nucleus of its cells to grow and develop into a living animal but it took much longer to recover from peripheral nerve injury. Genes that are normally active in response to nerve damage were activated to a lesser degree. All of this suggests that the importin beta1 that normally helps inform the extended nerve cell about injury is, indeed, produced locally in the axon and that this protein found in the axon is a key part of the nerve repair signaling process.
"The data shows conclusively that importin beta1 protein is produced in axons, Rotem's work has validated the importins' crucial role in nerve repair," said Dr. Michael Fainzilber, senior author and professor at the Weizmann Institute.
Twiss said that next steps will be to better describe how the signaling process involving importin beta1 delivers a signal to begin nerve ce
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