General Information
Symbol
Dmel\dl
Species
D. melanogaster
Name
dorsal
Annotation Symbol
CG6667
Feature Type
FlyBase ID
FBgn0260632
Gene Model Status
Stock Availability
Gene Snapshot
Dorsal is a transcription factor that functions with Dif, downstream of the Toll pathway. It contributes to certain functions of the Toll pathway, notably the dorsoventral patterning of early embryo. [Date last reviewed: 2016-06-30]
Also Known As
Dorsal, NFκB, GSd447
Genomic Location
Cytogenetic map
Sequence location
2L:17,436,830..17,450,364 [-]
Recombination map
2-53
Sequence
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
GO Summary Ribbons
Families, Domains and Molecular Function
Gene Group Membership (FlyBase)
Protein Family (UniProt, Sequence Similarities)
-
Summaries
Gene Group Membership
NUCLEAR FACTOR - KAPPA B -
The NF-κB transcription factor family share an N-terminal Rel homology domain. NF-κB transcription factors play a major role in development and immunity. (Adapted from FBrf0155649 and FBrf0210750).
UniProt Contributed Function Data
Embryonic developmental protein (PubMed:2598266, PubMed:10072776). The lateral or ventral identity of a cell depends upon the concentration of this protein in its nucleus during the blastoderm stage (PubMed:2598266). A morphogenetic protein that specifically binds to the kappa B-related consensus sequence 5'-GRGAAAANCC-3', located in the enhancer region of zygotic genes such as Zen, Twist, Snail and Decapentaplegic. Mediates an immune response in larvae (PubMed:10072776). Part of a signaling pathway involving NF-kappa-B and Toll-related receptors, that functions in the apoptosis of unfit cells during cell competition (PubMed:25477468). May be part of a NF-kappa-B and Tollo signaling cascade that regulates development of the peripheral nervous system (PubMed:18000549).
(UniProt, P15330)
Phenotypic Description from the Red Book (Lindsley and Zimm 1992)
dl: dorsal
Embryos produced by homozygous dl females form normal cellular blastoderm but at gastrulation develop into yolk-filled tube of dorsal hypoderm. Hair pattern of cuticle characteristic of dorsal hypoderm; ventral structures, such as denticle belts, lacking. Normally, dorsal infoldings occupy entire circumference of embryo. Evidence of anterior-posterior differentiation includes possible mouth armature structures anteriorly, small spiracles posteriorly, and orientation of hairs. The periodicity of stripes of ftz expression in pre gastrulation embryos, as revealed by antibody staining, displays the pattern normally characteristic of the dorsum circumferentially in embryos produced by dl females (Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32. Embryos produced by dl/dl and dl/Df(2L)TW137 indistinguishable, suggesting dl to be amorphic. Penetrance complete; expression constant. Embryos of dl2 females lack all structures normally derived from the ventral half of the egg, including mesoderm, endodermal gut, ventral nervous system, and ventral hypoderm. dl1 and to a lesser extent dl2, females produce embryos with reduced capacity for neurogenesis in response to an absence of dl function (Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 317-26). dl germ line dependent; homozygous germ-line clones produce dorsalized embryos (Schupbach and Wieschaus, 1986, Dev. Biol. 113: 443-48). Embryos of dl/+ females produced at 29 develop into comparatively normal-looking larvae; they mainly lack internal organs, such as mesoderm and parts of the anterior and posterior gut; often ventral hypoderm including denticle belts reduced; phenotype sensitive to genetic background. At 22, dl/+ females produce normal embryos. Developmental fate of ventrally located cells on cellular blastoderm apparently shifted to that of more dorsally located cells. The phenotype of embryos produced by dl/dl females partially rescued by the injection of wild-type cytoplasm but not RNA (Santamaria and Nusslein-Volhard, 1983, EMBO J. 2: 1695-99; Anderson and Nusslein-Volhard, 1944, Nature 34: 225-27). Developmental profiles show transcript to be present only in ovaries and pre-cellular-blastoderm stages of embryogenesis. In situ hybridization indicates that ovarian transcript accumulates in nurse cells from stage 5 to 11; number of transcripts per genome equivalent in these polytene cells remains low and constant until stage 10, at which time there is a dramatic increase in the relative numbers of transcripts. After a lag of one or two nuclear divisions, transcript begins to accumulate in the oocyte; by stage 12 there is little detectable transcript in the nurse cells. It appears as though the nurse-cell transcript is transferred to the oocyte and thus to the embryo; transcript seems to be uniformly distributed in stage 14 oocytes (Steward, Ambrosio, and Schedl). dl protein is uniformly distributed throughout cytoplasm of early embryo; in the syncytial blastoderm a gradient of expression is achieved by the graded transport of dl protein into nuclei, with the highest nuclear concentrations found ventrally; protein remains cytoplasmic dorsally. Maternal dorsalizing mutants prevent nuclear localization and ventralized embryos show dorsal as well as ventral nuclear localization (Steward, Zusman, Huang, and Schedl, 1988, Cell 55: 487-95; Rushlow, Han, Manley, and Levine, 1989, Cell 59: 1165-77; Steward, 1989, Cell 59: 11179-88; Roth, Stein, and Nusslein-Volhard, 1989, Cell 59: 1189-1202).
Gene Model and Products
Number of Transcripts
6
Number of Unique Polypeptides
2

Please see the GBrowse view of Dmel\dl or the JBrowse view of Dmel\dl 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
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Low-frequency RNA-Seq exon junction(s) not annotated.
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)
FBtr0081005
2489
677
FBtr0081006
2833
677
FBtr0081007
4724
999
FBtr0301383
2590
677
FBtr0301384
2504
677
FBtr0340250
4481
999
Additional Transcript Data and Comments
Reported size (kB)
4.4, 2.8 (northern blot)
2.8 (longest cDNA)
2.8 (northern blot)
Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
RefSeq ID
GenBank
FBpp0080558
75.3
677
8.10
FBpp0080559
75.3
677
8.10
FBpp0080560
111.6
999
5.04
FBpp0290597
75.3
677
8.10
FBpp0290598
75.3
677
8.10
FBpp0309222
111.6
999
5.04
Polypeptides with Identical Sequences

The group(s) of polypeptides indicated below share identical sequence to each other.

