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General Information
Symbol
Df(2L)dp-79b
Species
D. melanogaster
Name
Deficiency (2L) dumpy
FlyBase ID
FBab0001773
Feature type
Also Known As
Df(2L)dp79b, Df(2L)dp79b
Computed Breakpoints include

22A2-22A3;22D5-22E1

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

l(2)10685 << bk1 << cpb << aop << bk2 << l(2)00231

Genetic mapping information
Comments

This deletion removes a single ribosomal protein-coding gene (though other genes are also removed).

Comments on Cytology

All limits from polytene analysis (FBrf0055572)

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

    Action potentials recorded from the ab3 sensilla of 'Δhalo' (Df(2L)dp-79b/Dp(2;2)dppd21) flies show complete absence of large amplitude spikes when challenged with insect repellent odorants DEET, IR3535 or picaridin.

    The function of olfactory receptor neurons that project to the DM2 glomerulus is impaired in Df(2L)dp-79b/Dp(2;2)dppd21 flies; responses to E2-hexenal and γ-valerolactone are abolished and responses to ethyl acetate and 2-heptanone are severely reduced. In contrast, DM2 projection-neuron response amplitudes are only moderately attenuated.

    The synthetic deletion created using Df(2L)dp-79b and Dp(2;2)dppd21 recombined onto the same chromosome (see FBrf0173068 and FBrf0159257) deletes Or22a and Or22b, resulting in antennal olfactory receptor neuron ab3A losing its odorant response. This genetic background is referred to as "Δab3A".

    Animals homozygous for the synthetic deletion created using Df(2L)dp-79b and Dp(2;2)dppd21 combined on to the same chromosome (see FBrf0173068 and FBrf0159257) constitute the 'empty neuron system', in which antennal olfactory receptor neuron ab3A loses its odorant response.

    The net plus-end (phase II) transport of lipid droplets along microtubules is disrupted in Df(2L)dp-79b/Tp(2;2)A446 embryos, resulting in the apical accumulation of droplets in the embryo.

    Animals homozygous for the synthetic deletion called "Δhalo" (in which Df(2L)dp-79b and Dp(2;2)dppd21 are recombined onto the same chromosome) have abnormal antennal electrophysiology: the ab3A neurons are unresponsive to a large panel of odours, in contrast to wild type. The ab3B neurons in the mutant flies show an odour response spectrum similar to that of wild-type flies, except that the response to pentyl acetate is greater than that of controls. Some mutant ab3A neurons show a low level of activity that consists largely of bursts of action potentials. These bursts typically contain 3 or 4 action potentials, with an interspike interval of 14 +/- 0.8 ms and occur at approximately 10 second intervals in the absence of odour stimulation. The frequency of bursts increases during responses of the neighbouring ab3B neuron, but the overall frequency of firing is still very low. All other neuronal classes in large basiconic sensilla of the antenna appear normal, as judged by testing them with the odours against which they normally respond most strongly. The ab3A neurons in "Δhalo" animals target the DM2 glomerulus as occurs in wild-type animals and there are no gross abnormalities in projections.

    Embryos homozygous for the synthetic deletion termed "Δ(halo)" (in which Df(2L)dp-79b and Dp(2;2)dppd21 are recombined onto the same chromosome) fail to exhibit cytoplasmic clearing of lipid droplets. The physical parameters of droplet motion are altered in these mutants; in phase II of clearing, the stall forces are altered in both plus-end and minus-end directed motion, resulting in unbalanced forces. This leads to a net plus-end directed transport of the droplets.

    The injection of halocGa RNA into embryos homozygous for "Δ(halo)" (in which Df(2L)dp-79b and Dp(2;2)dppd21 are recombined onto the same chromosome) partially rescues the cytoplasmic lipid drop clearing phenotype seen in these embryos. When embryos are injected in phase II, noticeable clearing is observed towards the end of phase II. and clouding fails to occur near the injection site.

    NOT in combination with other aberrations

    Flies heterozygous for the deletion do not show a Minute bristle phenotype.

    The Df(2L)dp-79b chromosome does not act as a dominant suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{wvar}KR3-2", a stable "brown-red" variant of the P{3'WP-2,wvar}2Lt insertion).

    Heterozygosity for Df(2L)dp-79b results in 1.3% X chromosome nondisjunction and 0.0% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.

    Df(2L)dp-79b in combination with a pair of introgressions from D.simulans spanning 30F1-31E7 to 35D7-36A14 Dsim\Int(2L)S and 21A1 to 22D1--23A2 Dsim\Int(2L)D Dsim\Int(2L)D produces fertile male flies. These flies are female sterile.

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

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

    Shows no maternal enhancement of dpphr4.

    Deficient embryos show a mutant midgut phenotype: visceral mesoderm does not develop.

    Germband retraction is abnormal in some homozygous embryos, tracheae are disconnected and optic lobes do not invaginate.

    sev6/sev+;SosJC2/Df(2L)dp-79b mutants exhibit an increase in the number of R7 cells compared to sev6/SosJC2 mutants with two functional aop copies.

    Reduced brain.

    Heterozygotes exhibit wild type eye phenotype.

    Stocks (59)
    Notes on Origin
    Discoverer
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     

    The deletion 'Δhalo' is a synthetic deficiency that combines Df(2L)dp-79b and Dp(2;2)dppd21 (see FBrf0159257).

    The combination of aberrations Df(2L)dp-79b Dp(2;2)dppd21 is referred to as "Or22a/bΔhalo".

    The combination of aberrations Df(2L)dp-79b/Dp(2;2)dppd21 is referred to as 'Δhalo'.

    Synonyms and Secondary IDs (6)
    References (65)