Format

Send to

Choose Destination
Cell. 2007 May 18;129(4):801-12.

Nuclear translocation of CAM-associated protein activates transcription for long-term facilitation in Aplysia.

Author information

1
Department of Biological Sciences, Institute of Molecular Biology and Genetics, RIO, College of Natural Sciences, Seoul National University, San 56-1 Silim-dong Gwanak-gu, Seoul 151-747, Korea.

Abstract

Repeated pulses of serotonin (5-HT) induce long-term facilitation (LTF) of the synapses between sensory and motor neurons of the gill-withdrawal reflex in Aplysia. To explore how apCAM downregulation at the plasma membrane and CREB-mediated transcription in the nucleus, both of which are required for the formation of LTF, might relate to each other, we cloned an apCAM-associated protein (CAMAP) by yeast two-hybrid screening. We found that 5-HT signaling at the synapse activates PKA which in turn phosphorylates CAMAP to induce the dissociation of CAMAP from apCAM and the subsequent translocation of CAMAP into the nucleus of sensory neurons. In the nucleus, CAMAP acts as a transcriptional coactivator for CREB1 and is essential for the activation of ApC/EBP required for the initiation of LTF. Combined, our data suggest that CAMAP is a retrograde signaling component that translocates from activated synapses to the nucleus during synapse-specific LTF.

PMID:
17512412
DOI:
10.1016/j.cell.2007.03.041
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center