βFTZ-F1, β FTZ-F1, ftz-f1α, ftzf1, αftz-f1
transcription factor - nuclear receptor - zinc finger - bridges early and late gene expression during the process of metamorphosis - acetylations of Ftz-F1 and histone H4K5 are required for the fine-tuning of ecdysone biosynthesis during metamorphosis
Gene model reviewed during 5.55
Gene model reviewed during 5.45
Low-frequency RNA-Seq exon junction(s) not annotated.
Transposon inserted in intron
Gene model reviewed during 6.02
The 816aa (β) form of ftz-f1 protein is identical to the 1043aa (α) ftz-f1 isoform in the carboxy terminal 2/3 of the protein. The unique N-terminal region of the β ftz-f1 isoform is acidic and is likely to function as a transactivation domain. Polyclonal antibodies were prepared against bacterially expressed ftz-f1 protein and used to analyze the distribution of β ftz-f1 protein on polytene chromosomes. Staining that was reproducible in location and intensity was seen at 166 sites along the euchromatic genome in late prepupal stages, 55 of these represent ecdysone-regulated puffs.
One of a couple of protein products.
The "early" and "late" DNA-binding activity was subsequently shown to be encoded by two different isoforms of the ftz-f1 protein.
Monomer; forms a complex with ftz.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ftz-f1 using the Feature Mapper tool.
Expression increases as the gut clears before pupation.
ftz-f1 transcript expression is upregulated in the ring gland very late in larval development; expression levels are higher at "cleared gut" stage than at the earlier "blue gut" stage.
ftz-f1 DNA-binding activity is first observed in 1.5-4hr embryos and then diminishes.
GBrowse - Visual display of RNA-Seq signalsView Dmel\ftz-f1 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.
There is a cell-autonomous requirement for βftz-f1 activity during metamorphosis for the majority of γ neurons to be appropriately pruned.
Nonsense-mediated mRNA decay (NMD) down-regulates a distinct splice isoform(s) of this gene.
Expression is enriched in embryonic gonads.
ftz-f1 is required for muscle driven morphogenetic events at the prepupal-pupal transition.
Temporally restricted expression of ftz-f1 is important for late embryogenesis, the normal moulting process and early metamorphosis.
Mutants show defects in the hallmarks of the prepupal-pupal transition i.e. head eversion, leg elongation and salivary gland cell death.
The ftz-f1 gene product provides competence for stage-specific responses to ecdysone.
Adjacent and conserved ftz and cofactor binding sites within the en intron enhancer are necessary and sufficient for transcriptional activation. The cofactor sites can be specifically bound by ftz-f1, and the ftz homeodomain and ftz-f1 bind cooperatively in vitro.
Hr46 receptor represses the early genes activated by the late-larval ecdysone pulse and with the help of Eip75B, provides a temporal linkage between the two ecdysone responses by controlling the expression of ftz-f1.
Temporal profile of gene expression is not altered in Eip74EF mutant background.
Promoter analysis has identified an upstream element required for temporally restricted expression of ftz-f1. Multiple factors that bind to the ftz-f1 promoter region have been identified by electrophoresis mobility shift assays.
Ectopic expression of ftz-f1 at first instar, late second instar or early prepupal periods causes developmental defects. The sensitive stages slightly precede the endogenous ftz-f1 expression times. Premature expression at late second instar causes a failure in the second ecdysis, though third instar mouthooks and anterior spiracles form. Premature expression of ftz-f1 induces the Edg78E and Edg84A genes which have strong ftz-f1 binding sites upstream of their transcription start sites.
ftz-f1 and Hr39 bind as monomers to oligonucleotides corresponding to the ftz-f1 recognition element (F1RE) located within the zebra element of ftz promoter. Antagonism between the two receptors contributes to the net F1RE-dependent transcription of a reporter gene in cotransfection assays. Results suggest common target genes may be coregulated at the transcriptional level by a mechanism of competition between ftz-f1 and Hr39 monomers for binding to a common element.
Biochemical studies led to the identification multiple DNA-binding proteins (including ftz-f1 and ttk) that regulate ftz gene expression through the proximal enhancer, to mediate stripe establishment and maintenance.
A developmental isoform of ftz-f1, βftz-f1, is distinct from the embryonic αftz-f1 form: it is expressed as a product of the previously identified midprepupal chromosome puff at 75CD. Indirect immunofluorescent staining for ftz-f1 on the polytene chromosomes reveals binding to over 150 chromosomal targets, including 75CD itself and prominant late prepupal puffs predicted to be regulated by midprepupal puff proteins.
Evolutionary history for nuclear receptor genes, in which gene duplication events and swapping between domains of different origins took place, is studied.
Mutant peptides in the DNA-binding domain demonstrate that in addition to the zinc finger motif, the basic region abutting the C-terminal end of the zinc finger motif is involved in sequence specific DNA binding.