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General Information
Symbol
Dmel\ftz
Species
D. melanogaster
Name
fushi tarazu
Annotation Symbol
CG2047
Feature Type
FlyBase ID
FBgn0001077
Gene Model Status
Stock Availability
Gene Snapshot
In progress.Contributions welcome.
Also Known As
Dm-Ftz
Key Links
Genomic Location
Cytogenetic map
Sequence location
3R:6,864,324..6,866,244 [+]
Recombination map
3-48
Sequence
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
GO Summary Ribbons
Protein Family (UniProt)
Belongs to the Antp homeobox family. (P02835)
Summaries
Gene Group (FlyBase)
HOX-LIKE HOMEOBOX TRANSCRIPTION FACTORS -
HOX-like (HOXL) homeobox transcription factors are sequence-specific DNA binding proteins that regulate transcription. They encompass transcription factors encoded by the Hox genes of the Antennapedia and the Bithorax gene complexes and genes closely related in sequence. HOXL transcription factors are major regulators of animal development. (Adapted from FBrf0232555).
Protein Function (UniProtKB)
May play a role in determining neuronal identity, may be directly involved in specifying identity of individual neurons. Required during embryogenesis for the process of body segmentation. Homeotic protein, required in alternating segment primordia, it specifies the correct number of segments.
(UniProt, P02835)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
ftz: fushi tarazu
Null loss-of-function mutations result in embryonic lethality. Animals survive to the end of embryogenesis and exhibit a pair-rule mutant phenotype in the cuticle. This same phenotype is observable in animals at the beginning of segmentation of the germ band. Prior to deposition of cuticle, ftz- animals have two rather than three mouth (gnathocephalic) segments and five as compared to ten trunk metameres. The material deleted is derived from the even-numbered parasegments, ps2 through ps12. Similar metameric deletions/fusions are seen in the neuromeres of the ventral nerve cord of the CNS. The name of the locus derives from the phenotype and is Japanese for "segment" (fushi) "deficient" (tarazu) (N.B. - there is only one letter t in tarazu; it is at the start of the word i.e., there is no second t preceding the z). Temperature-sensitive alleles of the gene have shown that the temperature-critical period for viability and phenotype falls between 1 and 4 hours of embryogenesis with the mid point of 2.5 hours at the blastoderm stage. The recovery of clones of ftz- cells created by X-ray-induced somatic exchange after cellular blastoderm have demonstrated that ftz+ activity is not necessary for normal cuticular morphogenesis subsequent to this point in development. In addition to these recessive null and hypomorphic alleles there are two classes of dominant gain-of-function lesions at the ftz locus. The first, ftz- Regulator of postbithorax-like, causes a variable transformation of the posterior haltere into posterior wing. The second, ftz-Ultra-abdominal-like, is associated with a patchy transformation of the adult first abdominal segment toward third abdominal identity. The former (ftzRpl) lesion also shows a recessive loss-of-function phenotype while the latter class (ftzUal) has no discernable embryonic phenotype and is homozygous viable. The fact that these dominant alleles produce mutant phenotypes that mimic lesions in the BXC has been interpreted as demonstrating a regulatory link between the segment enumeration genes and the homeotics.
Summary (Interactive Fly)
transcription factor - homeodomain - Antp class - pair rule gene - modulates Runt-dependent activation and repression of segment-polarity gene transcription
Gene Model and Products
Number of Transcripts
1
Number of Unique Polypeptides
1

Please see the GBrowse view of Dmel\ftz or the JBrowse view of Dmel\ftz for information on other features

To submit a correction to a gene model please use the Contact FlyBase form

Protein Domains (via Pfam)
Isoform displayed:
Pfam protein domains
InterPro name
classification
start
end
Protein Domains (via SMART)
Isoform displayed:
SMART protein domains
InterPro name
classification
start
end
Comments on Gene Model
Gene model reviewed during 5.50
Sequence Ontology: Class of Gene
Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0081625
1774
410
Additional Transcript Data and Comments
Reported size (kB)
1.9 (northern blot)
1.8 (northern blot)
Comments
External Data
Crossreferences
Rfam - A collection of RNA sequence families of structural RNAs including non-coding RNA genes as well as cis-regulatory elements
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
RefSeq ID
GenBank
FBpp0081139
46.5
410
6.99
Polypeptides with Identical Sequences

There is only one protein coding transcript and one polypeptide associated with this gene

Additional Polypeptide Data and Comments
Reported size (kDa)
68 (kD observed)
413 (aa); 45 (kD predicted)
Comments
External Data
Post Translational Modification
Phosphorylated at as many as 16 sites.
(UniProt, P02835)
Crossreferences
PDB - An information portal to biological macromolecular structures
Linkouts
Sequences Consistent with the Gene Model
Mapped Features

Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ftz using the Feature Mapper tool.

External Data
Crossreferences
Linkouts
Gene Ontology (18 terms)
Molecular Function (3 terms)
Terms Based on Experimental Evidence (3 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN002388214
(assigned by GO_Central )
Biological Process (14 terms)
Terms Based on Experimental Evidence (6 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (9 terms)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN002388214
(assigned by GO_Central )
traceable author statement
traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN002902589
(assigned by GO_Central )
traceable author statement
traceable author statement
Cellular Component (1 term)
Terms Based on Experimental Evidence (0 terms)
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN002388214
(assigned by GO_Central )
Expression Data
Expression Summary Ribbons
Colored tiles in ribbon indicate that expression data has been curated by FlyBase for that anatomical location. Colorless tiles indicate that there is no curated data for that location.
For complete stage-specific expression data, view the modENCODE Development RNA-Seq section under High-Throughput Expression below.
Transcript Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
northern blot
Stage
Tissue/Position (including subcellular localization)
Reference

