FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Su(H)2
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General Information
Symbol
Dmel\Su(H)2
Species
D. melanogaster
Name
FlyBase ID
FBal0016303
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Su(H)AR9, AR9, l(2)br7AR9
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

Unclear, may be a complicated chromosomal aberration.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

embryonic/first instar larval cuticle & embryonic head | germ-line clone

proneural cluster & dorsal mesothoracic disc

Detailed Description
Statement
Reference

When expression is driven using Scer\GAL4da.PU, Su(H)Scer\UAS.T:Avic\GFP,T:SV5\V5 rescues viability of Su(H)2/Su(H)8, although adult flies have some wing and eye defects (reminiscent of reduced N function).

In Su(H)2 homozygous embryos, the early steps of proventricular development including the formation of the ball-like evagination at the ectoderm/endoderm boundary occur normally. However, at stage 14, the anterior boundary cells of the keyhole region fail to invaginate into the endodermal cell layer, but arrest anteriorly and do not move inwards until the final stages of embryonic development (16 and 17). In addition, the posterior boundary cells of the endodermal component of the proventriculus rim collapses in these animals.

Mutant embryos show normal boundary cell differentiation in the hindgut.

Wing primordium is established but does not grow. Lateral inhibition fails in the notum, causing an excess of neural precursors.

In Su(H)8/Su(H)2 mutant wing discs, each proneural cluster is enlarged as compared to wild-type.

Homozygous clones in the anterior ventral compartment of the leg result in fusion between the distal femur and proximal tibia, and cells in the clone fail to form joint tissue.

Dorsal mitotic clones in the wing encompassing the LII and LII veins cause an autonomous thickening of dorsal LIII but does not affect vein differentiation in the ventral surface. Ventral clone covering LII results in the differentiation of a thicker LII.

Dorsal, ventral and dorsoventral clones that extend to the wing margin produce extensive scalloping.

Clones in the thorax produce patches of naked cuticle, due to the differentiation of the ectopic SOPs into neurons. Clones in the wing that reach the wing margin show a loss of margin and blade tissue due to the requirement for N at the D/V boundary. Wing veins also appear thicker.

Homozygous embryos derived from germ-line clones exhibit a strong neurogenic cuticular phenotype and fail to hatch. The number of neuroblasts and sensory precursors that segregate from the ventral and dorsolateral neuroectoderm, respectively, is greatly increased. This leads to hypertrophy of the CNS and PNS and failure of ventral and head cuticle to develop. No defect is seen in the nervous system when rescued by wild type paternal copy of Su(H). Heterozygous embryos derived from germ-line clones survive to adulthood.

Lethality during the first day of pupal development. Supernumerary cells stained in mutant imaginal discs have adopted a sensory organ precursor (SOP) fate instead of the epidermal fate they would normally express. The excess SOPs arise from the proneural clusters of potential precursor cels that appear in the imaginal discs during the development of wild type bristles. The wing pouch region of the wing imaginal disc and the retinal field of the eye-antennal imaginal disc are dramatically reduced. Identical phenotype is seen when transheterozygous with Df(2L)TE35BC-24, Su(H)1, Su(H)8 or Su(H)IB115.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference

Su(H)[+]/Su(H)2 is an enhancer of visible | adult stage phenotype of Scer\GAL4sca-109-68, hamUAS.cMa

NOT Enhancer of
Statement
Reference

Su(H)[+]/Su(H)2 is a non-enhancer of visible phenotype of Scer\GAL4pnr-MD237, fredRNAi.UAS

Suppressor of
Statement
Reference

Su(H)[+]/Su(H)2 is a suppressor | partially of visible | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU

NOT Suppressor of
Statement
Reference

Su(H)[+]/Su(H)2 is a non-suppressor of visible phenotype of Scer\GAL4pnr-MD237, fredRNAi.UAS

Other
Statement
Reference
Phenotype Manifest In
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference

Su(H)[+]/Su(H)2 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, fredRNAi.UAS

