A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Aberration Dmel\Df(3R)e-BS2

General Information
SymbolDmel\Df(3R)e-BS2SpeciesD. melanogaster
NameDeficiency (3R) ebonyFlyBase IDFBab0002769
Feature typechromosomal_deletion
Also Known AsDf(3R)eBS2, Df(3R)eBS2, Df(3R)eB52
Computed Breakpoints include 93C3;93F14
Deleted segment93C3--93F14
Sequence coordinates
Member of large scale dataset(s)
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Description
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FB2013_03
FB2013_02
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hide Nature of the Aberration
Cytological Order
Progenitor
Mutagen
 
Class of aberration (relative to progenitor)
Breakpoints
93B;93F14
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data bk1 << l(3)93Dm << E(Egfr)C22 << bk2 << sar1
Genetic mapping information
Comments
hide 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)
 
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DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
hide Gene Deletion & Duplication Data
hide Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted
Molecular Data
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Complementation Data
Molecular Data
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Complementation Data
Molecular Data
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Complementation Data
Molecular Data
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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.
hide Stocks ( 2 )
Bloomington
Kyoto
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Discoverer
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hide Synonyms & Secondary IDs ( 9 )
Reported As
Symbol Synonym
Df(3R)e-BS2
 
Df(E2F1)(3R)e-BS2
Name Synonym
Deficiency (3R) ebony
 
Secondary FlyBase IDs
hide References ( 33 )
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All research papers listed in FlyBase were published before 2011