Comment: reference states 0-12 hr AEL

radioisotope in situ
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
Expression was examined at four phases of embryonic stage 5. The striped pattern becomes visible in phase 1 (0-5'), all stripes except stripe 7 are expressed during phase 2 (5-17'), and their spacing and expression levels become largely uniform by phase 3 (17-30'). The stripes initially appear less clearly separated and more graded.
Stripes of ftz expression diminish in width and intensity in evehs.PS embryos as the level of ectopic eve protein increases. Timing suggests that eve is a direct regulator of ftz.
The ftz transcript is expressed in every even numbered parasegment in a pair-rule pattern of the blastoderm stage embryo. The stripes of ftz expression are broad at first, and later in development become more refined. At stage 10, neural expression is appearant in the ventral nerve cord. By stage 11, ftz transcript levels are diminished.
The ftz transcripts are first detected in stage 3 embryos uniformly distributed between 20 and 70% egg length. This pattern is then resolved into seven stripes of expression in even numbered parasegments and persists through germband retraction.
ftz transcripts are first detected at the 11th nuclear division in early embryos at which point they are distributed throughout the embryo. A striped pattern is first seen at the 13th nuclear division. At the cellular blastoderm stage, ftz transcripts can be clearly seen to localize in discrete patches between 15% and 65% egg length that are separated by unlabelled cells. Each labelled cluster is 3-5 cells wide and is separated by 3-5 cell-wide patches of unlabelled cells. ftz transcripts continue to be detected at gastrulation and in early germ band extended embryos. No ftz transcripts are observed after 4 hrs of development.
ftz transcripts are most abundant in RNA from 0-6hr embryos and are also detected in 6-12hr RNA. They are not detected in RNA from later embryonic stages, larvae, or pupae.
ftz transcripts peak in 2-4hr embryos but are detected at all two hour intervals from 0-2 to 10-12 hours of embryogenesis.
Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
western blot
Stage
Tissue/Position (including subcellular localization)
Reference

Comment: reference states 3-14 hr AEL

embryonic/larval hindgut

Comment: reference states 12-15 hr AEL

Additional Descriptive Data
In csw mutant embryos, the seventh ftz stripe is expanded posteriorly.
The position of run protein stripes was compared to that of other segmentation genes. The run protein stripes lie anterior to the ftz protein stripes but overlap them partially. Two rows of run expression are anterior to a two-row region of overlap with ftz followed by two rows of ftz expression and then a region of non-expression before the next run stripe.
ftz protein expression is more intense in the posterior stripes (parasegments 10, 12, and 14) compared to more anterior stripes.
Filtered fluorescence imaging (FFI) was used to visualize low level ftz protein expression. The order of stripe formation is the following: 1+2, 5+3, 4+6+7. The shape of the stripes changes during maturation. Stripes 3-7 have a graded D/V distribution with more protein ventrally tapering off toward the dorsal midline. Stripes 1 and 2 are less graded. The stripes narrow with time and are wider in intermediate stages than in their mature form. For example, stripes 6 and 7 arise from expression in a region ~15 nuclei wide. ftz protein is also observed in anterior and posterior portions of the embryo with FFI in the cellularizing embryo. The anterior region is 12 nuclei wide and extends from 75-84% egg length. The posterior band of staining lies adjacent to the pole cells. ftz protein is also detected transiently in the interband regions during cellularization.
ftz protein is expressed in a segmentally repeated pattern in the embryonic CNS. Expression begins in a subset of neuronal precursor cells. It is eventually expressed in about 30 of the ~250 neurons in each hemisegment. Specific identified cells that express ftz protein include MP1, MP2, dMP2, vMP2, aCC, pCC, GMC1, RP1, RP2, and the glial precursor (GP). By stage 15, ftz protein is no longer detected in the nervous system.
ftz protein accumulation was assayed by western blot in embryos. An early peak of ftz protein is seen in 3-4 hr embryos. Protein levels subside and then rise to a second peak in 8-9hr embryos. Levels drop off again after 10 hours. No protein is detected after 14 hours. The pattern of protein distribution was determined by immunodetection. Between 3 and 5 hours of development, ftz protein is present in seven bands encircling the embryo. The order of appearance of the stripes is 2, 1+3, 5,6,7 (stripes are numbered from anterior to posterior). The bands are dynamic in width and position. Nuclei on the posterior edges of the stripes have a lower level of ftz protein. This is the region in which ftz protein expression is lost in stripes 1-5 when stripe narrowing occurs. Beginning at 5-6hr of development, staining becomes apparent in neuronal precursors in the CNS. A third stage of expression occurs in 12-15hr embryos. Expression is observed in the hindgut. Light staining is also observed in the proventriculus and in the dorsal posterior ectoderm.
At the cellular blastoderm stage of embryonic development ftz protein is expressed as a stripe in every even numbered parasegment.
ftz protein is first detected at the cellular blastoderm stage in a pattern of seven stripes, each about 4 nuclei wide, in the anterior-posterior axis. The most posterior stripe is wider, averaging 5 nuclei across. The space between stripes is about 4 nuclei across. The stripes become narrower at the beginning of gastrulation at which point they are about 3 nuclei across and the spaces between enlarge to about 5 cell nuclei. The staining in stripes can be followed nearly to the time of full germ band extension. The stripes disappear before the germ band is fully extended. In germ band extended embryos, ftz protein is observed in clusters of cells in the embryonic CNS. The staining is repeated bilaterally in 15 segmental units including the regions where the gnathocephalic segments are forming.
Marker for
 
Subcellular Localization
CV Term
Evidence
References
Expression Deduced from Reporters
Reporter: P{ftz3'Δ347}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ftz/lacD}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ftz/lacE}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ftz/lacG}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ftz-lacA}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ftz-lacB}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ftz-lacC}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{ftz-lacF}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter:
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{GAL4-ftz.ng}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{Prox323}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{Prox406}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{Prox531}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{UPHZ50D1}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{UPHZ50D2}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{UPHZ50H}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{UPHZ50HS}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{UPHZ50T}
Stage
Tissue/Position (including subcellular localization)
Reference
High-Throughput Expression Data
Associated Tools

