FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Gene: Dmel\Su(H)
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General Information
Symbol
Dmel\Su(H)
Species
D. melanogaster
Name
Suppressor of Hairless
Annotation Symbol
CG3497
Feature Type
FlyBase ID
FBgn0004837
Gene Model Status
Stock Availability
Gene Summary
Transcriptional regulator that plays a central role in Notch signaling, a signaling pathway involved in cell-cell communication that regulates a broad spectrum of cell-fate determinations (PubMed:10673509, PubMed:1617729, PubMed:21262215, PubMed:8674407). Binds directly the 5'-GTGRGAR-3' DNA consensus sequence, which is present in the regulatory region of several genes (PubMed:10673509). Acts as a transcriptional repressor when it is not associated with Notch proteins (PubMed:10673509). When associated with some Notch protein, it acts as a transcriptional activator that activates transcription of Notch target genes (PubMed:10673509). Required for transcription of Sim (PubMed:10673509). Specifically binds to the immunoglobulin kappa-type J segment recombination signal sequence (PubMed:1617729, PubMed:1617730, PubMed:1744127). Required for neurogenesis in imaginal disks (PubMed:1617730, PubMed:7813798). In the larval brain, might play a role as a transducer of Notch signaling during type II neuroblast development (PubMed:21262215). Also functions independently of the Notch pathway, in the development of the bristle sensory organ precursor cell (PubMed:12642500). (UniProt, P28159)
Contribute a Gene Snapshot for this gene.
Also Known As

SuH, l(2)br7, CSL, Supressor of Hairless, l(2)35Bh

Key Links
Genomic Location
Cytogenetic map
Sequence location
Recombination map
2-50
RefSeq locus
NT_033779 REGION:15039488..15043334
Sequence
Genomic Maps
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
Gene Ontology (GO) Annotations (36 terms)
Molecular Function (10 terms)
Terms Based on Experimental Evidence (9 terms)
CV Term
Evidence
References
enables DNA binding
inferred from direct assay
inferred from direct assay
inferred from physical interaction with UniProtKB:Q9VWP5
inferred from physical interaction with FLYBASE:ebi; FB:FBgn0263933
inferred from physical interaction with FLYBASE:Smr; FB:FBgn0265523
inferred from physical interaction with FLYBASE:N; FB:FBgn0004647
Terms Based on Predictions or Assertions (5 terms)
CV Term
Evidence
References
Biological Process (19 terms)
Terms Based on Experimental Evidence (11 terms)
CV Term
Evidence
References
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
involved_in long-term memory
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:Psn; FB:FBgn0284421
inferred from mutant phenotype
Terms Based on Predictions or Assertions (8 terms)
CV Term
Evidence
References
Cellular Component (7 terms)
Terms Based on Experimental Evidence (7 terms)
CV Term
Evidence
References
located_in cytoplasm
inferred from direct assay
is_active_in nucleus
inferred from direct assay
located_in nucleus
inferred from direct assay
inferred from physical interaction with FLYBASE:N; FB:FBgn0004647
inferred from genetic interaction with FLYBASE:ebi; FB:FBgn0263933
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
is_active_in nucleus
inferred from biological aspect of ancestor with PANTHER:PTN000071433
located_in nucleus
inferred from electronic annotation with InterPro:IPR015351, InterPro:IPR037095
Protein Family (UniProt)
Belongs to the Su(H) family. (P28159)
Summaries
Gene Group (FlyBase)
UNCLASSIFIED DNA BINDING DOMAIN TRANSCRIPTION FACTORS -
This group comprises DNA-binding transcription factors that do not classify under other domain-based transcription factor groups in FlyBase.
CSL-NOTCH-MASTERMIND TRANSCRIPTION FACTOR COMPLEX -
The CSL-Notch-Mastermind transcription factor complex consisting of the CSL protein, Su(H), and mastermind (mam) protein, in complex with Notch intracellular domain (generated by ligand-stimulated N-cleavage), up-regulates transcription of Notch-responsive genes. (Adapted from FBrf0232880).
Pathway (FlyBase)
NOTCH SIGNALING PATHWAY CORE COMPONENTS -
The Notch receptor signaling pathway is activated by the binding of the transmembrane receptor Notch (N) to transmembrane ligands, Dl or Ser, presented on adjacent cells. This results in the proteolytic cleavage of N, releasing the intracellular domain (NICD). NICD translocates into the nucleus, interacting with Su(H) and mam to form a transcription complex, which up-regulates transcription of Notch-responsive genes. (Adapted from FBrf0225731 and FBrf0192604). Core pathway components are required for signaling from the sending cell and response in the receiving cell.
Protein Function (UniProtKB)
Transcriptional regulator that plays a central role in Notch signaling, a signaling pathway involved in cell-cell communication that regulates a broad spectrum of cell-fate determinations (PubMed:10673509, PubMed:1617729, PubMed:21262215, PubMed:8674407). Binds directly the 5'-GTGRGAR-3' DNA consensus sequence, which is present in the regulatory region of several genes (PubMed:10673509). Acts as a transcriptional repressor when it is not associated with Notch proteins (PubMed:10673509). When associated with some Notch protein, it acts as a transcriptional activator that activates transcription of Notch target genes (PubMed:10673509). Required for transcription of Sim (PubMed:10673509). Specifically binds to the immunoglobulin kappa-type J segment recombination signal sequence (PubMed:1617729, PubMed:1617730, PubMed:1744127). Required for neurogenesis in imaginal disks (PubMed:1617730, PubMed:7813798). In the larval brain, might play a role as a transducer of Notch signaling during type II neuroblast development (PubMed:21262215). Also functions independently of the Notch pathway, in the development of the bristle sensory organ precursor cell (PubMed:12642500).
(UniProt, P28159)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
Su(H): Suppressor of Hairless
Homozygous lethal; hemizygotes die in the pupal stage, between head eversion and the beginning of eye pigmentation. Heterozygotes in the absence of H are wild type in phenotype. Suppresses H; Su(H)/+; H/+ have 7-10 more bristles that H/+ alone; besides affecting the bristle phenotype of H, all alleles tend to enhance its wing-vein phenotype of shortening L4 and L5. Su(H) is without effect on the lethal phenotype of homozygous H. One homozygous-lethal allele acts as a dominant enhancer of H. Most alleles are amorphic or hypomorphic; heterozygous deficiencies for the locus also suppress, and duplications enhance H (Nash, 1970). Enhanced genotypes have 10-15 fewer bristles and a far more extreme loss of microchaetae on the thorax than their unenhanced counterparts. The number of bristles in H/+ flies is inversely related to the dose of Su(H)+, with the number of bristles varying from fewer than ten with four doses to approximately 35 with one dose. Some combinations of hypomorphic alleles produce occasional escapers; survivors have distinctive phenotypes, which are described under entries for specific alleles.
Su(H)3
A leaky allele; trans heterozygotes with Su(H)1 show 20% survival; almost viable with Su(H)7; semilethal with Su(H)2, Su(H)4, Su(H)6, and Su(H)8; lethal in combination with Su(H)16. Survivors have vestigial wings and halteres and eyes somewhat reduced and rough; bristles normal.
Su(H)7
Homozygous lethal; in trans heterozygotes with other alleles produces rare escapers, which have an extreme mutant phenotype; wings and halteres similar to those of an extreme vestigial allele; eyes, although large, have rough glazed appearance and the flies are almost achaetous, having fewer than ten macrochaetae per fly; acrostichal hairs and other microchaetae reduced in number and disturbed in arrangement; tarsal claws also much reduced.
Su(H)16
Homozygous lethal; acts as a dominant enhancer of H, with about the same effect as heterozygosity for a duplication for the locus.
Summary (Interactive Fly)

