Gene model reviewed during 5.46
Gene model reviewed during 5.49
None of the polypeptides share 100% sequence identity.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Fbp1 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Fbp1 in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
The Fbp1 enhancer functions as a complex ecdysone response unit integrating spatial and temporal cues in a specific response to the hormonal signal.
In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.
The in vitro characterisation of the EcR/usp binding site its ecdysone- dependent in vivo occupancy in different genetic backgrounds support the conclusion that the Fbp1 enhancer is a primary target of the EcR.
Fbp1 upstream sequences from -138bp to -68bp are involved in regulating the 20-hydroxyecdysone inducibility, developmental and tissue specificity of Fbp1 expression. Sequences between -1386bp and -138bp are required for the full level of transcription.
The steroid hormone 20-hydroxyecdysone can regulate RNA levels of a single gene both positively and negatively depending on hormone concentration. br can modify the direction of the gene's response to a hormone signal.