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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Key Links
    Nature of the Allele
    Mutations Mapped to the Genome
    Additional Notes

    An 11bp deletion (agtcagtgcgc), which results in frameshift within residue Pro-374 and early translation termination after the addition of 114 novel amino acids. Note that FBrf0194614 reports that WASp3 is a deletion of 13bp extending from 1121-1134bp in WASp3.

    Associated Sequence Data
    DNA sequence
    Protein sequence
    Progenitor genotype
    Nature of the lesion

    WASp3 carries an intergenic deletion of 13 bp (1121-1134bp) that results in a frameshift, and subsequently the loss of the VVCA domain.

    An 8 nucleotide deletion (24652013 cggaaaca 24652006), replaced with 4 nucleotides (ggtg). This results in frameshift after residue Pro-309 of the protein and termination after 120 additional residues.

    Small intragenic deletion resulting in a predicted frameshift which causes the cytoskeleton-interacting carboxy-terminal domain to be lost.

    Expression Data
    Reporter Expression
    Additional Information
    Marker for
    Reflects expression of
    Reporter construct used in assay
    Human Disease Associations
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Modifiers Based on Experimental Evidence ( 0 )
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
    Disease-implicated variant(s)
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In

    actin filament & eye photoreceptor cell | somatic clone

    adult thorax & microchaeta & external sensory organ precursor cell IIa (with Df(3R)3450)

    adult thorax & microchaeta & external sensory organ precursor cell IIb (with Df(3R)3450)

    embryonic peripheral nervous system & external sensory organ | germ-line clone (with Df(3R)3450)

    embryonic peripheral nervous system & neuron | supernumerary | germ-line clone (with Df(3R)3450)

    microvillus & eye photoreceptor cell | somatic clone

    Detailed Description

    Homozygous embryos have a wild-type muscle pattern.

    WASp3 double mutant clones in the adult thorax exhibit external sensory cell loss and an excess of neurons.

    Only 14% of actin foci in embryos maternally and zygotically mutant for WASp3 invade into founder cells, compared to 35% in wild type. The depth of invasion is also reduced.

    Within WASp3 pIIa-pIIb cells, an apical actin-rich structure (ARS) is formed as in wild type, but its apical area is markedly reduced and, in about 50% of cases, the stalk of the normal 'umbrella shape' is not formed properly.

    Homozygous embryos derived from females carrying homozygous germline clones show severe myoblast fusion defects.

    WASp3 mutants exhibit muscle attachment defects but do not display unfused myoblasts.

    WASp3D3-035/WASp3 transheterozygotes exhibit a myoblast fusion phenotype.

    The cuticles of WASp3 mutants have abnormally thin denticles, which often display bent extremities.

    WASp3/Df(3R)3450 mutants show a frequent loss of dorsocentral and scutellar bristles. The notopleural bristles are missing. They also show loss of microchaetae.

    WASp1/WASp3 transheterozygotes survive to pharate adults. In these flies, many rhabdomeres do not obtain the normal characteristic oval shape, but rather are pointed and squared, with 2-3% of the mutant rhabdomeres split. The same phenotypes are seen in WASp3 homozygous somatic clones. In these clones F-actin accumulation along the photoreceptor apical surface is delayed and disorganised. At 48 hours there are regions of the photoreceptor cell in which the apical surface has not expanded and/or primordial microvillar projections have not formed. These regions are characterised by little or no F-actin enrichment compared with neighbouring wild-type cells. Ultrastructural analysis at this stage reveals loss of adherens junctions between mutant photoreceptors, no separation or elimination of cell-cell contacts between photoreceptor cells and a lack of primordial microvillar projections. While the initiation of rhabdomere microvilli formation is delayed, WASp3 mutant photoreceptor cells do form microvilli with an actin cytoskeleton core. At 72 hours, the developing mutant rhabdomeres are smaller in size or malformed compared with wild-type.

    Syncytial blastoderm stage WASp3 germ-line clone embryos have wild-type nuclear morphology and distribution during nuclear division cycles 12-14. There are also no obvious cytoskeletal defects in mutants at these stages. In WASp3/Df(3R)3450 embryos from WASp3 germ-line clone carrying mothers, axon bundles in the ventral nerve cord appear thicker and defasciculated. Most of these embryos contain one to two segments with axon bundles collapsed at the midline (73% of embryos, n = 41). WASp3 mutant germ-lines undergo normal oogenesis and nurse cell development.