GBrowse - Visual display of RNA-Seq signals

View Dmel\ftz in GBrowse 2
RNA-Seq by Region - Search RNA-Seq expression levels by exon or genomic region
Reference
See Gelbart and Emmert, 2013 for analysis details and data files for all genes.
Developmental Proteome: Life Cycle
Developmental Proteome: Embryogenesis
External Data and Images
Linkouts
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
FLIGHT - Cell culture data for RNAi and other high-throughput technologies
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
Flygut - An atlas of the Drosophila adult midgut
Images
Alleles, Insertions, and Transgenic Constructs
Classical and Insertion Alleles ( 31 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 110 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of ftz
Transgenic constructs containing regulatory region of ftz
Deletions and Duplications ( 40 )
Phenotypes
For more details about a specific phenotype click on the relevant allele symbol.
Lethality
Allele
Other Phenotypes
Allele
Phenotype manifest in
Allele
antennal segment 3 & bract | ectopic, with Scer\GAL4Dll-md23
Orthologs
Human Orthologs (via DIOPT v7.1)
Homo sapiens (Human) (32)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
3 of 15
No
Yes
 
3 of 15
No
Yes
 
3 of 15
No
Yes
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
Model Organism Orthologs (via DIOPT v7.1)
Mus musculus (laboratory mouse) (32)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
3 of 15
No
Yes
 
3 of 15
No
Yes
3 of 15
No
Yes
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
 
2 of 15
No
No
 
2 of 15
No
No
 
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
Rattus norvegicus (Norway rat) (36)
3 of 13
Yes
No
3 of 13
Yes
No
2 of 13
No
Yes
2 of 13
No
Yes
2 of 13
No
No
2 of 13
No
No
2 of 13
No
No
2 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
Xenopus tropicalis (Western clawed frog) (26)
2 of 12
Yes
No
2 of 12
Yes
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
Danio rerio (Zebrafish) (36)
3 of 15
Yes
No
3 of 15
No
Yes
3 of 15
Yes
No
3 of 15
No
Yes
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
2 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
Caenorhabditis elegans (Nematode, roundworm) (9)
2 of 15
Yes
Yes
2 of 15
Yes
No
1 of 15
No
No
1 of 15
No
No
 
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
1 of 15
No
No
Arabidopsis thaliana (thale-cress) (3)
1 of 9
Yes
Yes
1 of 9
Yes
No
1 of 9
Yes
No
Saccharomyces cerevisiae (Brewer's yeast) (2)
1 of 15
Yes
Yes
1 of 15
Yes
No
Schizosaccharomyces pombe (Fission yeast) (0)
No records found.
Orthologs in Drosophila Species (via OrthoDB v9.1) ( EOG09190CCT )
Organism
Common Name
Gene
AAA Syntenic Ortholog
Multiple Dmel Genes in this Orthologous Group
Drosophila melanogaster
fruit fly
Drosophila suzukii
Spotted wing Drosophila
Drosophila simulans
Drosophila sechellia
Drosophila erecta
Drosophila yakuba
Drosophila ananassae
Drosophila pseudoobscura pseudoobscura
Drosophila persimilis
Drosophila willistoni
Drosophila virilis
Drosophila mojavensis
Drosophila grimshawi
Orthologs in non-Drosophila Dipterans (via OrthoDB v9.1) ( EOG091503G8 )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Musca domestica
House fly
Glossina morsitans
Tsetse fly
Lucilia cuprina
Australian sheep blowfly
Orthologs in non-Dipteran Insects (via OrthoDB v9.1) ( None identified )
No non-Dipteran orthologies identified
Orthologs in non-Insect Arthropods (via OrthoDB v9.1) ( None identified )
No non-Insect Arthropod orthologies identified
Orthologs in non-Arthropod Metazoa (via OrthoDB v9.1) ( None identified )
No non-Arthropod Metazoa orthologies identified
Paralogs
Paralogs (via DIOPT v7.1)
Drosophila melanogaster (Fruit fly) (15)
3 of 10
3 of 10
3 of 10
2 of 10
2 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
1 of 10
Human Disease Associations
FlyBase Human Disease Model Reports
    Disease Model Summary Ribbon
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Allele
    Disease
    Evidence
    References
    Potential Models Based on Orthology ( 0 )
    Human Ortholog
    Disease
    Evidence
    References
    Modifiers Based on Experimental Evidence ( 0 )
    Allele
    Disease
    Interaction
    References
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Disease Associations of Human Orthologs (via DIOPT v7.1 and OMIM)
    Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
    Homo sapiens (Human)
    Gene name
    Score
    OMIM
    OMIM Phenotype
    DO term
    Complementation?
    Transgene?
    Functional Complementation Data
    Functional complementation data is computed by FlyBase using a combination of the orthology data obtained from DIOPT and OrthoDB and the allele-level genetic interaction data curated from the literature.
    Interactions
    Summary of Physical Interactions
    esyN Network Diagram
    Show neighbor-neighbor interactions:
    Select Layout:
    Legend:
    Protein
    RNA
    Selected Interactor(s)
    Interactions Browser

    Please see the Physical Interaction reports below for full details
    RNA-protein
    Physical Interaction
    Assay
    References
    protein-protein
    Physical Interaction
    Assay
    References
    Summary of Genetic Interactions
    esyN Network Diagram
    esyN Network Key:
    Suppression
    Enhancement