transcription factor - integrase domain - Notch pathway - Notch intracellular domain associates with Su(H) and Mastermind, a transcriptional coactivator - operates as molecular switch on Notch target genes: within activator complexes, including intracellular Notch, or within repressor complexes, including the antagonist Hairless

Gene Model and Products
Number of Transcripts
2
Number of Unique Polypeptides
1

Please see the JBrowse view of Dmel\Su(H) 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
Structure
Protein 3D structure   (Predicted by AlphaFold)   (AlphaFold entry P28159)

If you don't see a structure in the viewer, refresh your browser.
Model Confidence:
  • Very high (pLDDT > 90)
  • Confident (90 > pLDDT > 70)
  • Low (70 > pLDDT > 50)
  • Very low (pLDDT < 50)

AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.

Experimentally Determined Structures
Crossreferences
PDB - An information portal to biological macromolecular structures
Comments on Gene Model

Gene model reviewed during 5.52

Gene model reviewed during 5.57

Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0080700
2950
594
FBtr0346621
2633
594
Additional Transcript Data and Comments
Reported size (kB)

2.9 (northern blot)

3.4 (northern blot)

Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
UniProt
RefSeq ID
GenBank
FBpp0080261
66.9
594
7.02
Polypeptides with Identical Sequences

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

594 aa isoforms: Su(H)-PA, Su(H)-PC
Additional Polypeptide Data and Comments
Reported size (kDa)

75-80 (kD observed)

550, 485 (aa); 62, 54 (kD predicted)

Comments
External Data
Subunit Structure (UniProtKB)

Interacts with activated cleaved Notch. Interacts with Hairless, this interaction preventing its DNA-binding activity. Interacts with insv (via BEN domain).

(UniProt, P28159)
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\Su(H) using the Feature Mapper tool.

External Data
Crossreferences
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Linkouts
Expression Data
Testis-specificity index

The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).