    Hemizygotes complete nearly all stages of imaginal development and die as young adults, most commonly failing to eclose from the pupal case. Those that eclose can survive for a few days, but are lethargic and passive in their behaviour. WASp3/Df(3R)3450 embryos derived from WASp3 homozygous female germline clones do not survive. Embryos derived from WASp3 homozygous female germline clones with a wild-type paternal contribution of WASp develop normally, giving rise to viable and fertile adults. WASp3/Df(3R)3450 embryos derived from WASp3 homozygous female germline clones have normal cuticles. The initial selection of sensory organ determination appears to occur normally in these embryos, but they have an excess of neurons (a near doubling of normal numbers) in the mature peripheral nervous system (PNS). A corresponding reduction in the number of PNS nonneuronal support cells is seen; the number of cells expressing shaft and socket cell markers is reduced, although only mild effects on sheath cell numbers are seen. RP2 neuroblasts are duplicated. The mitotic spindles in the notum of WASp3/Df(3R)3450 pupae are positioned within the plane of the epithelium and along the anterior-posterior axis of the fly, as in wild type. The pI division in the lineage of the thoracic microchaetae is normal in WASp3/Df(3R)3450 pupae. However, subsequent events in the differentiation of this sensory organ lineage differ substantially from wild type. Either of the two pI daughter cells may divide after pI (in wild type the anterior pIIb cell always divides before the posterior pIIa cell) and the divisions of both of the pI daughter cells are morphologically identical and resemble the pattern seen in wild-type pIIb cells (both cell divisions are nonplanar and generate two daughter cells of different sizes).

    External Data
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Enhancer of
    NOT Enhancer of

    WASp[+]/WASp3 is a non-enhancer of visible phenotype of Df(3L)Exel8098/Cip4Δ32

    Suppressor of
    NOT Suppressor of

    WASp[+]/WASp3 is a non-suppressor of visible phenotype of Df(3L)Exel8098/Cip4Δ32

    Phenotype Manifest In
    Enhanced by
    Suppressed by
    Enhancer of
    NOT Enhancer of

    WASp[+]/WASp3 is a non-enhancer of wing hair | increased number phenotype of Df(3L)Exel8098/Cip4Δ32

    Suppressor of
    NOT Suppressor of
    Additional Comments
    Genetic Interactions

    WASp3 enhances the myoblast fusion defects seen in Vrp1f06715 embryos.

    Pak3del WASp3 double mutant embryos have a more severe myoblast fusion defect than either single mutant.

    Heterozygosity for WASp3 does not suppress the split microchaete phenotype caused by expression of Abp1Scer\UAS.T:Myr-Src64B,T:Avic\GFP under the control of Scer\GAL4sca.PU.

    AP-47SHE-11 suppresses the external sensory cell loss and excess neurons seen in WASp3 mutant thorax clones, instead producing the extra socket cell phenotype seen in AP-47SHE-11 mutants alone.

    Expression of psidinScer\UAS.cKa under the control of Scer\GAL4slbo.2.6 in a WASp3 heterozygous background has little or no effect on border cell migration.

    The reduced ectodermal apical cell surface size observed in osupd-4 mutant embryos at mid germ-band extension is rescued in osupd-4; WASp3/+ embryos.

    WASp3/+ has no effect on the fraction of wing cells that have multiple wing hairs in Cip4Δ32/Df(3L)Exel8098 adults.

    Myoblast fusion does not occur in DA1 muscles in Arp66Bschwachling, WASp3 double mutants.

    A WASp3/+ background intensifies the appearance of unfused myoblasts in SCARk13811 mutants.

    A WASp3 heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.PC.PD.Scer\UAS mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.

    sn3, m1, f36a; shaV15 and sn3, m1, f36a; WASp3 quadruple mutants show further impairment to denticle formation compared to sn3, m1, f36a triple mutants, with mutants exhibiting regions of naked cuticle where denticles lie in wild-type animals.

    The dorsal hairs on the abdominal segments of sn3, m1, f36a triple mutants are severly reduced in size, and in some cases, hairs are abrogated leaving abnormal naked regions. This phenotype is more severe in sn3, m1, f36a; WASp3 quadruple mutants.

    The extra notopleural bristles induced by expression of AbiScer\UAS.T:Myr1 under the control of Scer\GAL4sca-537.4 can be partially suppressed by WASp3.

    The short and split microchaetae phenotype of Sra-1Scer\UAS.T:Myr1; Scer\GAL4sca.PC flies is suppressed by WASp3/+.

    The bristle phenotype due to HemScer\UAS.T:Myr1; Scer\GAL4sca-537.4 is dominantly suppressed by WASp3.

    Xenogenetic Interactions
    Complementation and Rescue Data
    Fails to complement
    Images (0)
    Stocks (1)

    Stated to be lost.

    Notes on Origin
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (6)
    References (31)