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General Information
Symbol
Df(1)KA14
Species
D. melanogaster
Name
FlyBase ID
FBab0000483
Feature type
Computed Breakpoints include

7F1;8C6

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

lix << bk1 << su(Cbx) << l(1)7Fd << bk2 << fliD

Genetic mapping information
Comments
Comments on Cytology

Ref: Craymer and Roy, 1980, D. I. S. 55: 200--204

Left limit of break 1 from polytene analysis (FBrf0034402) Right limit of break 1 from inclusion of Nrg (FBrf0044177) Limits of break 2 from polytene analysis (FBrf0034402)

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

Transmission rate of Dp(1;f)J21A through females to progeny is 28%, Df(1)KA14 has no effect on transmission.

NOT in combination with other aberrations

Shows dominant enhancement of dominant haltere phenotype caused by Ubx195 and Ubx9.22.

Does not cause unconditional lethality in hybrid females when heterozygous with D.simulans chromosome.

No second site non-complementing phenotype with zipEbr and zipmhc-c6.1.

Shows no maternal enhancement of dpphr4.

Most of the VUM neurons and also the median neuroblast degenerate. Midline glial cells fail to migrate posteriorly, but this may be an indirect effect due to the absence of VUM neurons. Dorsal medial cell numbers correspond to wild type. Thus midline neurons appear to be dispensible with regard to dorsal meidal cell formation.

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

Midgut development of mutant embryos is wild type.

Homozygous embryos have reduced heads compared to wild-type.

Heterozygosity for this deletion enhances the mutant ovarian phenotype of ovoD2.

The Bolwig organ, hypopharyngeal organ and laterohypopharyngeal organ are absent in homozygous embryos. The frontal ganglion and frontal connective are shifted anteriorly. The supraoesophageal ganglion is reduced in size and no supraoesophageal commissure forms. The optic lobes are almost completely deleted.

More than six-fold reduction in sex ratio and significant levels of female lethality is observed when in combination with Sxlf1. Female lethality is also reduced when in combination with da1 but restored when in combination with emcML.

Ocular segment, dorsomedial papilla, pharyngeal sense organ, Bolwig's organ, antennal sense organ and pharyngeal monoscolopidial chordotonal organ are deleted.

Hemizygous embryos were examined with polarised light microscopy and antibody staining: indistinct striations and altered staining properties in antibody assay.

Heterozygotes have ocelli placed far back on the head and there is a slight indentation in the cuticle beneath the postvertical bristles.

Germ-line clones lethal (Garcia-Bellido and Robbins, 1983, Genetics 103: 235-47)

Stocks (2)
Notes on Origin
Discoverer

Lefevre.

 
Balancer / Genotype Variants of the Aberration
 
Separable Components
 
Other Comments
 
Synonyms and Secondary IDs (6)
References (68)