dCREB2, CREB, CrebB-17A, dCREB2-b, dCREB2-a
Gene model reviewed during 5.53
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 6.12
Gene model reviewed during 6.32
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.43
Evidence for alternative splicing from FBrf0083527.
Gene model reviewed during 5.42
Gene model reviewed during 5.46
Gene model reviewed during 5.56
The product of the longest CrebB transcript ("dCREB-2a") acts as a PKA-dependent transcriptional activator in transient transfection assays. This activation is blocked when an alternately spliced CrebB transcript (dCREB-2b") is cotransfected with the transcriptional activator ("dCREB-2a").
The product of the longest CrebB transcript ("dCREB-2a") acts as a PKA-dependent transcriptional activator in transient transfection assays. This activation is blocked when an alternately spliced CrebB transcript (dCREB-2b") is cotransfected with the transcriptional activator ("dCREB-2a"). When the middle 2 leucines in the bZIP domain of the antagonist protein (dCREB-2b") are changed to valine, the antagonist is no longer able to block transcriptional activation.
DNA binding assayed
g430806 and g1110570 appear to be alternative splice variants. It is unclear is either is a complete sequence
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\CrebB using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\CrebB in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
CrebB-17A binds to the Ubx cAMP response element (CRE), located in an enhancer, and ubiquitous expression of a dominant negative form of CrebB-17A suppresses CRE-mediated reporter gene expression and reduces lab expression in the endoderm.
CrebB-17A acts in parallel with Fas2 to cause an increase in synaptic strength. cAMP initiates these parallel changes to achieve long-term synaptic enhancement. Expression of the CrebB-17A repressor in the dnc mutant blocks functional but not structural plasticity. Expression of the CrebB-17A activator increases synaptic strength, but only in Fas2 mutants that increase bouton number, due to increased presynaptic transmitter release. Expression of CrebB-17A in a Fas2 mutant background genetically reconstitutes cAMP-dependent plasticity. Thus, cAMP initiates parallel changes in CrebB-17A and Fas2 to achieve long-term synaptic enhancement.
Long term memory formation can be prevented by an inducible repressor form of CrebB-17A.
Long term memory (LTM) is blocked specifically by induced expression of a repressor isoform of CrebB-17A. LTM formation is enhanced after induced expression of an activator form of CrebB-17A. LTM formation depends on phosphorylation of the CrebB-17A product. FlyBase curator comment: see FBrf0180428 for re-examination of these conclusions in light of discovery that CrebB-17Aa.hs actually encodes a mutant form of CrebB-17A isoform a. In contrast to results reported in FBrf0080505, FBrf0180428 reports that heat shock of CrebB-17Aa.hs was found to exert no effect on LTM in 1x training session - though assay was carried out at 5, as opposed to 7 days. CrebB-17Ab.hs, however, does have an effect on LTM.
Over-expression of the b isoform of CrebB-17A completely blocks long-term memory, but leaves anaesthesia resistant memory and learning unaffected.