FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\RanBPMΔ
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General Information
Symbol
Dmel\RanBPMΔ
Species
D. melanogaster
Name
FlyBase ID
FBal0230247
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

RanBPMΔ is a deletion of the region between the FRT sequences in P{RS3}RanBPMCB-6232-3 and PBac{WH}RanBPMf06647 (i.e. exons 1 and 11)

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

Deletion resulting from recombination between the directly repeated FRT sites in P{RS3}RanBPMCB-6232-3 and PBac{WH}RanBPMf06647. P element sequences remain.

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

Complementation tests show that RanBPMΔ is lethal in trans with Df(2R)12 and RanBPMf06647, is semi-lethal with RanBPMCB-6232-3, and is temperature-sensitive lethal with RanBPMΔN.

RanBPMΔ homozygous mutants exhibit an increase in cell size and terminal filament misalignment.

RanBPMΔ homozygous mutants expressing RanBPMS.Scer\UAS under the control of Scer\GAL4arm.PS exhibit an increase in cell size and terminal filament misalignment, although niche organization is less disrupted than in RanBPMΔ homozygous mutants not expressing RanBPMS.Scer\UAS. There is also a significant decrease in the number of cap cells in this genotype, possibly as a result of higher than normal expression of the short RanBPM isoform in the germline stem cell niche. An approximate 30% increase in the mean number of germline stem cells per cap cell in mutant females expressing RanBPMS.Scer\UAS under the control of Scer\GAL4arm.PS compared to heterozygous controls. An increase of approximately 30% is observed in cap cell surface area in RanBPMΔ/RanBPMΔ ; Scer\GAL4arm.PS > RanBPMS.Scer\UAS mutants.

Homozygous RanBPMΔ mutant terminal cells cells in mosaic niches are larger than wild-type, while both mutant and wild-type cells in mosaic terminal filaments are disorganised. The number of germline stem cells per niche is significantly higher in mosaics compared to non-mosaic controls. This is not caused by a decrease in the size of germline stem cells attached to mutant cap cells, or to an increase in cap cell number, as the number of cap cells in non-mosaic niches is not significantly different from mosaic niches. The mean surface area of homozygous RanBPMΔ mutant cap cells is increased by 30% relative to controls.

Homozygous RanBPMΔ mutants do not exhibit a difference in germline stem cell division or any obvious defects in the development of egg chambers. Within mosaic niches, RanBPMΔ mutant cap cells are attached to twice as many spectrosomes as normal, whereas the wild-type cap cells in the same niches are attached to normal numbers of spectrosomes. Individual mutant cap cells in mosaic niches are observed to contact as many as three spectrosomes, allowing the attachment of up to five spectrosomes to the mosaic cap cell cluster. The 2.2-fold increase in the number of germline stem cells attached to RanBPMΔ cap cells is greater than the 30% increase in mutant cap cell surface area, indicating a relative increase in the adhesive properties of RanBPMΔ cap cells compared to wild-type cap cells.

Loss of RanBPM from follicle cells in RanBPMΔ genetic mosaics can disrupt epithelial organization, causing the single-layered epithelium to become multilayered, which is sometimes associated with fusion of adjacent egg chambers. This phenotype is incompletely penetrant and preferentially affects follicle cells at the anterior and posterior poles of an egg chamber. Loss of RanBPM also causes defects in the morphogenesis of dorsal appendages, the prominent extended chorion structures at the anterior dorsal surface of the eggshell. Dorsal appendages surrounded by RanBPMΔ mutant cells are much shorter and paddle-like compared to wild-type.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference

RanBPMCB-6232-3/RanBPMΔ has egg chamber phenotype, enhanceable by shg[+]/shg2

RanBPMCB-6232-3/RanBPMΔ has ovary phenotype, enhanceable by shg[+]/shg2

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

The following alleles can be ordered into an allelic series based on their relative strength at 25[o]C: RanBPMΔ > RanBPMf06647 > RanBPMΔN > RanBPMCB-6232-3.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (1)