期刊
JOURNAL OF NEUROSCIENCE
卷 33, 期 17, 页码 7475-7487出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4387-12.2013
关键词
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资金
- NIH [RO1s NS35575, HL/AR59649, NS063245]
- McKnight Foundation
- UW-Madison Institute of Aging
- Neuroscience Training Program
CREB-responsive transcription has an important role in adaptive responses in all cells and tissue. In the nervous system, it has an essential and well established role in long-term memory formation throughout a diverse set of organisms. Activation of this transcription factor correlates with long-term memory formation and disruption of its activity interferes with this process. Most convincingly, augmenting CREB activity in a number of different systems enhances memory formation. In Drosophila, a sequence rearrangement in the original transgene used to enhance memory formation has been a source of confusion. This rearrangement prematurely terminates translation of the full-length protein, leaving the identity of the enhancing molecule unclear. In this report, we show that a naturally occurring, downstream, in-frame initiation codon is used to make a dCREB2 protein off of both transgenic and chromosomal substrates. This protein is a transcriptional activator and is responsible for memory enhancement. A number of parameters can affect enhancement, including the short-lived activity of the activator protein, and the time-of-day when induction and behavioral training occur. Our results reaffirm that overexpression of a dCREB2 activator can enhance memory formation and illustrate the complexity of this behavioral enhancement.
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