-0.41

Transcript Expression
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
organism

Comment: maternally deposited

epidermis

Comment: reference states 16-24 hr APF

macrochaeta

Comment: assayed at 17h, 21h, 30h APF

microchaeta

Comment: assayed at 17h, 21h, 30h APF

tormogen cell

Comment: assayed at 17h, 21h, 30h APF

tormogen cell

Comment: reference states 24 hr APF

trichogen cell

Comment: reference states 24 hr APF

northern blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data

Su(H) is stronglyly detected in all macrochaete socket cells 17, 21 and 30 hours APF. It is also observed in microchaetes at these stages.

Su(H)@ transcripts are detected throughout development by RNAase protection.

Su(H) transcripts are present throughout the syncytial embryo. During cellularization, the rapid disappearance of putative maternal transcripts reveals a transient striped pattern. Transcripts are next observed from stage 11 on in external sensory organs. In the thoracic and abdominal segments the es cells were identified as the tormogen and trichogen. In late third instar larvae, expression is observed in many larval and imaginal tissues but not in the CNS. Transcripts are broadly distributed in the discs but in a nonuniform pattern. In the wing disc, transcripts are most abundant in the posterior region of the wing pouch. In the leg disc, expression is also observed in a posterior zone of the disc. In the eye-antennal disc, low levels of expression are observed posterior to the morphogenetic furrow and and in the central antennal region while higher levels are observed in the vicinity of the furrow and along the margins of the disc. In 16-24hr pupae, Su(H) is expressed in many tissues including developing muscle and epidermis. In michrochaetae and macrochaetae, expression is observed in a couple of large cells that appear to be the tormogen and trichogen. Expression in the tormogen occurs at a higher level.

Su(H) transcripts are detected in RNA from embryos, adult males and adult females.

Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
western blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data

Su(H) protein is observed in the nucleus in all cells in the third instar wing disc. It was sometimes observed in the surrounding cytoplasm of both macrochaete and microchaete SOPs. It is observed in the nucleus and cytoplasm of socket cells. It does not co-localize with N protein at the apicolateral membrane in socket cells.

Su(H) protein is strongly expressed in prohemocytes in the medullary zone of the lymph gland and is weakly expressed in differentiated hemocytes in the cortical zone.

Su(H) protein isdetected by western blots in extracts from embryos, third instar wingdiscs, and nota dissected from 24hr APF pupae. It's expression was studiedduring SOP specification by immunolocalization. In wing discs of latethird instar larvae, it is expressed at a low level in all nuclei. It ispresent equally in macrochaete SOPs and the neighboring proneuralclusters. A similar observation was made fro microchaete SOPs in thedeveloping notum at 14hr APF. In this case, Su(H) protein is detected inboth the microchaete SOPs and the surrounding epithelial cells. FollowingSOP division, no difference in staining is seen between SOPIIa and SOPIIb.With further differentiation of SOPIIa and SOPIIb, Su(H) proteinexpression is observed specifically in the socket cell. This is true insocket cells of the machrochaetes, microchaetes and the interommatidialbristle. Su(H) protein is also expressed in a small number of embryonicsense organ cells per segment. These support cells show a 'socket-like'morphology.

Marker for
Subcellular Localization
CV Term
Evidence
References
located_in cytoplasm
inferred from direct assay
is_active_in nucleus
inferred from direct assay
located_in nucleus
inferred from direct assay
inferred from physical interaction with FLYBASE:N; FB:FBgn0004647
inferred from genetic interaction with FLYBASE:ebi; FB:FBgn0263933
Expression Deduced from Reporters
High-Throughput Expression Data
Associated Tools