677 aa isoforms: dl-PA, dl-PB, dl-PD, dl-PE
999 aa isoforms: dl-PC, dl-PF
Additional Polypeptide Data and Comments
Reported size (kDa)
994 (aa); 190 (kD observed); 110 (kD predicted)
85 (kD observed)
83 (kD observed)
75 (kD predicted)
677 (aa); 75.6 (kD predicted)
Comments
lwr protein was shown to bind and conjugate smt3 protein to dl protein. In addition, lwr protein releives the inhibition of dl protein nuclear uptake by cact protein in cultured cells.
The unique C-terminal portion of the large dl protein isoform has a transactivation domain and is able to induce the expression of a reporter gene in transient transfection assays in mouse 3T3 cells. The C-terminal activation domain was mapped by deletion mapping to between residues 576 and 638.
Two mutant dl proteins (dlS234P.Scer\adh1 and dlC233R.Scer\adh1) that activate transcription but are insensitive to inhibition by cact were isolated by a yeast assay. These mutant dl proteins are able to enter the nucleus, bind DNA, and activate transcription but are unable to bind cact protein. The surface of dl protein that is likely to bind cact protein was identified.
Two mutant dl proteins (dlS234P.Scer\adh1 and dlC233R.Scer\adh1) that activate transcription but are insensitive to inhibition by cact were isolated by a yeast assay. These mutant dl proteins are able to enter the nucleus, bind DNA, and activate transcription but are unable to bind cact protein. The surface of dl protein that is likely to bind cact protein was identified.
Small sequential deletions in the dl protein were used to map various functional regions of the protein. Sequences that are necessary for DNA binding map between residues 47 and 230. Two regions were mapped which are involved with inhibitor binding. Loss of sequences between residues 218-245 (region I) or residues 322-241 (region II)abolishes binding to cact protein. Deletions in residues 246-321 (between regions I and II) reduce but do not abolish cact binding. Mutation of highly conserved residues 231-237 in region I nearly abolishes binding. Mutation of sequences in region II containing the nuclear localization signal (residues 335-340) result in near or complete failure to bind cact protein. Finally, point mutations in the region I sequence can uncouple DNA binding and inhibitor interactions.
Disulfide crosslinking studies were used to show that dl and cact proteins exist as three different complexes in the embyro. Complex 1 (190kD) is a dl homodimer (dl2). Complex 2 (270kD)consists of a complex 1 and a cact molecule (dl2cact). Complex 3 is a cact protein complex. In wild type embryos, complex 1 was observed as the major form of dl protein and complex 2 was a minor form. Virtually no dl monomer was detected. Mutant analysis indicates that complex 1 is a cytoplasmic form while complex 2 is mainly nuclear.
Immunoprecipitation studies in embryos which contain a dl-lacZ protein fusion construct show that the dl protein can self associate in a protein complex. In early embryonic extracts, dl protein is found in large complexes of about 200kD. These are thought to be either dl homodimers and cact protein or dl protein multimers.
The cact binding site on the dl protein was localized to the region between amino acids 168 and 350 and is thought to include residues around aa270. This is within the RH domain (amino acid 47-341) and overlaps with or is adjacent to the nuclear localization signal. It overlaps with a region shown to be necessary for dl protein to be retained in the cytoplasm (FBrf0056112).
Cotransfection experiments in Schneider cells show that dl protein activates CAT expression from a zen-CAT construct. CAT activity is enhanced in the presence of either Tl or Pka-C1 proteins. Both Tl and Pka-C1 proteins affect dl protein nuclear localization and dl protein activity in the nucleus. Evidence suggests that the signalling pathway from Tl to dl proteins acts through Pka-C1 protein. dl mutant constructs were tested to map the regions of dl protein required for responses to Tl and Pka-C1 proteins.
External Data
Subunit Structure (UniProtKB)
Interacts with tamo via the nuclear localization signal. Interacts with emb, a component of the nuclear pore complex.
(UniProt, P15330)
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\dl using the Feature Mapper tool.

External Data
Crossreferences
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Linkouts
Gene Ontology (44 terms)
Molecular Function (8 terms)
Terms Based on Experimental Evidence (7 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
Biological Process (30 terms)
Terms Based on Experimental Evidence (10 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (23 terms)
CV Term
Evidence
References
traceable author statement
non-traceable author statement
traceable author statement
non-traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
non-traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
traceable author statement
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
Cellular Component (6 terms)
Terms Based on Experimental Evidence (4 terms)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (4 terms)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
inferred from biological aspect of ancestor with PANTHER:PTN000652441
(assigned by GO_Central )
inferred by curator from GO:0000381
non-traceable author statement
Expression Data
Transcript Expression
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
northern blot
Stage
Tissue/Position (including subcellular localization)
Reference

Comment: reference states 0-2.5 hr AEL

Comment: reference states >=6 hr AEL

Additional Descriptive Data
The larger form of dl transcript is expressed in a tissue specific manner. It is present in larvae and adults of both sexes. The intensity of the band increases upon immune challenge especially in larvae and adult males. dl transcripts are present at low levels in the gut and fat body of unchallenged larvae. The levels are enhanced in the larval fat body after immune challenge. In embryos the larger dl transcript is present from 6-9hr embryos on through embryogenesis.
dl transcripts are detected uniformly in embryos up until the cellular blastoderm stage.
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
mass spectroscopy
Stage
Tissue/Position (including subcellular localization)
Reference
western blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
Only the larger isoform of dl protein can be found in larval neuromuscular junctions.
The larger form of dl protein translocates into the nucleus after bacterial challenge.
cact colocalizes with Fas2 at the larval neuromuscular junction, but is shifted more cytoplasmically than is Fas2.
dl protein is diffusely distributed in the nucleus and cytoplasm of somatic muscles during the last hours of larval development, and though the first four hours of pupariation. dl protein is enriched in the subsynaptic reticulum of type I synaptic boutons. Four hours after pupariation, dl protein is shifted to the nucleus. In adults, the dl protein distibution is similar to that in larvae.
Up until embryonic stage 3, dl protein is localized primarily in the cytoplasm. Between stages 3 and 4 dl protein is localized to nuclei along the ventral side of the embryo and persists through grastrulation.
The dl protein is expressed throughout the embryo, however, by stage 2 markedly higher levels of staining are detected in the ventral region, which persists through gastrulation. dl protein is located primarily in the cytoplasm of nurse cells, and the embryo and moves into the ventral nuclei at cleavage cycle 11. This transition to nuclear localization is proposed to be required for dl function, as it is not observed in dl mutants.
dl protein is cytoplasmic until embryonic cleavage cycle 10, at which point it becomes nuclear. A specific nuclear transport system is proposed to be required for wild type dl function.
Marker for
 
