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General Information
Symbol
Df(3R)e-BS2
Species
D. melanogaster
Name
Deficiency (3R) ebony
FlyBase ID
FBab0002769
Feature type
Also Known As
Df(3R)eBS2, Df(3R)eBS2, Df(3R)eB52
Computed Breakpoints include

93C3;93F14

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

bk1 << l(3)93Dm << E(Egfr)C22 << bk2 << sar1

Genetic mapping information
Comments
Comments on Cytology

Cytology based on in situ hybridization

Limits of break 1 from polytene analysis (FBrf0054506) Left limit of break 2 from polytene analysis (FBrf0075280) Right limit of break 2 from polytene analysis (FBrf0093061)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Genes NOT Deleted / Disrupted
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
NOT in combination with other aberrations

Homozygous embryos show defects in commissure formation. The commissures are tightly fasciculated into a single bundle in late stage 12 and early stage 13 embryos and remain poorly separated into mid-stage 13 (in contrast to wild-type embryos which show clear commissural separation by mid-stage 13). Partial commissural fusions and distortions remain common in late stage 13 and early stage 14 homozygous embryos. The commissural axons form a dense bundle at the dorsal boundary of the nerve cord in homozygotes (in contrast to wild type where they interdigitate amongst the midline glia). The commissural bundles are thicker and the longitudinal fibres are sparser than normal. The pCC axon does not extend as far anteriorly in homozygous embryos as in wild type at stage 12/1, and appears stalled after minimal outgrowth. The pCC axon frequently remains stalled at early stage 13, although many late stage 13 embryos show nearly normal extension of the pCC axon into the next anterior segment. 95% of embryos show delayed longitudinal growth in, on average, more than 50% of their segments. Additional morphological defects are seen by mid to late stage 14 in homozygous embryos. The formation of midgut constrictions is blocked, resulting in a large, poorly organised gut. The midgut mass displaces and fragments the nerve cord, particularly in upper abdominal segments, resulting in both commissural and longitudinal discontinuities in the nerve cord.

Homozygous embryos die before hatching.

Dominantly causes tergite defects in less than 50% of run3 heterozygotes.

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

Stocks (2)
Notes on Origin
Discoverer
 
Balancer / Genotype Variants of the Aberration
 
Separable Components
 
Other Comments
 
Synonyms and Secondary IDs (9)
Reported As
Name Synonyms
Deficiency (3R) ebony
Secondary FlyBase IDs
    References (33)