JBrowse - Visual display of RNA-Seq signals

View Dmel\Su(H) in JBrowse
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
DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
FlyExpress - Embryonic expression images (BDGP data)
  • Stages(s) 1-3
  • Stages(s) 4-6
  • Stages(s) 7-8
  • Stages(s) 9-10
  • Stages(s) 11-12
  • Stages(s) 13-16
Alleles, Insertions, Transgenic Constructs, and Aberrations
Classical and Insertion Alleles ( 74 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 71 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of Su(H)
Transgenic constructs containing regulatory region of Su(H)
Aberrations (Deficiencies and Duplications) ( 146 )
Inferred from experimentation ( 146 )
Gene disrupted in
Gene not disrupted in
Inferred from location ( 7 )
Variants
Variant Molecular Consequences
Alleles Representing Disease-Implicated Variants
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
dorsal mesothoracic disc & neuron
embryonic/first instar larval cuticle & embryonic head | germ-line clone
eye disc & neuron | somatic clone | cell autonomous
macrochaeta & adult abdomen
macrochaeta & leg
mesothoracic tergum & sensory organ cell & pupa | somatic clone
neuron & eye | somatic clone
neuron & eye | supernumerary | somatic clone
photoreceptor cell & axon & larva
photoreceptor cell R8 & eye disc | ectopic | somatic clone
photoreceptor cell R8 & eye disc | somatic clone
proneural cluster & dorsal mesothoracic disc
Orthologs
Human Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Homo sapiens (Human) (2)
14 of 14
Yes
Yes
7 of 14
No
Yes
Model Organism Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Rattus norvegicus (Norway rat) (3)
14 of 14
Yes
Yes
11 of 14
No
Yes
7 of 14
No
Yes
Mus musculus (laboratory mouse) (2)
14 of 14
Yes
Yes
6 of 14
No
Yes
Xenopus tropicalis (Western clawed frog) (2)
7 of 13
Yes
Yes
1 of 13
No
No
Danio rerio (Zebrafish) (3)
14 of 14
Yes
Yes
13 of 14
No
Yes
7 of 14
No
Yes
Caenorhabditis elegans (Nematode, roundworm) (1)
12 of 14
Yes
Yes
Anopheles gambiae (African malaria mosquito) (1)
12 of 12
Yes
Yes
Arabidopsis thaliana (thale-cress) (0)
Saccharomyces cerevisiae (Brewer's yeast) (0)
Schizosaccharomyces pombe (Fission yeast) (2)
8 of 12
Yes
Yes
5 of 12
No
Yes
Escherichia coli (enterobacterium) (0)
Other Organism Orthologs (via OrthoDB)
Data provided directly from OrthoDB:Su(H). Refer to their site for version information.
Paralogs
Paralogs (via DIOPT v9.1)
Human Disease Associations
FlyBase Human Disease Model Reports
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 2 )
Potential Models Based on Orthology ( 1 )
Modifiers Based on Experimental Evidence ( 9 )
Disease Associations of Human Orthologs (via DIOPT v9.1 and OMIM)
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
Interaction Browsers

Please see the Physical Interaction reports below for full details
protein-protein
Physical Interaction
Assay
References
Summary of Genetic Interactions
Interaction Browsers

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
Subunit Structure (UniProtKB)
Interacts with activated cleaved Notch. Interacts with Hairless, this interaction preventing its DNA-binding activity. Interacts with insv (via BEN domain).
(UniProt, P28159 )
Linkouts
BioGRID - A database of protein and genetic interactions.
DroID - A comprehensive database of gene and protein interactions.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Pathways
Signaling Pathways (FlyBase)
Metabolic Pathways
FlyBase
External Links
External Data
Linkouts
KEGG Pathways - A collection of manually drawn pathway maps representing knowledge of molecular interaction, reaction and relation networks.
Reactome - An open-source, open access, manually curated and peer-reviewed pathway database.
SignaLink - A signaling pathway resource with multi-layered regulatory networks.
Class of Gene
Genomic Location and Detailed Mapping Data
Chromosome (arm)
2L
Recombination map
2-50
Cytogenetic map
Sequence location
FlyBase Computed Cytological Location
Cytogenetic map
Evidence for location
35B8-35B8
Limits computationally determined from genome sequence between P{EP}elBEP2039&P{PZ}osprJ571 and P{lacW}Su(H)k07904
Experimentally Determined Cytological Location
Cytogenetic map
Notes
References
35B8-35B9
(determined by in situ hybridisation)
35B8-35B10
(determined by in situ hybridisation)
35B9-35B10
(determined by in situ hybridisation)
35B-35C
(determined by in situ hybridisation)
Experimentally Determined Recombination Data
Left of (cM)
Notes
Stocks and Reagents
Stocks (38)
Genomic Clones (15)
 

Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete

cDNA Clones (25)
 

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 JBrowse for alignment of the cDNAs and ESTs to the gene model.

cDNA clones, fully sequenced
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
Antibody Information
Laboratory Generated Antibodies
Commercially Available Antibodies
 
Cell Line Information
Publicly Available Cell Lines
 
    Other Stable Cell Lines
     
      Other Comments

      The Su(H) product has a dual role, both as a N-independent repressor of transcription and as a N-dependent activator of transcription.

      Mutant analysis suggests that dx signalling is dependent on the activity of Su(H).

      dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.

      Su(H) has a N independent function during the development of bristle sensory organ precursor cells.

      Neither E(spl) nor Su(H) seem to be involved in the N pathway that directs the neuron/glia choice in the PNS.

      Su(H) has three distinct functions in the development of external mechanosensory organs; N-dependent transcriptional activation, an auto-repression function, both of which direct cell fate decisions, and an auto-activation function required for normal socket cell differentiation.

      The Su(H) phenotype is epistatic to that of H during wing disc development.

      During wing development Su(H) can activate the expression of some N target genes independently of N. Activation of other N target genes depends on the joint activity of Su(H) and the intracellular fragment of the N protein; without the N fragment Su(H) acts as a repressor of these genes. Su(H) activity is inhibited by H, suggesting that the activation of Su(H) by N involves the release of Su(H) from an inhibitory complex which contains H.