Subcellular Localization
CV Term
Evidence
References
Expression Deduced from Reporters
High-Throughput Expression Data
Associated Tools

GBrowse - Visual display of RNA-Seq signals

View Dmel\dl 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
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
Alleles, Insertions, Transgenic Constructs and Phenotypes
Classical and Insertion Alleles ( 61 )
For All Classical and Insertion Alleles Show
 
Allele of dl
Class
Mutagen
Associated Insertion
Stocks
Known lesion
    0
    --
      0
      --
      Other relevant insertions
      insertion of mobile activating element
      Name
      Expression Data
      miscellaneous insertions
      Name
      Expression Data
      Transgenic Constructs ( 81 )
      For All Alleles Carried on Transgenic Constructs Show
      Transgenic constructs containing/affecting coding region of dl
      Allele of dl
      Mutagen
      Associated Transgenic Construct
      Stocks
      Transgenic constructs containing regulatory region of dl
      reporter construct
      Name
      Expression Data
      Deletions and Duplications ( 20 )
      Summary of Phenotypes
      For more details about a specific phenotype click on the relevant allele symbol.
      Lethality
      Allele
      Sterility
      Allele
      Other Phenotypes
      Allele
      Phenotype manifest in
      Allele
      axon & eye photoreceptor cell, with Scer\GAL4GMR.PF
      axon & eye photoreceptor cell, with Scer\GAL4MT14
      mushroom body & axon, with Scer\GAL47B
      mushroom body & axon, with Scer\GAL4ey-OK107
      Orthologs
      Human Orthologs (via DIOPT v7.1)
      Homo sapiens (Human) (4)
      Species\Gene Symbol
      Score
      Best Score
      Best Reverse Score
      Alignment
      Complementation?
      Transgene?
      9 of 15
      Yes
      Yes
       
      8 of 15
      No
      Yes
      6 of 15
      No
      No
      1 of 15
      No
      No
      Model Organism Orthologs (via DIOPT v7.1)
      Mus musculus (laboratory mouse) (4)
      Species\Gene Symbol
      Score
      Best Score
      Best Reverse Score
      Alignment
      Complementation?
      Transgene?
      9 of 15
      Yes
      Yes
       
      8 of 15
      No
      Yes
      6 of 15
      No
      No
      1 of 15
      No
      No
       
      Rattus norvegicus (Norway rat) (3)
      8 of 13
      Yes
      Yes
      4 of 13
      No
      Yes
      3 of 13
      No
      Yes
      Xenopus tropicalis (Western clawed frog) (3)
      6 of 12
      Yes
      Yes
      5 of 12
      No
      Yes
      1 of 12
      No
      Yes
      Danio rerio (Zebrafish) (3)
      8 of 15
      Yes
      Yes
      8 of 15
      Yes
      Yes
      4 of 15
      No
      No
      Caenorhabditis elegans (Nematode, roundworm) (0)
      No orthologs reported.
      Arabidopsis thaliana (thale-cress) (0)
      No orthologs reported.
      Saccharomyces cerevisiae (Brewer's yeast) (0)
      No orthologs reported.
      Schizosaccharomyces pombe (Fission yeast) (0)
      No orthologs reported.
      Orthologs in Drosophila Species (via OrthoDB v9.1) ( EOG091902FV )
      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 erecta
      Drosophila yakuba
      Drosophila ananassae
      Drosophila pseudoobscura pseudoobscura
      Drosophila virilis
      Drosophila mojavensis
      Orthologs in non-Drosophila Dipterans (via OrthoDB v9.1) ( EOG091500S5 )
      Organism
      Common Name
      Gene
      Multiple Dmel Genes in this Orthologous Group
      Musca domestica
      House fly
      Glossina morsitans
      Tsetse fly
      Lucilia cuprina
      Australian sheep blowfly
      Mayetiola destructor
      Hessian fly
      Aedes aegypti
      Yellow fever mosquito
      Aedes aegypti
      Yellow fever mosquito
      Anopheles darlingi
      American malaria mosquito
      Anopheles gambiae
      Malaria mosquito
      Culex quinquefasciatus
      Southern house mosquito
      Culex quinquefasciatus
      Southern house mosquito
      Culex quinquefasciatus
      Southern house mosquito
      Orthologs in non-Dipteran Insects (via OrthoDB v9.1) ( EOG090W056Y )
      Organism
      Common Name
      Gene
      Multiple Dmel Genes in this Orthologous Group
      Bombyx mori
      Silkmoth
      Danaus plexippus
      Monarch butterfly
      Heliconius melpomene
      Postman butterfly
      Heliconius melpomene
      Postman butterfly
      Apis florea
      Little honeybee
      Apis florea
      Little honeybee
      Apis mellifera
      Western honey bee
      Apis mellifera
      Western honey bee
      Bombus impatiens
      Common eastern bumble bee
      Bombus terrestris
      Buff-tailed bumblebee
      Linepithema humile
      Argentine ant
      Linepithema humile
      Argentine ant
      Megachile rotundata
      Alfalfa leafcutting bee
      Nasonia vitripennis
      Parasitic wasp
      Nasonia vitripennis
      Parasitic wasp
      Nasonia vitripennis
      Parasitic wasp
      Nasonia vitripennis
      Parasitic wasp
      Nasonia vitripennis
      Parasitic wasp
      Dendroctonus ponderosae
      Mountain pine beetle
      Tribolium castaneum
      Red flour beetle
      Tribolium castaneum
      Red flour beetle
      Pediculus humanus
      Human body louse
      Rhodnius prolixus
      Kissing bug
      Cimex lectularius
      Bed bug
      Acyrthosiphon pisum
      Pea aphid
      Acyrthosiphon pisum
      Pea aphid
      Zootermopsis nevadensis
      Nevada dampwood termite
      Orthologs in non-Insect Arthropods (via OrthoDB v9.1) ( EOG090X053D )
      Organism
      Common Name
      Gene
      Multiple Dmel Genes in this Orthologous Group
      Strigamia maritima
      European centipede
      Ixodes scapularis
      Black-legged tick
      Stegodyphus mimosarum
      African social velvet spider
      Stegodyphus mimosarum
      African social velvet spider
      Tetranychus urticae
      Two-spotted spider mite
      Daphnia pulex
      Water flea
      Orthologs in non-Arthropod Metazoa (via OrthoDB v9.1) ( EOG091G07RW )
      Organism
      Common Name
      Gene
      Multiple Dmel Genes in this Orthologous Group
      Strongylocentrotus purpuratus
      Purple sea urchin
      Human Disease Model Data
      FlyBase Human Disease Model Reports
        Alleles Reported to Model Human Disease (Disease Ontology)
        Download
        Models ( 0 )
        Allele
        Disease
        Evidence
        References
        Interactions ( 1 )
        Comments ( 0 )
         
