生物谷報道：5月18日,，韓國首爾大學姜奉均（音譯）教授宣布發(fā)現(xiàn)促進形成長時記憶的蛋白質(zhì)。
姜奉均教授在世界上第一次發(fā)現(xiàn)“傳遞記憶信號逆行性轉(zhuǎn)錄因子”
生物的記憶主要分為持續(xù)1-2小時的短時記憶和通過反復學習能夠持續(xù)24小時以上的長時記憶,。在形成長時記憶方面，蛋白質(zhì)合成和基因表達均不可或缺,。
姜奉均領導的科研組在傳達外界刺激的神經(jīng)體系中發(fā)現(xiàn)了存在于神經(jīng)鍵內(nèi)被稱為“CAMAP”的蛋白質(zhì),，該蛋白質(zhì)將學習信號傳達到細胞核后，合成能夠形成長時記憶的蛋白質(zhì),。
科研組針對海兔進行實驗的結果,，發(fā)現(xiàn)一種使細胞結合的粘附蛋白質(zhì)——“CAMAP”起到了將信號從神經(jīng)鍵傳達到細胞核的傳達作用,。同時,，在細胞核中與其它蛋白質(zhì)“CREB”結合，起到形成長時記憶所需的轉(zhuǎn)錄因子作用,，并誘導基因表達,。
如果反復刺激海兔的尾部，反應會變得敏感,?？紤]到高級動物也存在這種類似的現(xiàn)象，科研組預測如果人類反復聽取英語單詞,，會長時間留在記憶之中,。
科研組表示，在“外界刺激→神經(jīng)鍵→細胞核→長時記憶蛋白子形成及基因表達”這一信號傳達鏈中,，確認了起到連接環(huán)作用的蛋白質(zhì)性質(zhì),。
原始出處:
Cell, Vol 129, 801-812, 18 May 2007
Article
Nuclear Translocation of CAM-Associated Protein Activates Transcription for Long-Term Facilitation in Aplysia
Seung-Hee Lee,1,7 Chae-Seok Lim,1,7 Hyungju Park,1,7 Jin-A Lee,1 Jin-Hee Han,1 Hyoung Kim,1 Ye-Hwang Cheang,1 Sue-Hyun Lee,1 Yong-Seok Lee,1 Hyoung-Gon Ko,1 Dong-Hyuk Jang,1 Hyongkyu Kim,2 Maria C. Miniaci,6,8 Dusan Bartsch,3 Eunjoon Kim,4 Craig H. Bailey,6 Eric R. Kandel,5,6 and Bong-Kiun Kaang1,
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
2 College of Medicine, Chungbuk National University, Cheongju 361-763, Korea
3 Department of Molecular Biology, Central Institute of Mental Health, Mannheim 68159, Germany
4 Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea
5 Howard Hughes Medical Institute, 1051 Riverside Drive, New York, NY 10032, USA
6 New York State Psychiatric Institute, Kavli Institute for Brain Sciences, Center for Neurobiology and Behavior, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Corresponding author
Bong-Kiun Kaang
kaang@snu.ac.kr
Summary
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.