      Su(H) activity is required to upregulate sim expression in the mesectoderm, and to prevent ectopic expression of sim dorsally in the neurectoderm in cellularising embryos.

      Su(H) is essential to determine outer but not inner cell fates in the sensory organ cell lineage.

      N is processed in a ligand-dependent manner to generate a phosphorylated cytoplasmic domain that preferentially associates with Su(H). Localization studies suggest that the relative levels of Su(H), Dl and N regulate nuclear entry of the N/Su(H) complex.

      Mutants isolated in a screen of the second chromosome identifying genes affecting disc morphology.

      N-inducible expression of HLHmδ and HLHmγ both in cultured cells and in vivo is dependent on functional Su(H) protein.

      Factors, in addition to Su(H), must exist to confer tissue-specific expression of vg and to regulate the spatial and temporal features of vg expression within the wing pouch. Su(H) has differential roles in the dorsal and ventral wing boundary cells. Su(H) represses the vg quadrant enhancer at the D/V boundary.

      Su(H) is required for only a subset of the asymmetric divisions that depend on the function of numb and N. Su(H) appears to act downstream of numb in the same genetic pathway in determining the fates of the IIa daughter cells, the hair cell and the socket cell, and Su(H) is negatively regulated by numb.

      Subcellular localisation of Su(H) during N signalling is analysed.

      Su(H) binds to and activates the vg dorsal/ventral boundary enhancer.

      Su(H) directly participates in N lateral signalling during sensory organ precursor (SOP) specification. N, H and Su(H) exhibit dose-dependent genetic interactions.

      Su(H) is required for all aspects of N function at the wing dorsoventral boundary.

      The genes of the E(spl) complex mediate only a subset of N activities during imaginal development. Comparisons of mutant phenotypes suggests that the N pathway bifurcates after the activation of Su(H) and that E(spl) activity is not required when the consequence of N function is the transcriptional activation of downstream genes. Transcriptional activation mediated by Su(H) and transcriptional repression mediated by E(spl) could provide greater diversity in the response of individual genes to N activity.

      The proximal upstream region of E(spl) complex genes contains multiple specific binding sites for Su(H). Integrity of these sites and Su(H) activity are required not only for normal levels of E(spl) complex gene expression in imaginal disc proneural clusters but also for their transcriptional response to hyperactivity of the N receptor. Su(H) is a direct regulatory link between N receptor activity and the expression of E(spl) complex genes, extending the known lineage of the N cell-cell signaling pathway.

      Activation of N, mediated through Su(H), is sufficient to direct wg expression in the wing.

      Su(H) protein binds to TGTGGGAA sequence located 616bp upstream of the transcription initiation site of E(spl).

      There is a strict genetic requirement for Su(H) activity for cell fate choices during early neurogenesis.

      Glutathione-S-transferase (GST) fusion proteins and the yeast two hybrid system demonstrate the H protein can inhibit the in vitro DNA binding activity of Su(H) through direct protein-protein interactions. Co-transfection assays in S2 cells demonstrate transcriptional activation driven by Su(H) is also inhibited by H.

      The dx gene product regulates the subcellular localisation of a transcription factor, Su(H), via antagonistic interactions with the N ankyrin repeats.

      Notum cells require Su(H) activity for receiving the lateral inhibitory signal. The DNA binding protein encoded by the Su(H) gene may act downstream of the N receptor to implement the epidermal non-sense organ precursor (SOP) fate.

      Yeast two-hybrid system assays and in vitro interaction studies demonstrate the sub-transmembrane region of N, structurally equivalent to the amino terminal part of mRAM23, is involved in the interaction with Su(H).

      Mutations can act as dominant modifiers of the activated N eye phenotype (FBrf0064452).

      In vitro binding assays demonstrate the H gene product can inhibit the DNA binding of Su(H) through direct protein-protein interactions. Consistent with this, transcriptional activation driven by Su(H) in transfected S2 cells is inhibited by H. These results support a model in which H acts, in part, as a negative regulator of Su(H) activity.

      Su(H) shows allele specific interactions with N, Dl, dx and mam.

      In cultured Drosophila cells, the Su(H) product is sequestered in the cytoplasm when coexpressed with N protein and is translocated to the nucleus when N protein binds its Dl protein ligand.

      N activity may regulate nuclear events by controlling the activity of the Su(H) DNA-binding protein.

      Decreasing or increasing the level of Su(H) function confers mutant phenotypes that closely resemble those associated with gain and loss of H activity, respectively.

      The sequence similarity between Su(H) and the integrase domain is not of functional significance as Tyr315 is not required for gene function in vivo.

      Genetic interactions with H suggest that Su(H) might be involved in cell fate specification in the adult PNS.

      Isolated from a genomic library using the murine RBP-JΚ cDNA as a probe, under low stringency conditions.

      Su(H) has been cloned and characterised.