        Human Orthologs (via DIOPT v7.1)
        Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
        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 look at the Interaction Group reports for full details of the physical interactions
        protein-protein
        Interacting group
        Assay
        References
        RNA-RNA
        Interacting group
        Assay
        References
        RNA-protein
        Interacting group
        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
        suppressible
        External Data
        Subunit Structure (UniProtKB)
        Interacts with tamo via the nuclear localization signal. Interacts with emb, a component of the nuclear pore complex.
        (UniProt, P15330 )
        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.
        Pathways
        Genomic Location and Detailed Mapping Data
        Chromosome (arm)
        2L
        Recombination map
        2-53
        Cytogenetic map
        Sequence location
        2L:17,436,830..17,450,364 [-]
        FlyBase Computed Cytological Location
        Cytogenetic map
        Evidence for location
        36C8-36C9
        Limits computationally determined from genome sequence between P{lacW}Mhck10423&P{lacW}Cask03902 and P{lacW}Aac11k06710
        Experimentally Determined Cytological Location
        Cytogenetic map
        Notes
        References
        36C9-36C9
        ; Limits computationally determined from genome sequence between P{lacW}Mhck10423&P{lacW}Cask03902 and P{lacW}Aac11k06710
        Location inferred from insertion in: dl[GSd447]
        36C-36C
        (determined by in situ hybridisation)
        Experimentally Determined Recombination Data
        Left of (cM)
        Right of (cM)
        Notes
        Stocks and Reagents
        Stocks (26)
        Genomic Clones (20)
        cDNA Clones (40)
         

        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)
        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
         