    Please look at the allele data for full details of the genetic interactions
    Starting gene(s)
    Interaction type
    Interacting gene(s)
    Reference
    Starting gene(s)
    Interaction type
    Interacting gene(s)
    Reference
    External Data
    Linkouts
    BioGRID - A database of protein and genetic interactions.
    DroID - A comprehensive database of gene and protein interactions.
    InterologFinder - Protein-protein interactions (PPI) from both known and predicted PPI data sets.
    MIST (genetic) - An integrated Molecular Interaction Database
    MIST (protein-protein) - An integrated Molecular Interaction Database
    Pathways
    Gene Group - Pathway Membership (FlyBase)
    External Data
    Linkouts
    SignaLink - A signaling pathway resource with multi-layered regulatory networks.
    Genomic Location and Detailed Mapping Data
    Chromosome (arm)
    3R
    Recombination map
    3-48
    Cytogenetic map
    Sequence location
    3R:6,864,324..6,866,244 [+]
    FlyBase Computed Cytological Location
    Cytogenetic map
    Evidence for location
    84A6-84A6
    Limits computationally determined from genome sequence between P{PZ}pb04498 and P{lacW}l(3)L2100L2100
    Experimentally Determined Cytological Location
    Cytogenetic map
    Notes
    References
    84B1-84B1
    (determined by in situ hybridisation)
    84B1-84B2
    (determined by in situ hybridisation)
    Experimentally Determined Recombination Data
    Left of (cM)
    Right of (cM)
    Notes
    Stocks and Reagents
    Stocks (23)
    Genomic Clones (20)
    cDNA Clones (12)
     

    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.

    cDNA clones, fully sequences
    BDGP DGC clones
    Other clones
    Drosophila Genomics Resource Center cDNA clones

    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.

    cDNA Clones, End Sequenced (ESTs)
    BDGP DGC clones
      RNAi and Array Information
      Linkouts
      DRSC - Results frm RNAi screens
      GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
      Antibody Information
      Laboratory Generated Antibodies
      Commercially Available Antibodies
       