      Homozygous lethal; hemizygotes die in the pupal stage, between head eversion and the beginning of eye pigmentation. Heterozygotes in the absence of H are wild type in phenotype. Suppresses H; Su(H)/+; H/+ have 7-10 more bristles that H/+ alone; besides affecting the bristle phenotype of H, all alleles tend to enhance its wing-vein phenotype of shortening L4 and L5. Su(H) is without effect on the lethal phenotype of homozygous H. One homozygous-lethal allele acts as a dominant enhancer of H. Most alleles are amorphic or hypomorphic; heterozygous deficiencies for the locus also suppress and duplications enhance H (Nash, 1970). Enhanced genotypes have 10-15 fewer bristles and a far more extreme loss of microchaetae on the thorax than their unenhanced counterparts. The number of bristles in H/+ flies is inversely related to the dose of Su(H)+, with the number of bristles varying from fewer than ten with four doses to approximately 35 with one dose. Some combinations of hypomorphic alleles produce occasional escapers; survivors have distinctive phenotypes, which are described under entries for specific alleles.

      Relationship to Other Genes
      Source for database merge of

      Source for merge of: Su(H) anon-WO0257455.3

      Additional comments

      Source for merge of Su(H) anon-WO0257455.3 was sequence comparison ( date:051113 ).

