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General Information
Symbol
Df(1)N19
Species
D. melanogaster
Name
FlyBase ID
FBab0000596
Feature type
Also Known As
N19
Computed Breakpoints include

17A1;18A2

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

wupA << bk1 << fliH << bk2

Genetic mapping information
Comments
Comments on Cytology

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

First chromosome breakpoint is 20kb distal to the first chromosome breakpoint of T(1;Y)B137.

Limits of break 1 from polytene analysis (FBrf0076124) 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)N19 weakly decreases transmission.

Df(1)svr/Df(1)N19 and Df(1)N71/Df(1)N19 double heterozygous females have reduced viability; only 30% and 8% respectively survive compared to control flies. Viability is recovered if the Df(1)svr/Df(1)N19 or Df(1)N71/Df(1)N19 females also carry SxlM1.

NOT in combination with other aberrations

29% of Df(1)N19 homozygous embryos show defects in germ-band extension.

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.

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

Deficient embryos show an uninterpretable mutant midgut phenotype.

Homozygous embryos are very abnormal compared to wild-type.

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

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.

'Sloppy' ventral cord.

Stocks (2)
Notes on Origin
Discoverer

Lefevre.

 
Balancer / Genotype Variants of the Aberration
 
Separable Components
 
Other Comments
 
Synonyms and Secondary IDs (5)
References (48)