      Other Information
      Relationship to Other Genes
      Source for database identify of
      Source for identity of: ftz CG2047
      Source for database merge of
      Additional comments
      Other Comments
      DNA-protein interactions: genome-wide binding profile assayed for ftz protein in 2-3 hr embryos; see BDTNP1_TFBS_ftz collection report.
      The LRALL motif is needed for the strong segmentation function of ftz.
      Nucleotides 1374 to 1570 contains the minimal signal required for RNA localisation of ftz in the blastoderm and ovary.
      Parasegment widths are defined early in the embryo by the relative levels of ftz and eve proteins at stripe junctions.
      Two RNA instability elements in the protein-coding region of ftz have been identified; the 63bp "FIE5-1" and 69bp "FIE5-2" elements. The function of both elements is position dependent; RNAs are destabilised when the elements are present within the coding region, but not when embedded in the 3' UTR. Each instability element is sufficient to destabilise a normally stable mRNA (RpLP2) but the destabilising activity is dependent on their position within the mRNA.
      ftz may represent a category of LXXLL motif-dependant coactivators for nuclear receptors.
      ftz influences ftz-f1 activity by interacting with its AF-2 domain in a manner that mimics a nuclear receptor co-activator.
      ttk accessory peptide N-terminal to the first zinc finger directly interacts with DNA, both in specific and nonspecific DNA-protein complexes.
      ftz and eve are expressed in the pole cells of nos- embryos.
      The phosphorylation state of the Thr-263 residue of ftz appears to be irrelevant for ftz function in the developing central nervous system.
      ftz transcript localization in blastoderm embryos involves sqd, which selectively binds to the ftz 3' UTR.
      Both positively and negatively regulated ftz target genes respond to ftz with the same kinetics as autoregulation. The rate limiting step is the time required for regulatory proteins to enter or be cleared from the nucleus. The matching of these processes is probably important for the rapid and synchronous progression of expression from one class of segmentation genes to the next.
      slp1 protein may be a direct repressor of the ftz gene in developing embryos.
      Amino acid residue T263 in the N-terminus of the ftz homeodomain is phosphorylated when ftz protein is in its active form, and phosphorylation probably affects a protein-protein interaction.
      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.
      Mutants are isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis: mutants exhibit pair-rule pattern defects.
      The AE1 enhancer element (which interacts with the ftz promoter in vivo) preferentially activates TATA-containing promoters when challenged with linked TATA-less promoters.
      Trl- and Iswi-mediated disruption of the chromatin structure within the promoter region of ftz activates transcription on the chromatin template.
      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.
      ftz and ftz-f1 encode mutually dependent cofactors that interact both in vitro and in vivo through a conserved domain in the ftz polypeptide.
      The nuclear hormone receptor ftz-f1 product is a cofactor for the homeodomain protein of ftz.
      ftz protein lacking the homeodomain can directly regulate ftz-dependent segmentation, suggesting that it can control target gene expression through interactions with other proteins. A likely candidate is the pair-rule protein prd.
      Analysis of Mmus\Hoxa7-Ecol\lacZ reporter constructs shows that the Mmus\Hoxa7 intron can function as an enhancer in Drosophila, and contains potential binding sites for cad and ftz.
      Probes labelled with digoxigenin, fluorescein and biotin allow detection of RNA of three different genes in three different colours.
      The gene product of ftz has homeodomain-independent activity. Activation of ftz-dependent en expression and activation of the ftz enhancer are homeodomain independent.
      Initiation of ftz transcription is regulated by the concentration of maternally loaded ttk. Altering the dose of ttk in embryos shifts the activation of ftz transcription either forward or backward during development but does not affect Kr activation.
      At least two sequences mediate destabilisation of the ftz mRNA. One is located in the 5' one third of the mRNA and another is located within a 201-nucleotide region of the 3' UTR, near the polyadenylation site, termed FIE3 (ftz instability element 3').
      The repression function of en::ftzEFE.hs is contributed by several domains, including the C-terminal region flanking the homeodomain and a conserved region found in the N-terminal repression domain.
      ftz protein has broad DNA recognition properties in vitro that are likely to be important determinants of its distribution on DNA in vivo.
      Most metazoan homeodomains share a preference for the TAAT motif, they can differ from each other in their preference for the bases immediately 3' to this core. This preference is determined, in part, by the identity of amino acid position 50. Because homeodomain sequences have been identified that possess at least 10 different amino acids at position 50 it is investigated whether multiple DNA binding specificities can be conferred by changing this position to a variety of amino acid side chains.
      Four neuroblast molecular markers (svp, pros, en and ftz) have been used to demonstrate that some neuroblasts are homologous between insects (Drosophila and Schistocerca). They have similar position, time of formation and time of gene expression. Results suggest that evolution of the insect CNS has occurred in part through altering the neuroblast pattern and fate.
      The ftz protein is specifically phosphorylated on serine and threonine residues at 3 to 4 hr after egg laying.
      Regulatory sequences that direct reporter gene expression in an Scr-like pattern in the anterior and posterior midgut are embedded in the regulatory region of the ftz gene.
      The sequence of the proximal part of the 'zebra' element of the ftz gene has been compared in a number of Drosophila species.
      Protein-protein interactions and phosphorylation are two factors that play a major role in determining the specificity of action of the homeodomain containing protein ftz.
      odd and nkd are required to restrict en expression. odd represses expression of ftz, an activator of en. nkd prevents activation of en by ftz without affecting ftz expression. In odd mutants the altered expression patterns of ftz, en and wg lead to the changes in positional identities of cells that causes mirror image duplications of the body pattern.
      run and h act on ftz with opposing effect via a common 32 bp element, the fDE1. run acts via transcriptional activation and h acts via transcriptional repression. The fDE1 contains a binding site for a small family of orphan nuclear receptor proteins that are uniformly expressed in blastoderm embryos.
      The heat induced phenotype of wild type embryos mimics the ftzUal1 mutant (a phenocopy), not only in the adult phenotype but also by several molecular and genetic criteria. The crucial lesion in this phenocopy is interference with proper ftz turnover, causing ftz overexpression.
      ftz mRNA degradation is mediated by a sequence specific factor that binds the 200bp FIE3 ftz instability element. Competition with excess FIE3 RNA hinders ftz mRNA decay.
      Within the hierarchy of genes expressed in GMC4-2a nub and pdm2 lie downstream of pros and ftz and upstream of eve.
