Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia

Seung Hee Lee; Chae Seok Lim; Hyungju Park; Jin A. Lee; Jin Hee Han; Hyoung Kim; Ye Hwang Cheang; Sue Hyun Lee; Yong Seok Lee; Hyoung Gon Ko; Dong Hyuk Jang; Hyongkyu Kim; Maria C. Miniaci; Dusan Bartsch; Eunjoon Kim; Craig H. Bailey; Eric R. Kandel; Bong Kiun Kaang

doi:10.1016/j.cell.2007.03.041

Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia

Seung Hee Lee, Chae Seok Lim, Hyungju Park, Jin A. Lee, Jin Hee Han, Hyoung Kim, Ye Hwang Cheang, Sue Hyun Lee, Yong Seok Lee, Hyoung Gon Ko, Dong Hyuk Jang, Hyongkyu Kim, Maria C. Miniaci, Dusan Bartsch, Eunjoon Kim, Craig H. Bailey, Eric R. Kandel, Bong Kiun Kaang

Department of Dentistry

Research output: Contribution to journal › Article › peer-review

47 Scopus citations

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.

Original language	English
Pages (from-to)	801-812
Number of pages	12
Journal	Cell
Volume	129
Issue number	4
DOIs	https://doi.org/10.1016/j.cell.2007.03.041
State	Published - 18 May 2007

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MOLNEURO

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Lee, S. H., Lim, C. S., Park, H., Lee, J. A., Han, J. H., Kim, H., Cheang, Y. H., Lee, S. H., Lee, Y. S., Ko, H. G., Jang, D. H., Kim, H., Miniaci, M. C., Bartsch, D., Kim, E., Bailey, C. H., Kandel, E. R., & Kaang, B. K. (2007). Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia. Cell, 129(4), 801-812. https://doi.org/10.1016/j.cell.2007.03.041

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title = "Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia",

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.",

keywords = "MOLNEURO",

author = "Lee, {Seung Hee} and Lim, {Chae Seok} and Hyungju Park and Lee, {Jin A.} and Han, {Jin Hee} and Hyoung Kim and Cheang, {Ye Hwang} and Lee, {Sue Hyun} and Lee, {Yong Seok} and Ko, {Hyoung Gon} and Jang, {Dong Hyuk} and Hyongkyu Kim and Miniaci, {Maria C.} and Dusan Bartsch and Eunjoon Kim and Bailey, {Craig H.} and Kandel, {Eric R.} and Kaang, {Bong Kiun}",

year = "2007",

month = may,

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Lee, SH, Lim, CS, Park, H, Lee, JA, Han, JH, Kim, H, Cheang, YH, Lee, SH, Lee, YS, Ko, HG, Jang, DH, Kim, H, Miniaci, MC, Bartsch, D, Kim, E, Bailey, CH, Kandel, ER & Kaang, BK 2007, 'Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia', Cell, vol. 129, no. 4, pp. 801-812. https://doi.org/10.1016/j.cell.2007.03.041

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T1 - Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia

AU - Lee, Seung Hee

AU - Lim, Chae Seok

AU - Park, Hyungju

AU - Lee, Jin A.

AU - Han, Jin Hee

AU - Kim, Hyoung

AU - Cheang, Ye Hwang

AU - Lee, Sue Hyun

AU - Lee, Yong Seok

AU - Ko, Hyoung Gon

AU - Jang, Dong Hyuk

AU - Kim, Hyongkyu

AU - Miniaci, Maria C.

AU - Bartsch, Dusan

AU - Kim, Eunjoon

AU - Bailey, Craig H.

AU - Kandel, Eric R.

AU - Kaang, Bong Kiun

PY - 2007/5/18

Y1 - 2007/5/18

N2 - 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.

AB - 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.

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SN - 0092-8674

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EP - 812

JO - Cell

JF - Cell

IS - 4

ER -

Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia

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