FB2025_05 , released December 11, 2025
Allele: Dmel\washΔ185
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General Information
Symbol
Dmel\washΔ185
Species
D. melanogaster
Name
FlyBase ID
FBal0219165
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
wash185
Key Links
Genomic Maps

Nature of the Allele
Cytology
Description

Imprecise excision of P{EPgy2}washEY15549 has deleted more than half of the coding region of wash and introduced two stop codons at positions 11 and 12.

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

An imprecise excision event leads to two stop codons at positions 11 and 12 due to an internal deletion of 1,029

nucleotides and the insertion of six nucleotides (ATGATG) at the junction.

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

washΔ185 homozygotes or washΔ185/Df(2R)BSC699 exhibit disrupted actin organization at outer ring canals in stage 7-9 egg chambers, premature ooplasmic streaming in stage 7 oocytes and disrupted cortical actin organization in stage 7-9 oocytes when compared to controls.

washΔ185 homozygotes and washΔ185/Df(2R)BSC699 transheterozygotes are viable.

washΔ185 homozygous females present normal oogenesis and fertility, as there are no obvious defects in ring canals, actin cables in nurse cells, border cell migration, morphology of egg chamber, morphology of laid eggs, or number of offspring, as compared to controls; washΔ185 homozygous adults present a mild decrease in lifespan under sugar-only diet, as compared to controls.

washΔ185 homozygous larval and pupal macrophages show defects in flattening and spreading, as shown by decreased cell spread area on uncoated glass surfaces; mutant pupal macrophages also present decreased cell spread areas on vitronectin-coated glass surfaces, associated with significantly shorter focal adhesions, but not on Concavalin A-coated surfaces, as compared to controls; mutant pupal macrophages present enlarged Vha55-marked lysosomes and defects in neutralizing lysosomal pH after phagocytosis, despite an apparently normal phagocytic uptake, as compared to controls; prepupal macrophages present a significant decrease in cell area and motility defects, as shown by significant decreases in migratory velocity and distance in unperturbed conditions, and decreased numbers of macrophages reaching lesions 30min, but not 5min, after lesion induction, as compared to controls. washΔ185 homozygous third instar larval fat body cells display increased lysosomes and autophagosomes under both normal and sugar-only diet, as compared to controls; under sugar-only diet, there is an increase in markers for active autolysosomes, and lysosomes and autophagosomes also present increased enlargement, as compared to wild-type controls.

washΔ185 is a suppressor of both bw[VDE2]/In(2R)bwVDe2 and bw[D]/Dp(?;2)bwD position effect variegation and is an enhancer of centromeric and heterochromatic (e.g. w[m4]/In(1)wm4) position effect variegation, but has not effect on telomeric position effect variegation. The washΔ185 mutant larval salivary glands present the following severe nuclear defects, despite apparently normal gland and gland cell shapes, as compared to controls: irregular shape, with a wrinkled nuclear envelope; significant decrease in volume; significant decrease in DNA content; chromosomes positioned irregularly and closer to the nuclear periphery; and Cajal body and nucleolus defects (as shown by the mis-localization of the markers Coilin and Fibrillarin).

Average dorsal trunk tube length is increased in stage 16 homozygous embryos compared to wild type.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhanced by
NOT suppressed by
NOT Enhancer of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

washΔ185/+ RpII140wimp/+ trans-heterozygotes exhibit disrupted actin organization at outer ring canals in stage 7-9 egg chambers, premature ooplasmic streaming in stage 7 oocytes and disrupted cortical actin organization in stage 7-9 oocytes when compared to controls.

Stage 7 oocytes show premature cytoplasmic streaming in washΔ185/+ ; RpII140wimp/+ females. The yolk granules show speeds of movement that are almost twice that seen in wild type and the movements are concerted and coordinated, in contrast to the uncoordinated, saltatory movements seen in wild-type oocytes at this stage. The normal gradient of microtubule organisation that is seen in wild-type oocytes at this stage is lost in the mutant oocytes. The oocyte nucleus is mislocalised in the mutant oocyte by stage 7 and contains to be mislocalised during later stages. The mutant stage 7 oocytes have a disrupted and discontinuous band of cortical actin.

Oocytes of washΔ185 Rho11B and washΔ185 capuEY12344 transheterozygous females undergo premature cytoplasmic streaming. The normal gradient of microtubule organisation that is seen in wild-type oocytes at stage 7 is lost in the mutant oocytes. The mutant stage 7 oocytes have disruptions in the cortical actin.

washΔ185/+ ; RpII140wimp/+ egg chambers show a loss of nurse cell integrity at stage 10a and incomplete stress fiber formation during during nurse cell dumping (stages 10b-11) compared to wild type. The actin network around the ring canals is abnormally expanded during nurse cell dumping in the mutant egg chambers. Inner ring canal formation appears to be unaffected, although ring canals separated from the nurse cell membrane can be found floating within the oocyte.

washΔ185 Arpc1Q25st egg chambers show a loss of nurse cell integrity at stage 10a and incomplete stress fiber formation during during nurse cell dumping (stages 10b-11) compared to wild type. The actin network around the ring canals is abnormal by stage 10b.

washΔ185/+ ; RpII140wimp/+ Arpc1Q25st egg chambers show a loss of nurse cell integrity at stage 10a and incomplete stress fiber formation during during nurse cell dumping (stages 10b-11) compared to wild type. The actin network around the ring canals is abnormal by stage 10b.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Partially rescued by
Not rescued by
Comments

The expression of washScer\UAS.T:Avic\GFP-EGFP driven by Scer\GAL4Hml.Δ rescues the increased mortality under sugar-only diet and partially rescues the decreased macrophage cell spread area on uncoated surfaces, observed in washΔ185 homozygotes.

washGFP, but not wash+NESΔNLS.GFP, rescues washΔ185 to viability and rescues their nuclear defects (i.e. rescues defects in nucleus shape, nucleus volume, Cajal body and nucleolus).

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

The washΔ185 chromosome originally carried a separable mutation which was responsible for the lethality of the chromosome.

Separable from an unrelated background lethal mutation, referred to as the 'not Wash lethal'.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (13)