PHILADELPHIA (July 30, 2012) When the longest cells in the body are injured at their farthest reaches, coordinating the cells' repair is no easy task. This is in part because these peripheral nerve cells can be extremely long up to one meter in adult humans which is a lot of distance for a molecular distress signal to cover in order to reach the "command center" of the cell's nucleus.
Scientists have believed this process to be even more challenging because their textbook understanding for many years has been that the axons the long extensions of nerve cells away from the main cell body containing the nucleus do not manufacture the proteins involved in the molecular signal themselves. Yet, in recent years, some scientists have begun to challenge that textbook understanding, with preliminary evidence that one key protein involved in setting off a distress signal for cellular repair, known as importin beta1, was locally produced in the axons. They just weren't sure how.
"Now these textbooks need to be rewritten," said Dr. Jeffery Twiss, a professor and head of the department of biology in Drexel University's College of Arts and Sciences. Twiss co-authored new research recently published in Neuron, led by collaborators from the Weizmann Institute of Science. "Our new research is one of the strongest indicators yet of molecular signaling from end to end in peripheral nerve cells."
These researchers have provided strong new evidence that the protein importin beta1 is indeed produced locally in the axons of peripheral nerve cells. They also found that the version of the protein, when found in the axon, is made using a different molecular recipe than the version found in the nucleus, where it performs different essential cell functions. These discoveries may help scientists better understand how subsequent steps operate in the distress signal and in nerve cell repair, so they can eventually control and enhance the process to spee
|Contact: Rachel Ewing|