        Developmental Studies Hybridoma Bank - Monoclonal antibodies for use in research
        Other Information
        Relationship to Other Genes
        Source for database identify of
        Source for identity of: dl CG6667
        Source for database merge of
        Source for merge of: dl anon- EST:GressD7
        Source for merge of: dl GSd447
        Additional comments
        Other Comments
        DNA-protein interactions: genome-wide binding profile assayed for dl protein in 2-3 hr embryos; see BDTNP1_TFBS_dl collection report.
        Gene expression is increased in response to the presence of two copies of Scer\GAL4hs.PB.
        Ventral signal dependent modification of cact and dl may be required for the graded nuclear import of dl.
        dl can activate transcription from zen and twi promoters, and additional Dsp1 inhibits the zen activation and increases the twi activation.
        dl protein is subject to signal-dependent phosphorylation while associated with cact protein in the cytoplasm. Phosphorylation of dl protein is required for its nuclear import.
        Dif and dl are functionally redundant in their ability to control Drs gene expression in larvae.
        A linear activation cascade spz-Tl-cact-dl/Dif leads to the induction of the Drs gene in larval fat body cells.
        An interplay of dl and twi proteins with Taf4 protein is required for the activation of mesoderm-determining gene expression in the embryo.
        The h and dl gene products continue to function as repressors in the setting up of segmentation in the absence of CtBP.
        Targeting of either tub or pll product to the plasma membrane by myristylation is sufficient to activate the signal transduction pathway that leads to translocation of the dl product. Activated Tl induces a localized recruitment of tub and pll proteins to the plasma membrane.
        Tl pathway is required for the nuclear import of dl in the immune response, but not required for the nuclear import of Dif. Cytoplasmic retention of both dl and Dif depends on cact protein. The two signalling pathways that target cact for degradation must discriminate between cact-dl and cact-Dif complexes.
        Transcript induced by MMS treatment of S1CII cells.
        nej is necessary for dl-mediated activation of the twi promoter.
        dl protein binds specifically to the tub, pll and cact proteins.
        The molecular evolution of the Rel/NF-κB and IκB proteins is studied in parallel. Phylogenetic analysis allows the structure of the putative ancestor genes to be defined and proposes and evolutionary model that clusters both families in a unique Rel/NF-κB/IκB superfamily.
        dl and twi proteins synergistically activate transcription in cell culture from a promoter containing binding sites for both factors. The Rel homology domain of the dl protein appears to be sufficient for the synergy. Protein-protein interaction assays show that dl and twi proteins bind to one another in vitro.
        tub, pll, cact and dl form a complex essential for signal transduction.
        Yeast two hybrid assay demonstrates both tub and pll interact with dl. Interactions have also been confirmed in an in vitro binding assay.
        cact forms a concentration gradient inversely correlated to the nuclear translocation gradient of dl. Genetic evidence indicates degradation of cact is required, but not sufficient, to translocate dl completely into the nucleus.
        Homodimerisation, nuclear targeting and interaction of dl with cact are mediated by the conserved Rel-homology domain of dl.
        Expression of dl causes lethality and the formation of melanotic tumours.
        dl and Dif have distinct DNA-binding characteristics and the proteins can heterodimerise in vitro. Mutants carrying no copies of dl and a single copy of Dif retain their full capacity to express the Dpt and CecA1 genes in response to bacterial challenge.
        The embryonic regulatory pathway, comprising the gene products between spz and cact (Tl, tub and pll) but not the genes acting upstream or downstream (ea and dl), is involved in the induction of the Drs gene in adults.
        Expression of pll enhances the transcriptional activity and nuclear localisation of dl.
        In embryos there is a gradient of cact protein. In ventral regions cact is degraded allowing dl to translocate into the nuclei, in dorsal regions cact persists, retaining dl in the cytoplasm.
        The dl product binds to multiple sites in the dpp second intron.
        cact inhibits nuclear translocation of dl on the ventral side of the embryo by binding to and retaining dl in the cytoplasm. cact is rapidly degraded in response to signalling from the dorsal ventral pathway between spz and dl/cact, this signal-dependent degradation does not require the presence of dl but does require sequences in the amino terminus or ankyrin repeats of the cact protein. Disruption of the dl-cact complex is a secondary result of cact degradation.
        Monitoring phosphorylation in mutant backgrounds demonstrates that phosphorylation of the dl protein is clearly affected. Therefore phosphorylation may play a role in regulating the dl protein. One of three mutations in the putative phosphorylation sites at residue 312, not at residue 290 or 324, markedly reduces the ability of the transgene to rescue dl mutant embryos.
        Molecular analysis suggests that sna protein acts over distances of 50-150bp to block the activity, but not the binding, of the dl activator to the rho 650bp enhancer.
        Increases in intra-cellular Ca2+ levels result in rapid destruction of cact protein and dephosphorylation of dl protein in a Drosophila cell line.
        dl protein enhances the biosynthesis and stability of cact.
        cact activity blocks the DNA binding and nuclear localisation functions of dl. dl transcriptional activating region is functional in the dl cact complex.
        Nuclear localisation of dl in the fat body during the immune response is controlled by the intracellular embryonic dorsoventral pathway, the Tl signalling pathway. dl alone does not control the expression of antibacterial peptide genes as these genes are inducible in its absence. dl is not involved in the formation of melanotic tumours of Tl or cact mutations nor in the induction of Dpt gene, or dl acts in concert with other proteins to affect cellular and/or humoral immunity.
        The dl regulatory gradient defines the limits of inductive interactions between germ layers after gastrulation.
        The tub protein can function in a novel way to enhance dl activity. In the absence of dl or when dl is cytoplasmic, tub is only found in the cytoplasm of transfected cells. When dl is localised to the nucleus, so is tub. tub can then function to enhance reporter gene expression, by cooperation with dl or as a Scer\GAL4-tub fusion protein. tub is capable of acting as both a chaperon or escort for dl as it moves to the nucleus and then as a transcriptional coactivator. The intracytoplasmic domain of Tl is sufficient for activating the signalling pathway that leads to dl-tub nuclear translocation in Schneider cells.
        dl can activate the CecA1 promoter, but to a lesser extent and in a less sequence-specific manner than Dif. The dl product exerts a dominant negative effect on Dif transactivation of CecA1.
