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General Information
D. melanogaster
FlyBase ID
Feature type
Also Known As
E(spl)Bx22, groBX22, Df(3R)E(spl)BX22, Df(3R)BX22
Computed Breakpoints include
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Class of aberration (relative to progenitor)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

bk1 << HLHm5 << gro << bk2

Genetic mapping information

Small deletion.

about 14-kb deletion (4 to 17.5 kb); about 14-kb inversion (-10.5 to -7.6 and 4 kb)

Comments on Cytology

Cytologically invisible deletion.

Left limit of break 1 from polytene analysis (citation unavailable) Right limit of break 1 from inclusion of E(spl) (FBrf0055903) Left limit of break 2 from inclusion of E(spl) (FBrf0055903) Right limit of break 2 from polytene analysis (citation unavailable)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Genes NOT Deleted / Disrupted
Complementation Data
Molecular Data
Genes Duplicated
Complementation Data
Completely duplicated
Partially duplicated
Molecular Data
Completely duplicated
Partially duplicated
Genes NOT Duplicated
Complementation Data
Molecular Data
Affected Genes Inferred by Location
    Phenotypic Data
    In combination with other aberrations

    Inferred to overlap with: Df(3R)boss15.

    Inferred to overlap with: Df(3R)Espl-P11.

    Inferred to overlap with: Df(3R)R20.

    Inferred to overlap with: Df(3R)R27.

    Inferred to overlap with: Df(3R)R70.

    Inferred to overlap with: Df(3R)R75.

    Inferred to overlap with: Df(3R)X13.

    Eggs from Df(3R)Espl22/Df(3L)10H mothers exhibit an embryonic lethality significantly higher than from either Df(3L)10H/+ or Df(3R)Espl22/+ mothers. 50-60% had no cuticle. Cuticles from 5-10% of unhatched embryos show a duplication of the posterior spiracle accompanied by disorganised denticle belts.

    NOT in combination with other aberrations

    56% of heterozygous flies show duplication of the anterior postalar bristle.

    The Df(3R)Espl22 chromosome does not act as a dominant suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{wvar}KR3-2", a stable "brown-red" variant of the P{3'WP-2,wvar}2Lt insertion).

    Homozygous clones in the eye disc show a neurogenic phenotype.

    Phenotype manifest in: embryonic/larval dorsal vessel | precursor Homozygous embryos have an increased number of cardiac precursor cells.

    Df(3R)Espl22 single mutant and Df(3R)Espl22, osa308 double mutant clones in the eye show excess neuronal differentiation.

    No effect on the faf eye phenotype.

    Clones induced in the first larval instar generate single large patches that lack sensory bristles (macrochaetaes and microchaetes) in the notum. Clones induced in the late second or early third larval instar generate many small patches that lack sensory bristles in the notum. These areas correspond to areas of neural hyperplasia in the developing notum. Clones in the developing wing generate extra vein material. Clones in the developing eye cause the eye to be rough and scarred with highly disorganised ommatidia.

    In clones in the wing, the phenotype depends on where the clone lies. In the anterior compartment all clones abutting the wing margin cause local overgrowth and pattern duplications. Those abutting the wing margin and restricted to dorsal or ventral surfaces cause overgrowth of both dorsal and ventral cells. Clones at the wing margin cause loss of sensory organs and mild scalloping of the margin. Clones double mutant for sggM11 and Df(3R)Espl22 in the anterior wing differentiate anterior bristles (as for clones of sggM11 single mutants), however double mutant clones in the posterior compartment differentiate hairs typical of the posterior wing margin.

    The number of exit and dorsal roof glia in mutant embryos is higher than in wild-type embryos.

    Embryos exhibit fused muscles in patterned arrangements, particularly in the more dorsal regions of the embryo. The birefringent is clearly correlated with the expansion of the CNS and PNS, and the loss of epidermis and the degree to which myoblast fusion occurs. Where myoblast fusion fails conspicuous clusters of mesodermal cells are formed and if epidermal territories are expanded cells in these clusters may be recruited to fusion.

    Homozygotes display a wide dorsal shield that spans the width of the embryo with well formed telson and Filzkorper. One copy of P{ry+,HLHm5+,m6+,mX+,HLHm7+,E(spl+,gro+=E25R} is sufficient to rescue Df(3R)Espl22 to adulthood. Df(3R)Espl22/Df(3R)boss15 heterzygotes could be rescued to adulthood by the presence of the P{ry+,HLHm5+,m6+,mX+,HLHm7+=Ep} construct.

    Strong to full phenotypic reversion: 250--450 facets per eye. Viable when heterozygous with a Dl allele.

    Intermediate neurogenic phenotype. P element construct carrying a wild type E(spl) gene copy partially rescues the neurogenic phenotype: less severe neural hyperplasia.

    Stocks (2)
    Notes on Origin


    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments

    Deletion of 14kb removing gro, HLHm5, HLHm7 and E(spl).

    Synonyms and Secondary IDs (17)
    References (57)