      Nomenclature History
      Source for database identify of

      Source for identity of: Su(H) CG3497

      Nomenclature comments
      Etymology
      Synonyms and Secondary IDs (40)
      Reported As
      Symbol Synonym
      D
      E(H)
      RBP-Jkappa
      Su(H)
      (Shi et al., 2026, Malidarreh et al., 2025, Park et al., 2025, Wu et al., 2025, Breuer et al., 2024, Deichsel et al., 2024, Fenelon et al., 2024, Jain et al., 2024, Kim et al., 2024, Kim et al., 2024, Larnerd et al., 2024, Luo et al., 2024, Mattila et al., 2024, Megaly et al., 2024, Mönch et al., 2024, Nair and Baker, 2024, Pinot and Le Borgne, 2024, Sachan et al., 2024, Sood et al., 2024, Wang et al., 2024, Wang et al., 2024, Zhao et al., 2024, Aughey et al., 2023, Chen et al., 2023, Hodge et al., 2023, Josserand et al., 2023, Liu et al., 2023, Maier et al., 2023, Mo et al., 2023, Rosales-Vega et al., 2023, Yheskel et al., 2023, Yu et al., 2023, Chen et al., 2022, Ding et al., 2022, Falo-Sanjuan and Bray, 2022, Fechner et al., 2022, Gagliani et al., 2022, Jullien et al., 2022, Koca et al., 2022, Petridi et al., 2022, Ray and Li, 2022, Revici et al., 2022, Soares et al., 2022, Yasugi and Sato, 2022, Zhang and Edgar, 2022, Bonfini et al., 2021, Boukhatmi, 2021, Cattenoz et al., 2021, Chen et al., 2021, DeAngelis et al., 2021, Ferguson et al., 2021, Frankenreiter et al., 2021, Girard et al., 2021, Harnish et al., 2021, Irizarry and Stathopoulos, 2021, Johnson, 2021, Krishnan et al., 2021, Kuang et al., 2021, Nagel et al., 2021, Parkhitko et al., 2021, Resnik-Docampo et al., 2021, Sun et al., 2021, Zhou et al., 2021, Ahmed et al., 2020, Bahrampour and Thor, 2020, Cho et al., 2020, Cho et al., 2020, Feng et al., 2020, Girard et al., 2020, Haudry et al., 2020, Hung et al., 2020, Lan et al., 2020, Li et al., 2020, Li et al., 2020, Maier, 2020, Mehrotra et al., 2020, Nagel et al., 2020, Panta et al., 2020, Salazar et al., 2020, Sato and Yasugi, 2020, Serafini et al., 2020, Shen and Sun, 2020, Wang et al., 2020, Wei et al., 2020, Wilson et al., 2020, Yamamoto, 2020, Zhao et al., 2020, Banerjee et al., 2019, Chai et al., 2019, Flint Brodsly et al., 2019, Gahr et al., 2019, Houtz et al., 2019, Koca et al., 2019, Maier, 2019, Miller et al., 2019, Ng et al., 2019, Paddibhatla et al., 2019, Shokri et al., 2019, Simon et al., 2019, Singh et al., 2019, Smylla et al., 2019, Zacharioudaki et al., 2019, Alfred and Vaccari, 2018, Bala Tannan et al., 2018, Bischof et al., 2018, Giaimo et al., 2018, Gomez-Lamarca et al., 2018, Kavaler et al., 2018, Khajouei and Sinha, 2018, Ren et al., 2018, Salazar and Yamamoto, 2018, Von Stetina et al., 2018, Yang and Deng, 2018, Ahmad, 2017, Bhattacharya et al., 2017, Chan et al., 2017, Court et al., 2017, Koromila and Stathopoulos, 2017, Lin et al., 2017, Liu and Jin, 2017, Liu et al., 2017, Miller et al., 2017, Nagel et al., 2017, Praxenthaler et al., 2017, Shukla et al., 2017, Solis et al., 2017, Strilbytska et al., 2017, Wu et al., 2017, Xu et al., 2017, Xu et al., 2017, Zehender et al., 2017, Bivik et al., 2016, Chen et al., 2016, Han et al., 2016, Horvath et al., 2016, Hudry et al., 2016, Hunter et al., 2016, Jiang et al., 2016, Kockel et al., 2016, Morimoto et al., 2016, Nagel et al., 2016, Ramat et al., 2016, Saha et al., 2016, Slaninova et al., 2016, Tracy et al., 2016, Auer et al., 2015, Auer et al., 2015, Baëza et al., 2015, Dutta et al., 2015, Jiang et al., 2015, Mishra et al., 2015, Palmer et al., 2015, Praxenthaler et al., 2015, Reimels and Pfleger, 2015, Sachan et al., 2015, Schertel et al., 2015, Spratford and Kumar, 2015, Spratford and Kumar, 2015, Xing et al., 2015, Ahmad et al., 2014, Andrés et al., 2014, Boyle et al., 2014, Brockmann et al., 2014, Charng et al., 2014, Córdoba and Estella, 2014, Housden et al., 2014, Jia et al., 2014, Li et al., 2014, Li et al., 2014, Liu and Posakony, 2014, Loubéry and González-Gaitán, 2014, Loza-Coll et al., 2014, Mannervik, 2014, Nagel and Preiss, 2014, Pearson and Crews, 2014, Pézeron et al., 2014, Slattery et al., 2014, Wurmbach and Preiss, 2014, Xie et al., 2014, Zacharioudaki and Bray, 2014, Babaoğlan et al., 2013, Christiansen et al., 2013, Dai et al., 2013, Dai et al., 2013, Das et al., 2013, Das et al., 2013, Djiane et al., 2013, Jauffred et al., 2013, Langen et al., 2013, Lee et al., 2013, Li et al., 2013, Li et al., 2013, Maier et al., 2013, Morozov and Ioshikhes, 2013, Müller et al., 2013, Sasamura et al., 2013, Spokony and White, 2013.5.10, Sun and Spradling, 2013, Terriente-Felix et al., 2013, Tremmel et al., 2013, Xiong et al., 2013, Yu et al., 2013, Zeng et al., 2013, Zhang et al., 2013, Aboukhalil and Bulyk, 2012, Giagtzoglou et al., 2012, Heck et al., 2012, Kapuria et al., 2012, Liu and Posakony, 2012, Mou et al., 2012, Peng et al., 2012, Popkova et al., 2012, Rincon-Arano et al., 2012, Tokusumi et al., 2012, Troost and Klein, 2012, Zacharioudaki et al., 2012, Benhra et al., 2011, Bhattacharya and Baker, 2011, Cave et al., 2011, Di Stefano et al., 2011, Duan et al., 2011, Jiang et al., 2011, Kurth et al., 2011, Kuzina et al., 2011, Maier et al., 2011, Miura, 2011, Nicholson et al., 2011, O'Keefe et al., 2011, Ozdemir et al., 2011, Park et al., 2011, Perdigoto et al., 2011, Pérez et al., 2011, Quijano et al., 2011, Rebeiz et al., 2011, Ren et al., 2011, San-Juán and Baonza, 2011, Tong et al., 2011, Wang et al., 2011, Zhang et al., 2011, Aerts et al., 2010, Bardin et al., 2010, Beebe et al., 2010, Bernard et al., 2010, Issigonis and Matunis, 2010, Kim et al., 2010, Liefke et al., 2010, Monastirioti et al., 2010, Mourikis et