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General Information
D. melanogaster
Deficiency (1) Notch
FlyBase ID
Feature type
Also Known As
Df(1)N8, Df(1)N8, N8, N8
Computed Breakpoints include
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

l(1)3Bf << bk1 << crm << l(1)EA65 << bk2 << l(1)3Eb

Genetic mapping information
Comments on Cytology

Deletion of 17/19 bands.

Left limit of break 1 from polytene analysis (FBrf0004288) Right limit of break 1 from inclusion of crm (FBrf0038033) Left limit of break 2 from polytene analysis (FBrf0040178) Right limit of break 2 from polytene analysis (FBrf0004288)

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
Affected Genes Inferred by Location
    Phenotypic Data
    In combination with other aberrations

    Does not complement Df(1)w67k30.

    NOT in combination with other aberrations

    Df(1)N-8/+ wings show notching of the distal wing margin.

    Df(1)N-8/+ adult females show wing defects that include thickening of the longitudinal vein 5.

    Df(1)N-8/+ females ectopically expressing Hsap\ATXN1LScer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4hh.PU rarely survive to adult stage (less than 10%) and the survivors display severe wing defects including a further thickening of the vein L5 compared to Df(1)N-8/+ controls.

    Df(1)N-8 heterozygotes exhibit a dominant wing notching phenotype.

    Heterozygotes show loss of wing margin and wing vein thickening.

    Flies bearing Df(1)N-8 are generally smaller than wild-type flies and have a transient, slightly brown, eye phenotype shortly after eclosion.

    Df(1)N-8 flies exhibit a weak loss of wing margin.

    Shows dominant wing nicking which is enhanced by PsnW11 and PsnW6.

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

    Heterozygotes of Df(1)N-8 or N55e11 with Abl1,NrtM54 or In(3L)std11 show defects in eye development leading to rough eyes with high penetrance.

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

    Shows no maternal enhancement of dpphr4.

    Single cells from Df(1)N-8 embryos transplanted into the ventral neurogenic region of wild-type host embryos can give rise to both neural and epidermal cells.

    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. Midgut primordia do not fuse, and Malpighian tubules branch.

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

    Reveals antimorphic alleles of P{en1}wgen11.

    Hyperplasia of replicating sensory precursors: due to an increased number of ectodermal cells being recruited as sensory precursor cells. Extra precursor cells are recruited beyond the normal time window for neurogenesis in the PNS.

    Heterozygous females exhibit reduced viability and fertility.

    Stocks (2)
    Notes on Origin

    Mohr, 7 Oct. 1918.

    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (14)
    References (85)