Su(H)2 is an enhancer of wing vein phenotype of NAx-E2

Su(H)[+]/Su(H)2 is an enhancer of wing phenotype of Nnd-1

Su(H)[+]/Su(H)2 is an enhancer of wing vein phenotype of Nnd-1

Su(H)2 is an enhancer of phenotype of Delta9P

NOT Enhancer of
Statement
Reference

Su(H)2 is a non-enhancer of larval intersegmental nerve | heat sensitive phenotype of Nl1N-ts1

Su(H)2 is a non-enhancer of phenotype of NAx-M1

Su(H)2 is a non-enhancer of phenotype of NAx-59d

Su(H)2 is a non-enhancer of phenotype of Nl1N-B

Suppressor of
Statement
Reference

Su(H)[+]/Su(H)2 is a suppressor | partially of wing blade posterior compartment | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU

NOT Suppressor of
Statement
Reference

Su(H)2 is a non-suppressor of larval intersegmental nerve | heat sensitive phenotype of Nl1N-ts1

Su(H)2 is a non-suppressor of phenotype of NAx-M1

Su(H)2 is a non-suppressor of phenotype of Nl1N-B

Su(H)2 is a non-suppressor of phenotype of NAx-59d

Other
Additional Comments
Genetic Interactions
Statement
Reference

The wing blistering phenotype seen in the posterior compartment of wings in flies expressing EogtGD5084 under the control of Scer\GAL4en.PU in the presence of Dcr-2Scer\UAS.cDa is dominantly partially suppressed if the flies are also heterozygous for Su(H)2.

Su(H)2 Sox154AA/Su(H)8 Sox154AA; Su(H)RC-ΔASE mutants show a more dramatic socket differentiation defect than either single mutant. Most of the double mutant bristles have a convex (rather than concave) socket-shaft cuticular interface. Dome of these bulbous socket structures extend one or more small cuticular projections, while others extend one or two distinctly shaft-like structures.

The addition of Su(H)2/+ to freddsRNA.Scer\UAS, Scer\GAL4pnr-MD237 animals has no detectable effect on the freddsRNA.Scer\UAS phenotype. However when Su(H)2/+ is added to freddsRNA.Scer\UAS driven by Scer\GAL4GMR.PF, an enhancement of the rough eye phenotype is seen.

The neurogenic phenotype, but not the wing development phenotype, of Su(H)2/Su(H)8 is strongly suppressed by either HLHm7Scer\UAS.cdCa or E(spl)Scer\UAS.cNa driven by Scer\GAL4klu-G410. The wing development phenotype of Su(H)2/Su(H)8 is not suppressed by either Nint.SH.Scer\UAS or DlScer\UAS.cHa, or SerScer\UAS.cSa in combination with vgScer\UAS.cKa, driven by Scer\GAL4dpp.blk1. The wing development phenotype of Su(H)2/Su(H)8 is also not suppressed by HE31.

Su(H)2 has no effect on the wing disc proneural cluster phenotypes seen in NAx-59d or NAx-M1, or the lack of phenotype seen in Nl1N-B discs. The addition of Su(H)2/Su(H)8 has no effect on the wing disc proneural cluster phenotype seen in NECNΔ10-12.Scer\UAS/Scer\GAL4ptc-559.1 discs.

Scer\GAL4dpp.blk1-mediated or Scer\GAL4ptc-559.1-mediated expression of vgScer\UAS.cKa substantially rescues the wing blade phenotype. Scer\GAL4dpp.blk1-mediated expression of wgScer\UAS.cGa does not rescue loss of wing tissue.

Loss of a single copy of Su(H) in sno71e3 flies causes pupal lethality at 23oC and at 20oC some pupae eclose and exhibit severe wing margin defects.

Abruptex wing phenotype of NAx-E2 dominantly enhanced by Su(H)2.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments

When expression is driven using Scer\GAL4da.PU, Su(H)Scer\UAS.T:Avic\GFP,T:SV5\V5 rescues viability of Su(H)2/Su(H)8.

When expression of Su(H)Scer\UAS.cKa is driven by Scer\GAL4dpp.blk1 in a Su(H)2/Su(H)8 mutant the wing pouch size defect is rescued. When expression of Su(H)Scer\UAS.cKa is driven by Scer\GAL4klu-G410 in a Su(H)2/Su(H)8 mutant the neurogenesis and wing pouch size defects are rescued.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Ashburner.

Isolated from: Greece population.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (51)