FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\dpn1
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General Information
Symbol
Dmel\dpn1
Species
D. melanogaster
Name
FlyBase ID
FBal0031051
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description
Allele components
Component
Use(s)
Inserted element
Encoded product / tool
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 ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

No excess neuroblasts are seen in dpn1 mutant brains.

Type II neuroblasts are completely absent in the brains of late third larval instar dpn1/dpn7 larvae. The number of type I neuroblasts is close to that of wild type at 9-12 hours after larval hatching (ALH), but is reduced compared to wild type at 48 hours ALH, and does not reduce further from 48 hours to 96 hours ALH.

Mushroom body neuroblasts are progressively lost in dpn1/dpn7 mutants: at the late third instar larval stage nearly half of the mushroom body neuroblasts are missing, and by the start of pupariation, 90% of them are lost.

In the optic nerve of dpn1 homozygous third instar larvae,sporadic breaks are evident in the normally continuous area of S phase positive cells. These breaks can vary in size and location in the outer proliferation center (OPC) of the developing optic lobe, but can be found in the OPC of nearly all homozygous dpn1 mutant larvae. In addition, S-phase activity in the developing lamina appears compressed and disorganized. The number of photoreceptor axons in dpn1 and wild type mutant remains similar, however the number of lamina cells is decreased.

Viability of homozygous females: 13%. Viability of homozygous males: 20%.

Homozygotes die at various stages of development, with occasional adult survivors when conditions are especially favourable. Homozygous larvae are weak, but there are no consistant morphological defects when examined with antibodies that recognise neuronal nuclei, membranes or neuroblasts, or PNS cytoplasm, neuronal precursors or muscles. More than 50% of the males doubly heterozygous for dpn1 and a duplication for the achaete-scute complex die.

Flies homozygous for dpn1 or heterozygous for dpn1 and a deficiency show reduced viability and die at various stages of development: viabilities relative to controls are 1.5% in males and 8-10% in females. Males with 2 or 3 copies of sc+ and homozygous for dpn1 were never recovered. Females with 3 copies of sc+ and homozygous for dpn1 have improved viability whereas females with three copies of dpn+ and one copy of sc+ show reduced viability. dpn1 larvae and adults show limited movement and are extremely lethargic.

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

dpn[+]/dpn1 is an enhancer of visible | dominant phenotype of N55e11

Suppressor of
Other
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

dpn[+]/dpn1 is an enhancer of wing margin phenotype of N55e11

dpn[+]/dpn1 is an enhancer of eye phenotype of scrtjo11

dpn[+]/dpn1 is an enhancer of eye photoreceptor cell phenotype of scrtjo11

Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

Homozygous dpn1 suppresses the supernumerary neuroblast phenotype seen in erm1/Df(2L)erm2 mutant clones originating from a single type II neuroblast.

dpn1/+ enhances the wing notching phenotype seen in N55e11/+ flies (78% of flies have wing nicks).

dpn1/+ enhances the mild wing vein phenotype of Df(3R)E(spl)Δmγ-mβ-DK33-10.1 flies, such that the double mutant has prominent vein thickening at the tips of veins L4 and L5 as well as ectopic veins flanking vein L5 in 26% of wings.

prosV17/+ partially rescues the reduction in number of type I neuroblasts which is seen in the brains of late third larval instar dpn1/dpn7 larvae.

Whereas either single mutant shows escapers, dpn1, scrtjo11 double mutant embryos never hatch and exhibit a dramatic reduction of both central and peripheral nervous system nervous system. While eyes of dpn1 are normal, dpn1/+,scrtjo11 have an enhanced rough eye phenotype and more severe loss of photoreceptors than for scrtjo11 alone.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Viability of dpn1/dpn6 is unexpectedly high, perhaps due to transvection between the alleles.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (14)