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Volume 17, Number 13, Issue of July 1, 1997 pp. 4915-4920
Copyright ©1997 Society for Neuroscience

An NF-B-Like Transcription Factor in Axoplasm is Rapidly Inactivated after Nerve Injury in Aplysia

Received March 21, 1997; revised April 11, 1997; accepted April 1, 1997.

Michael Povelones¹, Kathy Tran², Dimitris Thanos², and Richard T. Ambron¹

¹ Departments of Anatomy and Cell Biology and ² Biochemistry and Molecular Biophysics, College of Physicians and Surgeons of Columbia University, New York, New York 10032

We found a protein in Aplysia neurons that has many characteristics of the transcription factor NF-B. Thus, the protein recognized a radiolabeled probe containing the B sequence from the human interferon- gene enhancer element (PRDII), and the binding was not affected by PRDIV, an ATF-2 enhancer sequence from the same gene. Binding was efficiently inhibited, however, by nonradioactive oligonucleotides containing H2, the B site from the major histocompatibility complex I gene promotor. In addition, recombinant mammalian IB-, which associates specifically with the P65 subunit of NF-B, inhibited the binding to the PRDII probe in a dose-dependent manner. The nuclear form of the Aplysia protein was constitutively active. Axoplasm, however, contained the constitutively active form as well as a latent form. The latter was activated by treatment with deoxycholate under the same conditions as mammalian NF-B. Based on these findings, we believe the protein to be a homolog of NF-B. To investigate the role of apNF-B in the axon, we crushed the peripheral nerves to the body wall. Surprisingly, there was a rapid loss of apNF-B binding at the crush site and, within 15 min, as far as 2.5 cm along the axon. In contrast, exposing either the intact animal or the nervous system in situ to levels of 5-HT that induce synaptic facilitation did not affect apNF-B activity.

Key words: NF-B; axon injury; transcription factor; axoplasm; DNA binding; injury signal; nuclear localization signal

This article has been cited by other articles:

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