        The dl-bHLH protein interactions mediating gene expression in the neuroectoderm and mesoderm are fundamentally distinct. Proximity between dl and bHLH binding sites is essential for synergistic activation of gene expression in the lateral neuroectoderm, where levels of dl product diminish. Sharp on/off patterns of gene expression in the presumptive mesoderm do not require linkage of these sites.
        A sequence within the RHD (Rel homology domain) is essential for inhibitor interactions. Point mutations within this sequence can uncouple DNA binding and inhibitor interactions in vitro.
        dl is an embryonic phosphoprotein and its phosphorylation state is regulated by an intracellular signaling pathway initiated by the transmembrane receptor Tl. Using a combined genetic and biochemical approach it is demonstrated that activation of Tl stimulates an increase in the extent of dl phosphorylation. Signal-dependent dl phosphorylation is modulated by three intracellular proteins, pll, tub and cact.
        Dorsal-ventral patterning is regulated by a signalling pathway that includes Tl and transcription factors, dl, that interact with related enhancers, rho. The κ enhancer from mouse is capable of generating lateral stripes of Ecol\lacZ gene expression in transgenic embryos in a pattern similar to that directed by rho enhancer. Results suggest that enhancers can couple conserved signalling pathways to divergent gene functions, dorso-ventral patterning and mammalian haematopoiesis.
        ems, a head-specific gap gene, may function as a co-repressor of dl, thereby linking the anteroposterior and dorsoventral systems st the molecular level.
        Disulfide cross-linking in crude extracts has identified two complexes of dl protein: a dl protein homodimer and a complex of the homodimer with cact protein. The distribution of the complex varies, the homodimer is the nuclear form of dl protein and a complex of the homodimer with cact protein prevails in the cytoplasm.
        dl directly represses tld gene expression in ventral regions of the early embryo. DNaseI footprinting reveals dl binds to at least three sites in the tld 5' flanking sequences that are required in vivo for ventral repression (423bp VRE element).
        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.
        The Tl signalling pathway generates a dl nuclear gradient which initiates the differentiation of the mesoderm, neuroectoderm and dorsal ectoderm by activating and repressing gene expression in the early embryo. A second signalling pathway controlled by the tor receptor kinase also modulates dl activity. The tor pathway selectively masks the ability of dl to repress gene expression but only has a slight effect on activation.
        dl gene product interacts with members of the HLH family, including da, ac and sc and dosage sensitive interactions that exist between dl, da, ac, sc and twi are required for the specification of both the embryonic mesoderm and neuroectoderm.
        Promoter fusions using elements of the twi, ve, da and sna promoters indicate that low affinity dl-binding sites restrict target gene expression to the presumptive mesoderm, where there are peak levels of dl expression, while high affinity sites in other target genes permit expression in ventrolateral regions where dl levels are intermediate. Activation by low levels of dl in lateral regions depends on cooperative interaction between dl and other basic helix loop helix proteins. Promoters containing the Et (veinlet) or Eds (dl and snail) E boxes display opposite behaviour in da and twi mutants, suggesting they are regulated by different basic helix loop helix proteins.
        A minimal 110bp Ventral Repression Element silencer in the zen promoter contains two dl binding sites as well as binding sites for additional nuclear factors present in early embryos. Mutations in the latter convert the minimal VRE into an enhancer, mediating transcriptional activation in ventral regions in response to dl. Thus dl is converted from an activator to a silencer by interactions with neighboring corepressors.
        dl binding sites from the zen promoter can mediate transcriptional activation of a heterologous promoter, but not repression. T-rich sequences close to the dl binding sites in the silencer region of the zen promoter are conserved between D.melanogaster, D.virilis and D.pseudoobscura.pseudoobscura.
        Increased cytoplasmic calcium concentration and the expression of constitutively active Tl receptors can induce the relocalisation of dl in culture cells. Activation of endogenous Pka-C1, expression of wild type Tl receptors or treatment of cells with activators of Pkc53E and radical oxygen intermediates have only a marginal effects on the cellular distribution of dl protein.
        Ecol\lacZ reporter gene constructs demonstrate the presence of dl maternal system cis-acting response elements in the 5' flanking region of tll.
        In addition to its role in embryogenesis, dl is involved in the immune response. In dl mutants the genes encoding antibacterial peptides retain their inducibility, suggesting multifactorial control.
        Cytoplasmic injection studies indicate that the putative Toll ligand appears to originate from a ventrally restricted zone extending along the anterior-posterior axis, and its diffusion or graded release are required to determine the slope of the nuclear dorsal protein gradient.
        dl and cact are phosphoproteins that form a stable cytoplasmic complex. The cact protein is stabilised by its interaction with dl protein, and the dl-cact complex dissociates when dl protein is targeted to the nucleus.
        The zygotic dpp gradient and the maternal dorsal gradient specify distinct, non-overlapping domains of the dorsal-ventral pattern.
        Double mutant combinations of dl with ea alleles demonstrate that spatial regulation of ea activity by localized zymogen activation is a key initial event in defining the polarity of the dorsal-ventral embryonic pattern.
        In vitro studies showed the cactus gene product can inhibit binding of dorsal protein to DNA.
        Expression of dl-lacZ fusion protein causes a partial loss of function dl phenotype, and downstream genes twi and zen are misregulated. The fusion protein localises to nuclei in manner indistinguishable from wild type dl protein. The dl-lacZ fusion provides some dl function: in a null dl background the fusion gene causes partial rescue of the phenotype. In vitro immunoprecipitation experiments show that dl and dl-lacZ proteins associate, suggesting that in wild type dl functions as an oligomer. Dominant female sterility caused by dl-lacZ is relieved by additional dl or Ecol\lacZ protein.
        dl acts in concert with basic HLH proteins (possibly including twi) to activate ve in both ventral and lateral regions. A dl activator site has been found in the neural ectoderm expression region of the ve promoter.
        Mutants of dl have been sequenced and their phenotypes studied. Results demonstrate that the dl protein has an amino terminal DNA binding domain and a carboxy terminal domain required for transcriptional activation/repression.
        dl binding site domain exchange experiments, using Ecol\lacZ reporter gene constructs, between the zen and twi promoters demonstrate that dl is intrinsically an activator and that repression requires additional factors present in the distal region of the zen promoter, the VR.
        In vitro mutagenesis alleles assayed in a cell free system indicate that the rel homology domain of dl, around amino acid 270, is the site at which the cact gene product binds.