      The expression pattern of ftz RNA during embryogenesis has been investigated.
      Comparisons of early development to that in other insects have revealed conservation of some aspects of development, as well as differences that may explain variations in early patterning events.
      NMR experiments determine the complete solution structure of the ftz homeodomain and compare it to that of the Antp homeodomain.
      In vivo crosslinking has been used to directly measure DNA binding of the homeodomain protein ftz. ftz protein binds at uniformly high levels throughout the length of their genetically identified target genes and at a lower, but significant level to genes ftz is not expected to regulate. Studies suggest that ftz and eve has similar DNA binding specificities in vivo.
      In situ hybridisation using pre-embedded methods have been used to demonstrate that mitochondrial large ribosomal RNA is associated with polar granules in the pole plasm of cleavage embryos.
      Transient expression assays using Ecol\CAT reporter gene constructs have been used to define the sequences responsible for the synergistic action of ftz and prd, these have been mapped to different regions of the two proteins. ftz protein has a synergistic effect on transcription of a target promoter in the presence of prd protein that is apparently entirely independent of binding of ftz protein to the promoter DNA. This synergism is dependent on the presence of homeodomain DNA binding sites in the promoter and does not occur at active promoters that are not regulated by homeodomain.
      The highly complex pattern of ttk expression suggests specific functions for ttk late in development that are separate from the regulation of ftz. Ectopic ttk expression causes complete or near complete repression of ftz and significant repression of eve, odd, h and runt.
      Expression of the trn pair rule stripes requires ftz and ems.
      Activity of the glutamine rich ftz activation domain is blocked by truncated TfIIB derivatives in Schneider L2 cells suggesting the block is mediated by interactions with TfIIB.
      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. DNaseI footprinting studies reveal the proximal enhancer contains a cluster of nuclear protein binding sites.
      The male Sxl exon is subject to Sxl regulation when a fragment containing the exon plus flanking intron sequences is placed in the introns of two different genes, ftz and w.
      wg expression is aberrantly activated and regulated in pair rule mutant embryos.
      The role of ftz in the regulation of run mRNA expression in the early embryo has been investigated.
      DNA elements both 3' and 5' to the coding region that are important in proper regulation of expression are the most evolutionarily conserved regions in the vicinity of gene homologs.
      The BRE region of Ubx includes binding sites for hb, ftz, tll, en and twi. The binding of their products and the interplay between them is responsible for generating the expression pattern directed by the BRE.
      The homologs of Antp, ftz, Scr, Dfd, Ama, bcd, zen, pb and lab, but not zen2 are all present in D.pseudoobscura.pseudoobscura, in the same linear order and similarly spaced along the chromosome as in D.melanogaster.
      The D.melanogaster ftz autoregulatory domain, AE, is a direct target for the ftz homeodomain gene product. Deletion analysis defines multiple elements redundantly involved in enhancer activity. Several of these elements are conserved in the AE homologs of D.virilis and D.hydei and in the developmentally regulated eve and Ubx genes. The AE homolog of D.virilis is functional in D.melanogaster.
      Specific DNA binding is an important but not sufficient determinant of the functional specificity of ftz in vivo. Binding of ftz to homeodomain binding site BS2 of en has been studied: specificity mutations only partially reduce enhancer activity as compared to null mutations of this site.
      Comparative analysis of the homeobox sequences reveals the subdivision of the Antp-type homeobox genes into three classes early in metazoan evolution, one includes Abd-B, the second includes abd-A, Ubx, Antp, Scr, Dfd and ftz, and the third includes zen, zen2, pb and lab.
      The induction of a ftz-specific ribozyme mimics the effects of known ftz mutations. Expression of the ftz ribozyme at the blastoderm stage caused ftz-like morphological defects in the resulting first instar larval cuticles: the second thoracic segment and the odd-numbered abdominal segments are completely deleted in the most severely affected cuticles. Expression during development of the central nervous system affects the morphology and/or migration of neurons.
      Expression analysed in CNS study of neuroblasts and ganglion mother cells, using a ftz-lacZ fusion gene.
      Distamycin and the ftz homeodomain peptide compete for their DNA binding sites. This demonstrates that minor groove binders can compete with the binding of proteins in the major groove, providing an experimental indication for the influence of biological activities exerted by DNA ligands binding in the minor groove.
      Mutational analysis of the helix-turn-helix motif has revealed a set of class-specific DNA backbone contacting residues, particularly Arg28 and Arg43 that are required for efficient target site recognition and full ftz activity both in vivo and in vitro.
      Post cellularization ftz expression is repressed by ectopic eve expression, precellularization ectopic eve expression stimulates ftz expression.
      Footprint analysis and tests in transformed embryos of Ubx-lacZ fusions bearing mutated footprinted regions suggest that ftz protein acts directly as a transcriptional activator of Ubx.
      In csw- embryos hb remains as a posterior cap and the seventh ftz stripe expands posteriorly, both due to lack of hkb repressing activity.
      Maternally supplied ttk protein helps to establish the timing of the onset of zygotic expression of eve and ftz thereby preventing premature activation.
      Upstream region deletion derivatives of ftz driving Ecol\lacZ expression have demonstrated that the ftz gene product acts as a DNA-binding transcriptional activator during embryogenesis.
      Mutant analysis shows that wild type ftz function is required to set up expression of ac and sc in row D of the embryonic proneural cluster.
      Pattern of hh expression in ftz mutants studied.
      The ttk product binds to the zebra stripe element of the ftz promoter, behaving as a transcriptional repressor.
      Apical localization of pair-rule transcripts restricts lateral protein diffusion allowing pair-rule proteins to define sharp boundaries and precise spatial domains.
      The DNA binding properties of the ftz homeodomain have been studied in vitro.
      Nuclear extracts prepared from developmentally staged embryos were transcriptionally active for several non-muscle genes: Tm2 non-muscle promoter, Act5C, ftz, Adh and en.
      Mutations in zygotic pair rule gene ftz interact with RpII140wimp. Ecol\lacZ reporter gene constructs demonstrate that mutations of ftz interact with RpII140wimp.
      Mutant ftz embryos do not alter the expression of the Ubx bx region enhancer element, BRE.
      The activator and repressor functions sufficient to generate a stripe pattern of transcription are encoded in the ftz promoter.
      Deletions and subfragments of the ftz scaffold attached region have been analysed in yeast and Drosophila to define the sequences involved in scaffold association.
