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General Information
D. melanogaster
FlyBase ID
Feature type
Also Known As
Computed Breakpoints include


Deleted Segment
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

bk1 << l(3)68Fh << l(3)69Ah << bk2 << app

Genetic mapping information
Comments on Cytology

Limits of break 1 from polytene analysis (FBrf0047765) Left limit of break 2 from polytene analysis (FBrf0047765) Right limit of break 2 from polytene analysis (FBrf0080317)

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
Phenotypic Data
In combination with other aberrations

Myoblast fusion is significantly compromised in Df(2R)Vrp1D30; Df(3L)BK9 double mutants. There is a greater percentage of hemisegments with a reduced number of nuclei in the double mutants than there is in the single mutants.

Fails to complement Df(3L)TP32.

NOT in combination with other aberrations

Df(3L)BK9 mutant embryos show mostly normal circular muscle morphology with only sporadic small gaps, probably a result of minor failures in circular myoblast fusion.

Df(3L)BK9 mutant embryos display defects in the fusion of longitudinal visceral muscle founder cells but the migration of the founder cells is unaffected. The fusion-defective phenotype is most severe in the anterior part of the gut, which is covered mostly in just mononucleated muscles at the end of embryogenesis.

Myoblast fusion is blocked at the bi- and tri-nuclear stage in Df(3L)BK9 mutant embryos.

Initial determination, budding and elongation of Malpighian tubules during stage 13-14 is normal in Df(3L)BK9 homozygous embryos. However rearrangement of tubule cells to produce elongated, 2 cell wide tubules is delayed (from stage 15 to stage 16-17) and partially disrupted. Tubule migration is defective from stage 15. The anterior tubules appear to follow a random path through the body cavity, sometimes doubling back on themselves and failing to form the usual kink at A2/A3.

By stage 13, when fusion is underway in wild-type (WT) embryos, Df(3L)BK9 homozygotes show clustering of fusion competent myoblasts (FCM) around muscle founder cells and extension of filopodia toward them. While some founders undergo an initial round of fusion to generate small syncytia others do not fuse. By stage 15, the FCM cease to extend filopodia toward the founders and precursors, and are eventually removed by macrophages. The unfused founders and precursors differentiate and attach to the epidermis at respective muscle-forming positions as miniature muscle fibers. While a wt DA1 myotube comprises an average of 15 nuclei at stage 15, in Df(3L)BK9 homozygotes 34% of the DA1 muscle founders remain unfused while the rest form bi- (53%) and tri-nucleated (13%) precursors.

Homozygous embryos have severely disturbed mesoderm differentiation; clusters of myoblasts, which fail to form myofibres at late stages of embryogenesis, are seen. Most of the unfused myoblasts are arranged near to formed myotubes. Development of the dorsal vessel is nearly undisturbed. Embryos undergo dorsal closure and develop until shortly before hatching. Muscle founder and precursor cells are formed normally in homozygous embryos. Homozygous ventral mesoderm cells transplanted into wild-type blastoderm embryos can give rise to clones in the ventral, lateral and dorsal somatic muscles of third instar larvae. The mutant clones are found in the same positions in the thoracic and abdominal segments as control clones and are the same size as control clones. Mini-muscles containing two to five nuclei are also seen as a part of clones derived from mutant transplanted cells.

Homozygous embryos do not complete dorsal closure.

Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.

Stocks (3)
Notes on Origin
Balancer / Genotype Variants of the Aberration
Separable Components
Other Comments
Synonyms and Secondary IDs (5)
References (27)