        Effects of Toll on dl in cotransfected Schneider cells examined: Toll can enhance nuclear localisation of dl and, independently, the ability of dl to activate transcription once in the nucleus. Pathway from Toll to dl may involve protein kinase A, and nuclear transport and activation of dl may result from phosphorylation of dl by protein kinase A.
        The dl gene product is required for ventral repression of tll expression of the stripe: bcd function is also required.
        The dl gene acts downstream of Tl: perivitelline fluid from dl mutant embryos is equivalent to that obtained from wild type embryos.
        The effect of the terminal system on the expression of 2 zygotic genes involved in dorsoventral patterning, sna and dpp, is mediated by a reduction in dl activity by the terminal system. Due to this interaction the poles adopt a more dorsalised fate than their counterparts in the middle of the embryo.
        dl is a sequence specific DNA binding protein that may mediate long range repression by interacting with the distal regions of the zen promoter. dl binding sites share sequence similarity with the conserved sites recognized by the rel and NF-ΚB proteins.
        A combination of promoter fusion-P-element transformation assays (1.2kb twi promoter fragment is sufficient to generate normal twi pattern of Ecol\lacZ expression) and in vitro DNA binding assays coupled with site directed mutagenesis (revealing four dl-binding sites in the twi promoter) have been used to establish a link between the dl-binding sites and twi expression in early embryos. The dorsal ventral limits of twi expression depend on the number and affinity of dl binding sites present in the twi promoter. dl-binding sites present in the twi promoter possess a lower affinity to those present in the zen promoter.
        Establishment of the mesoderm neuroectoderm boundary involves the interaction of twi, sna and dl proteins.
        Footprint analysis has been used to analyse transcription activation factors responsible for ventral specific expression of twi. dl has been found to bind the ventral activation region of twi and interact directly or indirectly with other DNA bound regulatory factors to activate twi expression in the presumptive mesoderm.
        Mutations in maternal dorsal class gene dl interact with RpII140wimp.
        dl appears to activate the expression of twi and sna and repress the expression of zen and dpp. Polar expression of dpp and zen requires the terminal system to override the repression of dl, and twi and sna polar expression require the terminal system to augment activation of dl.
        dl acts as a sequence specific trans-activator of the twi promoter. Gel retardation assays have been used to investigate binding of dl protein to synthetic oligonucleotides corresponding to the proximal and distal activator region of the twi promoter.
        Involved in the regulatory hierarchy responsible for the asymmetric distribution and function of zygotic regulatory gene products along the DV axis of early embryos.
        Establishment of the dl gradient involves selective nuclear transport. Truncated dl protein lacking C-terminal sequences accumulate predominantly in the nuclei of transfected Schneider cells while the full length protein is largely restricted to the cytoplasm.
        Mutations in dl result in a maternal effect phenotype with defects during the early stages of gastrulation and defects in the dorsoventral axis; embryos derived from homozygous females are dorsalised.
        Epistatic relationships exist between dorsalizing maternal effect mutations and "dppHin" alleles.
        opa-e is present at position 1417bp, identified as a stretch of 34 glutamine residues, within the dl locus.
        The expression of genes controlling neurogenesis is dependent on the previous activity of the genes controlling the development of the embryonic dorsal-ventral pattern.
        In homozygous embryos invagination of the ventral presumptive mesodermal cells fails to occur and the resulting embryos are devoid of internal organs.
        Embryos produced by homozygous dl females form normal cellular blastoderm but at gastrulation develop into yolk-filled tube of dorsal hypoderm. Hair pattern of cuticle characteristic of dorsal hypoderm; ventral structures, such as denticle belts, lacking. Normally, dorsal infoldings occupy entire circumference of embryo. Evidence of anterior-posterior differentiation includes possible mouth armature structures anteriorly, small spiracles posteriorly and orientation of hairs. The periodicity of stripes of ftz expression in pre-gastrulation embryos, as revealed by antibody staining, displays the pattern normally characteristic of the dorsum circumferentially in embryos produced by dl females (Carroll, Winslow, Twombly, and Scott, 1987). Embryos produced by dl/dl and dl/Df(2L)TW137 indistinguishable, suggesting dl to be amorphic. Penetrance complete; expression constant. Embryos of dl2 females lack all structures normally derived from the ventral half of the egg, including mesoderm, endodermal gut, ventral nervous system and ventral hypoderm. dl1 and to a lesser extent dl2, females produce embryos with reduced capacity for neurogenesis in response to an absence of dl function (Campos-Ortega, 1983). dl germ line-dependent; homozygous germ-line clones produce dorsalized embryos (Schupbach and Wieschaus, 1986). Embryos of dl/+ females produced at 29oC develop into comparatively normal-looking larvae; they mainly lack internal organs, such as mesoderm and parts of the anterior and posterior gut; often ventral hypoderm including denticle belts reduced; phenotype sensitive to genetic background. At 22oC, dl/+ females produce normal embryos. Developmental fate of ventrally located cells on cellular blastoderm apparently shifted to that of more dorsally located cells. The phenotype of embryos produced by dl/dl females partially rescued by the injection of wild-type cytoplasm but not RNA (Santamaria and Nusslein-Volhard, 1983; Anderson and Nusslein-Volhard, 1984). Developmental profiles show transcript to be present only in ovaries and pre-cellular-blastoderm stages of embryogenesis. In situ hybridization indicates that ovarian transcript accumulates in nurse cells from stage 5 to 11; number of transcripts per genome equivalent in these polytene cells remains low and constant until stage 10, at which time there is a dramatic increase in the relative numbers of transcripts. After a lag of one or two nuclear divisions, transcript begins to accumulate in the oocyte; by stage 12 there is little detectable transcript in the nurse cells. It appears as though the nurse-cell transcript is transferred to the oocyte and thus to the embryo; transcript seems to be uniformly distributed in stage 14 oocytes (Steward, Ambrosio, and Schedl, 1985). dl protein is uniformly distributed throughout cytoplasm of early embryo; in the syncytial blastoderm a gradient of expression is achieved by the graded transport of dl protein into nuclei, with the highest nuclear concentrations found ventrally; protein remains cytoplasmic dorsally. Maternal dorsalizing mutants prevent nuclear localization and ventralized embryos show dorsal as well as ventral nuclear localization (Steward, Zusman, Huang and Schedl, 1988; Rushlow, Han, Manley and Levine, 1989; Steward, 1989; Roth et al., 1989).
        Origin and Etymology
        Discoverer
        Etymology
        Identification
        External Crossreferences and Linkouts ( 88 )
        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.
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        BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