al., 2010, Pierce et al., 2010.8.10, Saj et al., 2010, Swanson et al., 2010, Terriente-Félix et al., 2010, Tokusumi et al., 2010, Tong et al., 2010, Wang and Hou, 2010, Andrews et al., 2009, Ayroles et al., 2009, Babaoglan et al., 2009, Bhattacharya and Baker, 2009, Boyle and Berg, 2009, Cai and Laughon, 2009, Firth and Baker, 2009, Guruharsha et al., 2009, Jin et al., 2009, Krejcí et al., 2009, Li et al., 2009, Ma et al., 2009, Mao and Freeman, 2009, Martinez et al., 2009, Miller et al., 2009, Moshkin et al., 2009, Mummery-Widmer et al., 2009, Patel et al., 2009, Roegiers et al., 2009, Sanders et al., 2009, Schaaf et al., 2009, Shyu et al., 2009, Simon et al., 2009, Song et al., 2009, Twombly et al., 2009, Vied and Kalderon, 2009, Becam and Milán, 2008, Cave and Caudy, 2008, Chang et al., 2008, Crocker et al., 2008, del Alamo and Mlodzik, 2008, Eastman and Maeder, 2008, Hayashi et al., 2008, Herranz et al., 2008, Kaspar et al., 2008, Le Gall et al., 2008, Liu and Posakony, 2008, Maier et al., 2008, Parks et al., 2008, Prince et al., 2008, Rand et al., 2008, Remaud et al., 2008, Sukhanova and Du, 2008, Talora et al., 2008, Terriente Felix and de Celis, 2008.1.16, Wang et al., 2008, Wheeler et al., 2008, Yamada et al., 2008, Arbouzova and McNeill, 2007, Christensen and Cook, 2007.5.8, Edenfeld et al., 2007, Furriols et al., 2007, Goodfellow et al., 2007, Grillenzoni et al., 2007, Jemc and Rebay, 2007, Kelly et al., 2007, Krejci and Bray, 2007, Lee and Lundell, 2007, Ohlstein and Spradling, 2007, Ohlstein and Spradling, 2007, Park et al., 2007, Sun and Deng, 2007, Tanaka et al., 2007, Vied and Kalderon, 2007, Zeitlinger et al., 2007, Zeitouni et al., 2007, Balakireva et al., 2006, Cohen et al., 2006, Fuwa et al., 2006, Gallagher and Knoblich, 2006, Gao and Laughon, 2006, Giebel and Wodarz, 2006, Hayward et al., 2006, Herranz and Milan, 2006, Hutterer et al., 2006, Jaekel and Klein, 2006, Jafar-Nejad et al., 2006, Jordan et al., 2006, Joshi et al., 2006, Kaspar and Klein, 2006, Koelzer and Klein, 2006, Langdon et al., 2006, Müller et al., 2006, Philippakis et al., 2006, Tsuda et al., 2006, Ward et al., 2006, Ward et al., 2006, Zinzen et al., 2006, Apitz et al., 2005, Baonza and Freeman, 2005, Birch-Machin et al., 2005, David et al., 2005, de Wit et al., 2005, Firth and Baker, 2005, Gao et al., 2005, Jafar-Nejad et al., 2005, Nagel et al., 2005, Peel et al., 2005, Stathopoulos and Levine, 2005, Tang et al., 2005, Thomas, 2005, Veraksa et al., 2005, Wong et al., 2005, Ahimou et al., 2004, Voas and Rebay, 2004, Michellod et al., 2003, Wesley and Mok, 2003, Kitagawa et al., 2001, Nagel et al., 2000, Weinmaster, 1997)
      anon-WO0257455.3
      l(1)br7
      l(2)k07904
      Name Synonyms
      lethal 7 in the black-reduced region
      lethal group D
      suppressor of Hairless
      suppressor of hairless
      suppressor-of-hairless
      transcription unit C
      Secondary FlyBase IDs
      • FBgn0003566
      • FBgn0004467
      • FBgn0021969
      • FBgn0022068
      • FBgn0063792
      Datasets (0)
      Study focus (0)
      Experimental Role
      Project
      Project Type
      Title
      Study result (0)
      Result
      Result Type
      Title
      External Crossreferences and Linkouts ( 110 )
      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 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/GCRP - The gene-centric reference proteome (GCRP) provides a 1:1 mapping between genes and UniProt accessions in which a single 'canonical' isoform represents the product(s) of each protein-coding gene.
      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
      AlphaFold DB - AlphaFold provides open access to protein structure predictions for the human proteome and other key proteins of interest, to accelerate scientific research.
      BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
      DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
      EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
      FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
      FlyMine - An integrated database for Drosophila genomics
      KEGG Genes - Molecular building blocks of life in the genomic space.
      MARRVEL_MODEL - MARRVEL (model organism gene)
      PDB - An information portal to biological macromolecular structures
      Linkouts
      BioGRID - A database of protein and genetic interactions.
      Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
      DroID - A comprehensive database of gene and protein interactions.
      DRSC - Results frm RNAi screens
      Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
      FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
      FlyCyc Genes - Genes from a BioCyc PGDB for Dmel
      Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
      Flygut - An atlas of the Drosophila adult midgut
      FlyMet - A comprehensive tissue-specific metabolomics resource for Drosophila.
      iBeetle-Base - RNAi phenotypes in the red flour beetle (Tribolium castaneum)
      Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
      KEGG Pathways - A collection of manually drawn pathway maps representing knowledge of molecular interaction, reaction and relation networks.
      MIST (genetic) - An integrated Molecular Interaction Database
      MIST (protein-protein) - An integrated Molecular Interaction Database
      Reactome - An open-source, open access, manually curated and peer-reviewed pathway database.
      SignaLink - A signaling pathway resource with multi-layered regulatory networks.
      References (949)