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General Information
D. melanogaster
Deficiency (1) Notch
FlyBase ID
Feature type
Also Known As
Df(1)N81k1, N81K1, Df(1)N81K
Computed Breakpoints include


Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Class of aberration (relative to progenitor)


Carries alleles
Transposon Insertions
Formalized genetic data

bk1 << N << dnc << bk2

Genetic mapping information

The proximal deletion breakpoint breaks within the dnc transcription unit removing the transcription start sites 1 and 2.

Breakpoint(s) molecularly mapped

-43.9 to -31.2 kb The zero coordinate used in locating the molecular lesions in the Notch deficiencies is the first Eco R1 site in Canton-S DNA proximal to the 3C7 breakpoint of In(1)N76b8 (Kidd et al., 1983); it is 1.1 kb to the right of the zero coordinate used by Artavanis-Tsakonas et al., 1983

Comments on Cytology

All limits from polytene analysis (FBrf0042381)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Partially deleted / disrupted
Molecular Data
Completely deleted
Partially deleted
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
Affected Genes Inferred by Location
    Phenotypic Data
    In combination with other aberrations

    The increased number of thoracic bristles seen in Df(1)N-81k1 heterozygotes is rescued almost to a wild-type number by Dp(1;2)51b.

    Lethal or semi-lethal when in combination with large deficiency alleles of E(spl).

    NOT in combination with other aberrations

    Scutellar bristle number is not effected in Df(1)N-81k1/+ mutant adults.

    Mutant flies have margin defects at the distal wing tip, moderate thickening of wing vein 5 and deltas at the ends of the wing veins.

    Heterozygotes show distal notching of the wing and thickening of the wing veins.

    en and nub expressing multidendritic (md) neurons in the dorsal cluster are greatly over produced in Df(1)N-81k1 mutants.

    heterozygous flies have small notches at the distal portion of the wing. This is made more variable by the addition of neurUAS.cLa, when driven by Scer\GAL4VMQ

    The cuticle secreted by zygotic N mutants is crinkled. In the complete absence of zygotic or maternal N the cuticle is very disorganized and thin and often has a hole in the middle. The cells at the leading edge of the closing dorsal epidermis are elongated compared to the wild type, appearing stretched, as do more ventral cells. The midline which eventually forms does not fall along a straight line. For embryos derived from mutant germline clones the defects are more pronounced and dorsal closure fails. The epidermis consists of isolated patches. Df(1)N-81k1 suppresses the dorsal hole phenotypes caused by hep1 and Df(2L)flp147E. Does not suppress dorsal-hole phenotype of pnr or zip mutants.

    The RP2 motoneuron duplicated at the expense of the RP2sib. The aCC motoneuron is duplicated at the expense of the pCC interneuron. The Usib fates are duplicated at the expense of the U neurons. The dMP2 is duplicated at the expense of the vMP2. No change was observable in EL cell fate. This phenotype is the reciprocal of that shown for numb mutants. Mutant embryos show excess neuroblast formation characteristic of neurogenic mutants.

    Heterozygotes have a marked increase in the number of bristles on the notum.

    Dominantly enhances the phenotype of flies carrying Brdmut123+GYmut in a wild-type background.

    Assymetric division of all the MP2 precursors formed is not altered, but the smaller vMP2 is transformed to the dMP2 fate. In numb1 Df(1)N-81k1 double mutants all MP2 neurons develop as dMP2.

    Embryos lacking Dl function, or maternal and zygotic N function, fail to develop principal midgut epithelial cells and no midgut epithelium develops.

    Hemizygotes exhibit severe defects in the optic lobe and Bolwig's organ. Bolwig's organ has an increased number of cells that form an irregular cluster within the surrounding hyperplastic brain. The number of cells within the optic lobe also seem slightly increased. The morphology of the optic lobe cells has changed, cells are rounded and arranged in a solid cluster.

    Homozygotes die as embryos. Heterozygotes show notching of the wing.

    Stocks (2)
    Notes on Origin


    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (11)
    References (43)