      The effect of hkb, fkh and tll on ftz expression has been studied.
      Germline transformation of ftz:lacZ promoter fusion genes demonstrate that the ftz promoter can be divided into three functional subunits (Hiromi, Cell 43: 603): an enhancer element, an element that influences neural expression and a region that is sufficient for the generation of the seven stripe pattern.
      ftz mutants exhibit pattern deletions that correspond to even numbered segments.
      Mutants show a deletion of all even numbered parasegments. Temperature sensitive alleles demonstrate that ftz is required for cell viability and pattern formation between 1--4 hours of embryogenesis.
      In saturation mutagenesis of a protein a background of nonsense mutations can complicate genetic analysis of the resulting mutations. Methods are proposed for elimination of those molecules containing stop codons at the target codon from the pool. Application of these methods should ensure that all changes are missense mutations, thereby simplifying genetic analysis.
      ftz has been cloned and sequenced. Comparison with Dhyd\ftz shows that the overall organisation of the gene is similar in both species.
      ftz protein distribution is altered in mutant cad embryos: stripes 2, 3 and 4 are abnormally spaced and reduced, posterior stripes stain stronger than anterior stripes.
      DNAse I footprinting of ftz binding sites near the two Antp promoters identifies a consensus sequence including ATTA, as does the consensus sequence for en, eve and bcd binding sites. DNA bending is proposed as an explanation for the presence of a shared motif between proteins with divergent recognition helices. The ATTA would not directly contact amino acid side chains of the recognition helix, but would be necessary for bending the DNA around the homeodomain, perhaps facilitating protein-DNA contacts.
      ftz protein directly activates transcription by binding to homeodomain binding sites in vitro. en protein represses transcriptional activation by ftz protein by competition for binding to homeodomain binding sites in vitro.
      Deletion analysis of the ftz upstream element defines several independent regulatory units, including at least two independent enhancers. The enhancers are autoregulated independently by the wild type ftz gene product and contain multiple binding sites for purified ftz homeodomain. Results suggest that the ftz gene product is one of the trans-acting factors that acts directly to positively regulate transcription of the ftz gene.
      The role of segment polarity genes in arm protein accumulation has been investigated.
      ftz-f1 encodes a transcriptional activator necessary for the proper expression of the ftz gene. The ftz-f1 product binds to two sites located within the zebra element of the ftz promoter and to two sites located within the ftz coding region.
      ftz transcription is activated in each parasegment through the "zebra stripe" promoter region and is then inhibited selectively in the odd numbered parasegments by repressors that bind directly to elements within this promoter region.
      cad can increase the level of transcription from ftz-Ecol\lacZ promoter fusion constructs in vitro.
      Injection of protein synthesis inhibitors into early embryos induces expression of ftz mRNA in virtually all regions of the embryo.
      The ability of ftz-Scer\GAL4 fusion genes to activate transcription has been studied in yeast cells, and suggests that ftz may act as a positive regulator of transcription.
      A transient expression assay has been employed to investigate the potential of homeobox genes to function as transcriptional activators.
      An investigation of the role of gap genes in expression from Ubx and Antp promoters in the blastoderm embryo reveals that a unique combination of gap genes and pair rule genes is required for their initial activation.
      Heat shock constructs have been used to distinguish between two models that try to explain the generation of embryonic pattern: the "cell identity" and parasegmental models.
      Novel ftz protein expression has been detected in very early embryos (before the cellular blastoderm stage) using a sensitive immunocytochemical staining technique.
      ftz protein is phosphorylated at multiple sites, and at different subsets of these sites during different stages of development.
      The development of the eve and ftz stripes in h-, run-, eve- and en- embryos demonstrates that individual cells are allocated to parasegments with respect to the anterior margins of the eve and ftz stripes.
      Genetic analysis demonstrates that ftz is not required for efficient homeotic gene expression in the visceral mesoderm.
      Cotransfection assays have been used to demonstrate that the homeodomain proteins encoded by ftz can specifically activate transcription of certain promoters by acting upon a common sequence to modulate gene transcription.
      ftz protein expression has been studied.
      The mutant phenotype of flies that direct normal ftz expression in blastoderm stripes but not in the developing CNS suggests that ftz controls cell identity during neurogenesis.
      The ftz enhancer-like upstream element (USE) has been sequenced, and the binding sites for embryonic nuclear proteins within this region have been determined by in vitro DNAase I footprinting.
      ftz binding sites inserted upstream of promoters act as ftz-dependent enhancers in culture cells. This suggests that ftz acts by binding to the inserted sites to activate the linked promoter. en is also able to bind to sites that confer ftz responsiveness.
      Inactivation of the ftz gene serves to significantly increase the penetrance of the hbD1 phenotype.
      The expression of ftz has been used as a positional marker to investigate the relationship between the dorsoventral and anteroposterior axes in the embryo.
      The pattern of ftz RNA and protein expression in blastoderm embryos with disrupted cellularisation has been studied.
      ftz protein expression has been analysed in various mutants that disrupt segmentation.
      The DNA sequences of the homeobox region of 11 Drosophila genes, including ftz, have been compared.
      Pattern defects caused by inappropriate h expression are due to misregulation of ftz and other segmentation genes, h behaves as a negative regulator of ftz.
      ftz transcript localization was compared to prd transcript localization.
      Cis-acting control elements of ftz have been mapped by P-element mediated transformation.
      Null loss-of-function mutations result in embryonic lethality. Animals survive to the end of embryogenesis and exhibit a pair-rule mutant phenotype in the cuticle. This same phenotype is observable in animals at the beginning of segmentation of the germ band. Prior to deposition of cuticle, ftz- animals have two rather than three mouth (gnathocephalic) segments and five as compared to ten trunk metameres. The material deleted is derived from the even-numbered parasegments, ps2 through ps12. Similar metameric deletions/fusions are seen in the neuromeres of the ventral nerve cord of the CNS. Temperature-sensitive alleles of the gene have shown that the temperature-critical period for viability and phenotype falls between 1 and 4 hours of embryogenesis with the mid-point of 2.5 hours at the blastoderm stage. The recovery of clones of ftz- cells created by X-ray-induced somatic exchange after cellular blastoderm have demonstrated that ftz+ activity is not necessary for normal cuticular morphogenesis subsequent to this point in development. In addition to these recessive null and hypomorphic alleles there are two classes of dominant gain-of-function lesions at the ftz locus. The first, ftz-Regulator of postbithorax-like, causes a variable transformation of the posterior haltere into posterior wing. The second, ftz-Ultra-abdominal-like, is associated with a patchy transformation of the adult first abdominal segment toward third abdominal identity. The former (ftzRpl) lesion also shows a recessive loss-of-function phenotype while the latter class (ftzUal) has no discernible embryonic phenotype and is homozygous viable. The fact that these dominant alleles produce mutant phenotypes that mimic lesions in the BXC has been interpreted as demonstrating a regulatory link between the segment enumeration genes and the homeotics.
