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Activation and Degradation of the Transcription Factor C/EBP During Long‐Term Facilitation in Aplysia
Author(s) -
Yamamoto Naoki,
Hegde Ashok N.,
Chain Daniel G.,
Schwartz James H.
Publication year - 1999
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1999.0732415.x
Subject(s) - aplysia , biology , transcription factor , activator (genetics) , protein kinase a , phosphorylation , cyclic amp response element binding protein , enhancer , microbiology and biotechnology , ccaat enhancer binding proteins , kinase , mitogen activated protein kinase , dna binding protein , biochemistry , creb , gene , neuroscience
: Long‐term facilitation (LTF) of the sensory‐to‐motor synapses that mediate defensive reflexes in Aplysia requires induction of the transcription factor Aplysia CCAAT/enhancer binding protein (ApC/EBP) as an early response gene. We examined the time course of ApC/EBP DNA binding during the induction of LTF : Binding activity was detected within 1 h of the sensitization treatment with serotonin, reached a maximum at 2 h, and decreased after 6 h. How are DNA binding and the turnover of ApC/EBP regulated ? We find that phosphorylation of ApC/EBP by mitogen‐activated protein (MAP) kinase is essential for binding. MAP kinase appears to be activated through protein kinase C. We also showed that ApC/EBP is degraded through the ubiquitin‐proteasome pathway but that phosphorylation by MAP kinase renders it resistant to proteolysis. Thus, phosphorylation by MAP kinase is required for ApC/EBP to act as a transcription activator as well as to assure its stability early in the consolidation phase, when genes essential for the development of LTF begin to be expressed.