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        ApoDroso - Functional genomic database for photoreceptor development, survival and function
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        Synonyms and Secondary IDs (17)
        Reported As
        Symbol Synonym
        anon-EST:GressD7
        dl
        (Araujo, 2017.8.28, Duneau et al., 2017, Koenecke et al., 2017, Louradour et al., 2017, Wang et al., 2017, Gao et al., 2016, Morris et al., 2016, Sarov et al., 2016, Chen et al., 2015, Liu et al., 2015, Schertel et al., 2015, Ugrankar et al., 2015, Ward et al., 2015, Yamamoto-Hino et al., 2015, Zhang et al., 2015, Carvalho et al., 2014, Esteves et al., 2014, Ferreira et al., 2014, Jiang and Singh, 2014, Rembold et al., 2014, Shin and Hong, 2014, Tevy et al., 2014, Garcia et al., 2013, Gueguen et al., 2013, Li and Gilmour, 2013, Matzat et al., 2013, McIlroy et al., 2013, Mulero et al., 2013, Quintin et al., 2013, Samaraweera et al., 2013, Shravage et al., 2013, Vaque et al., 2013, Vaqué et al., 2013, Garcia et al., 2012, Holmqvist et al., 2012, Japanese National Institute of Genetics, 2012.5.21, Kvon et al., 2012, Lemaitre et al., 2012, Reeves et al., 2012, Spokony, 2012.12.12, Spokony and White, 2012.5.22, Abruzzi et al., 2011, Ajuria et al., 2011, Friedman et al., 2011, Guan et al., 2011, Keller et al., 2011, Li et al., 2011, Marcu et al., 2011, Toku et al., 2011, van Uden et al., 2011, Aerts et al., 2010, Hill-Burns and Clark, 2010, Lund et al., 2010, Matova and Anderson, 2010, Mrinal and Nagaraju, 2010, Negreiros et al., 2010, Paddibhatla et al., 2010, Salzer et al., 2010, The modENCODE Consortium, 2010, The modENCODE Consortium, 2010, Boettiger and Levine, 2009, Dworkin et al., 2009, Fontenele et al., 2009, Liberman and Stathopoulos, 2009, Liberman et al., 2009, Obbard et al., 2009, Blanco and Gehring, 2008, Bornemann et al., 2008, Carrera et al., 2008, Kalamarz et al., 2008, Liu and Lehmann, 2008, Pope and Harris, 2008, Ratnaparkhi et al., 2008, Tan et al., 2008, Yano et al., 2008, Aerts et al., 2007, Ayyar et al., 2007, Beramendi et al., 2007, Christensen and Cook, 2007.5.8, DeLotto et al., 2007, Heckscher et al., 2007, Levine et al., 2007, Minidorff et al., 2007, Zeitouni et al., 2007, Anderson et al., 2006, Carneiro et al., 2006, Kim et al., 2006, Matova and Anderson, 2006, Minakhina and Steward, 2006, Mizutani et al., 2006, Molnar et al., 2006, Prothmann et al., 2006, Ratnaparkhi et al., 2006, Scuderi et al., 2006, Shirangi et al., 2006, Thoetkiattikul et al., 2005, Xavier-Neto, 2005, Lau et al., 2003, Uvell and Engstrom, 2003, Bhaskar et al., 2002, Bhattacharya and Steward, 2002, Jia et al., 2002, Lehmann et al., 2002, Gim et al., 2001, Luo et al., 2001, Steneberg and Samakovlis, 2001, Pickeral et al., 2000, Cantera et al., 1999)
        mat(2)dorsal
        Name Synonyms
        Dorsal
        (Min and Tatar, 2018, Palmer et al., 2018, Amourda and Saunders, 2017, Mussabekova et al., 2017, Gao et al., 2016, Lacy and Hutson, 2016, Signor et al., 2016, Yadav et al., 2016, Bandarra et al., 2015, Boija and Mannervik, 2015, Clifford and Adami, 2015, Kanoh et al., 2015, Li and Dijkers, 2015, Liu et al., 2015, Lucas et al., 2015, Shirinian et al., 2015, Keebaugh and Schlenke, 2014, Li et al., 2014, Lindsay and Wasserman, 2014, Mannervik, 2014, Rembold et al., 2014, Salazar-Jaramillo et al., 2014, Zhou et al., 2014, Costa et al., 2013, Ferrandon, 2013, Fontenele et al., 2013, Fuse et al., 2013, Gueguen et al., 2013, Lee et al., 2013, Matzat et al., 2013, Mbodj et al., 2013, Neckameyer and Argue, 2013, Tremmel et al., 2013, Bitra et al., 2012, Daniels et al., 2012, Haskel-Ittah et al., 2012, Kanodia et al., 2012, Lim and Thiery, 2012, Reeves et al., 2012, Rushlow and Shvartsman, 2012, Buechling et al., 2011, Guan et al., 2011, Kanodia et al., 2011, Kim et al., 2011, Mrinal et al., 2011, Nègre et al., 2011, Qian et al., 2011, Valanne et al., 2011, van Uden et al., 2011, Wang et al., 2011, Fakhouri et al., 2010, Khoueiry et al., 2010, Kuttenkeuler et al., 2010, Lund et al., 2010, Matova and Anderson, 2010, Paddibhatla et al., 2010, Rand et al., 2010, Sample and Shvartsman, 2010, Tanji et al., 2010, Tipping et al., 2010, Buchon et al., 2009, Cooper et al., 2009, Cronin et al., 2009, Fontenele et al., 2009, Kanodia et al., 2009, MacArthur et al., 2009, Mavrakis et al., 2009, Nie et al., 2009, Papatsenko et al., 2009, Towb et al., 2009, Araujo et al., 2008, Ching et al., 2008, Hong et al., 2008, Ishihara and Shibata, 2008, Kechris and Li, 2008, Levine et al., 2008, Liang et al., 2008, Ratnaparkhi and Courey, 2008, Reed et al., 2008, Tan et al., 2008, Xi et al., 2008, Beramendi et al., 2007, Copley et al., 2007, DeLotto et al., 2007, Harari-Steinberg et al., 2007, Korolchuk et al., 2007, Kuranaga and Miura, 2007, McElwain et al., 2007, Nibu et al., 2007, Waterhouse et al., 2007, Williams et al., 2007, Zeitlinger et al., 2007, Akira et al., 2006, Bergmann, 2006, Biemar et al., 2006, Chanut, 2006, Chen, 2006, Chen et al., 2006, Lawrence, 2006, Matova and Anderson, 2006, Nguyen and Frasch, 2006, Sivatchenko and Letsou, 2006, Xylourgidis et al., 2006, Zinzen et al., 2006, Hogarth et al., 2005, Stathopoulos and Levine, 2005, Cho, 2004, Cowden and Levine, 2003, Minakhina et al., 2003, Nibu et al., 2003, Park et al., 2003, Roth et al., 2003, Uvell and Engstrom, 2003, Avila et al., 2002, Bhaskar et al., 2002, Christophides et al., 2002, Jia et al., 2002, Lehmann et al., 2002, Roxstrom-Lindquist et al., 2002, Chen et al., 2000, Rutschmann et al., 2000)
        Embryonic polarity protein dorsal
        dorsal
        (Kato et al., 2018, Yu et al., 2018, Lence et al., 2016, Troutwine et al., 2016, Bandarra et al., 2015, Liu et al., 2015, Luo et al., 2015, Wu et al., 2015, Yamamoto-Hino et al., 2015, Zhou et al., 2015, Ambrosi et al., 2014, Cantera et al., 2014, Carvalho et al., 2014, Imler, 2014, Lee and Hyun, 2014, Shin and Hong, 2014, Taylor et al., 2014, Garcia et al., 2013, Matzat et al., 2013, Mulero et al., 2013, Nelson et al., 2013, Samaraweera et al., 2013, Shravage et al., 2013, Chiu et al., 2012, Garcia et al., 2012, Kvon et al., 2012, Ajuria et al., 2011, Cammarato et al., 2011, Kato et al., 2011, Keller et al., 2011, Marcu et al., 2011, Roth, 2011, Aerts et al., 2010, Goto et al., 2010, Mosca and Schwarz, 2010, Mrinal and Nagaraju, 2010, Salzer et al., 2010, Valanne et al., 2010, Avadhanula et al., 2009, Liberman et al., 2009, Schaaf et al., 2009, Zsindely et al., 2009, Blanco and Gehring, 2008, Bosveld et al., 2008, Crocker et al., 2008, Fu and Levine, 2008, Pal et al., 2008, Ratnaparkhi et al., 2008, Yano et al., 2008, Ayyar et al., 2007, Busse et al., 2007, Fu and Levine, 2007, Gregory et al., 2007, Kankel et al., 2007, Levine et al., 2007, Matova and Anderson, 2007, Shen and Tanda, 2007, Tanji et al., 2007, Wu and Silverman, 2007, Zeitouni et al., 2007, Zinzen and Papatsenko, 2007, Anderson et al., 2006, Prothmann et al., 2006, Senger et al., 2006, Shirangi et al., 2006, Beckstead et al., 2005, Beramendi et al., 2005, Bettencourt et al., 2004, Meinhardt, 2004, Bolatto et al., 2003, Yajima et al., 2003, Bhattacharya and Steward, 2002, Takano and Gusella, 2002, Cornwell and Kirkpatrick, 2001, Gim et al., 2001, Luo et al., 2001, Steneberg and Samakovlis, 2001, Cantera et al., 1999, Roth et al., 1989, Boulay et al., 1987)
        Secondary FlyBase IDs
        • FBgn0000462
        • FBgn0025325
        • FBgn0260285
        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 (900)