      Origin and Etymology
      Discoverer
      Etymology
      The name of the locus derives from the phenotype and is Japanese for 'segment' (fushi) 'deficient' (tarazu).
      Identification
      External Crossreferences and Linkouts ( 56 )
      Sequence Crossreferences
      NCBI Gene - Gene integrates information from a wide range of species. A record may include nomenclature, Reference Sequences (RefSeqs), maps, pathways, variations, phenotypes, and links to genome-, phenotype-, and locus-specific resources worldwide.
      GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
      GenBank Protein - A collection of sequences from several sources, including translations from annotated coding regions in GenBank, RefSeq and TPA, as well as records from SwissProt, PIR, PRF, and PDB.
      RefSeq - A comprehensive, integrated, non-redundant, well-annotated set of reference sequences including genomic, transcript, and protein.
      UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
      UniProt/TrEMBL - Automatically annotated and unreviewed records of protein sequence and functional information
      Other crossreferences
      BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
      Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
      Flygut - An atlas of the Drosophila adult midgut
      GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
      KEGG Genes - Molecular building blocks of life in the genomic space.
      modMine - A data warehouse for the modENCODE project
      PDB - An information portal to biological macromolecular structures
      Rfam - A collection of RNA sequence families of structural RNAs including non-coding RNA genes as well as cis-regulatory elements
      SignaLink - A signaling pathway resource with multi-layered regulatory networks.
      Linkouts
      BioGRID - A database of protein and genetic interactions.
      DPiM - Drosophila Protein interaction map
      DroID - A comprehensive database of gene and protein interactions.
      DRSC - Results frm RNAi screens
      FLIGHT - Cell culture data for RNAi and other high-throughput technologies
      FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
      FlyMine - An integrated database for Drosophila genomics
      Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
      InterologFinder - Protein-protein interactions (PPI) from both known and predicted PPI data sets.
      MIST (genetic) - An integrated Molecular Interaction Database
      MIST (protein-protein) - An integrated Molecular Interaction Database
      Synonyms and Secondary IDs (20)
      Reported As
      Symbol Synonym
      BG:DS07876.1
      Ual
      ftz
      (Graham et al., 2019, Shokri et al., 2019, Abed et al., 2018, Adamidou et al., 2018, Baron et al., 2018, Bischof et al., 2018, Lim et al., 2018, Hang and Gergen, 2017, Karaiskos et al., 2017, Transgenic RNAi Project members, 2017-, Vazquez-Pianzola et al., 2017, Bürglin and Affolter, 2016, Field et al., 2016, Hauptmann et al., 2016, Kwon et al., 2016, Ma et al., 2016, Ma et al., 2016, Sarov et al., 2016, Dahlberg et al., 2015, Dehghani and Lasko, 2015, Kok et al., 2015, Li et al., 2015, Zhao et al., 2015, Bischof and FlyORF project members, 2014.6.20, Ciglar et al., 2014, Guilgur et al., 2014, Jiang and Singh, 2014, Vazquez-Pianzola et al., 2014, Chen et al., 2013, Heffer and Pick, 2013, Heffer et al., 2013, Hernández et al., 2013, Jennings, 2013, Li and Gilmour, 2013, Samee and Sinha, 2013, Saunders et al., 2013, Surkova et al., 2013, Webber et al., 2013, Zeidler and Bausek, 2013, Andrioli et al., 2012, Aswani et al., 2012, Garcia et al., 2012, Ghosh et al., 2012, Japanese National Institute of Genetics, 2012.5.21, Kvon et al., 2012, Nikulova et al., 2012, Stern et al., 2012, Turki-Judeh and Courey, 2012, Abed et al., 2011, Chung et al., 2011, Fowlkes et al., 2011, Kaplan et al., 2011, Kim et al., 2011, Kuzin et al., 2011, Li and Arnosti, 2011, Li et al., 2011, Myasnikova et al., 2011, Nègre et al., 2011, Nien et al., 2011, Roy et al., 2011, Schroeder et al., 2011, Seong et al., 2011, Singh et al., 2011, Taliaferro et al., 2011, Thomas et al., 2011, Tsurumi et al., 2011, Walrad et al., 2011, Yoo et al., 2011, Braid et al., 2010, Gonsalvez et al., 2010, Haley et al., 2010, Heffer et al., 2010, Hueber et al., 2010, Prazak et al., 2010, Ribeiro et al., 2010, Scheuermann et al., 2010, The modENCODE Consortium, 2010, The modENCODE Consortium, 2010, Walrad et al., 2010, Wang et al., 2010, Yassin et al., 2010, Berry et al., 2009, Dienstbier et al., 2009, Fang et al., 2009, Fujioka et al., 2009, Herold et al., 2009, Hou et al., 2009, Iovino et al., 2009, Lee et al., 2009, Liu et al., 2009, Liu et al., 2009, Myasnikova et al., 2009, Ni et al., 2009, Pisarev et al., 2009, Saleh et al., 2009, Schaaf et al., 2009, Tchuraev and Galimzyanov, 2009, Weber et al., 2009, Zhai et al., 2009, Anderson and Pick, 2008, Andrioli et al., 2008, Beckervordersandforth et al., 2008, Fowlkes et al., 2008, Hanyu-Nakamura et al., 2008, Heffer and Pick, 2008, Hsouna and VanBerkum, 2008, Ishihama et al., 2008, Jennings et al., 2008, Juven-Gershon et al., 2008, Kwong et al., 2008, Larsen et al., 2008, McDermott and Kliman, 2008, Noyes et al., 2008, Schroeder and Gaul, 2008, Segal et al., 2008, Surkova et al., 2008, Surkova et al., 2008, Tarone et al., 2008, Aerts et al., 2007, Chicoine et al., 2007, Dorsten et al., 2007, Duboule, 2007, Mito et al., 2007, Negre and Ruiz, 2007, Ogishima and Tanaka, 2007, Prazak et al., 2007, Roy et al., 2007, Takada et al., 2007, Ullah et al., 2007, Vanderzwan-Butler et al., 2007, Vendra et al., 2007, Wang et al., 2007, Xing et al., 2007, Bartolome and Charlesworth, 2006, Choksi et al., 2006, Jamieson et al., 2006, Jennings et al., 2006, Keranen et al., 2006, Luengo Hendriks et al., 2006, Mogila et al., 2006, Tokunaga et al., 2006, Tucker and Chiquet-Ehrismann, 2006, Delanoue and Davis, 2005, Fox et al., 2005, Hoskins et al., 2005, Leaman et al., 2005, Pearson et al., 2005, Peel et al., 2005, Reinking et al., 2005, Sage et al., 2005, Shav-Tal and Singer, 2005, Snee et al., 2005, Berman et al., 2004, Grad et al., 2004, Riede, 2004, Ronshaugen and Levine, 2004, Hsouna et al., 2003, McDonald et al., 2003, Greenberg and Schedl, 2001, Hauptmann, 2001, Wilkie et al., 2001, Martinez Arias et al., 1988)
      l(3)84Ag
      Name Synonyms
      FUSHI-TARAZU
      Fushi Tarazu
      Fushi-Tarazu
      Ultra-abdominal-like
      Secondary FlyBase IDs
      • FBgn0014176
      Datasets (2)
      Study focus (2)
      Experimental Role
      Project
      Project Type
      Title
      • bait_protein
      ChIP characterization of transcription factor genome binding, Berkeley Drosophila Transcription Factor Network Project.
      • bait_protein
      Genome-wide localization of transcription factors by ChIP-chip and ChIP-Seq.
      References (983)