PKA-activated ApAF-ApC/EBP heterodimer is a key downstream effector of ApCREB and is necessary and sufficient for the consolidation of long-term facilitation

Jin A. Lee, Sue Hyun Lee, Changhoon Lee, Deok Jin Chang, Yong Lee, Hyoung Kim, Ye Hwang Cheang, Hyoung Gon Ko, Yong Seok Lee, Heejung Jun, Dusan Bartsch, Eric R. Kandel, Bong Kiun Kaang

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Long-term memory requires transcriptional regulation by a combination of positive and negative transcription factors. Aplysia activating factor (ApAF) is known to be a positive transcription factor that forms heterodimers with ApC/EBP and ApCREB2. How these heterodimers are regulated and how they participate in the consolidation of long-term facilitation (LTF) has not, however, been characterized. We found that the functional activation of ApAF required phosphorylation of ApAF by PKA on Ser-266. In addition, ApAF lowered the threshold of LTF by forming a heterodimer with ApCREB2. Moreover, once activated by PKA, the ApAF-ApC/EBP heterodimer transactivates enhancer response element-containing genes and can induce LTF in the absence of CRE- and CREB-mediated gene expression. Collectively, these results suggest that PKA-activated ApAF-ApC/EBP heterodimer is a core downstream effector of ApCREB in the consolidation of LTF.

Original languageEnglish (US)
Pages (from-to)827-838
Number of pages12
JournalJournal of Cell Biology
Volume174
Issue number6
DOIs
StatePublished - Sep 11 2006
Externally publishedYes

ASJC Scopus subject areas

  • Cell Biology

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