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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Allele class
    Nature of the Allele
    Allele class
    Mutations Mapped to the Genome
    Additional Notes

    351 bp deletion (removes bases 1962-2248 of the norpA cDNA FBrf0047660)

    Associated Sequence Data
    DNA sequence
    Protein sequence
    Progenitor genotype
    Nature of the lesion

    A 351-bp genomic deletion removing parts of exon 8, most of exon 9, and the entire intron 9, which corresponds to a 286-bp deletion in the norpA cDNA. The resulting protein is predicted to encode 436 N-terminal amino acids identical to the wild type protein, followed by a frame-shift, resulting in the substitution of 120 amino acids and a premature stop codon. The mutant protein would interrupt the catalytic domain and lack the C-terminal tail required for Gαq interaction and rhabdomere localization.

    Expression Data
    Reporter Expression
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    Human Disease Associations
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Modifiers Based on Experimental Evidence ( 0 )
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In
    Detailed Description

    norpA39 flies synchronize quickly to a 6-hour advancement in their light-dark cycle, similar to wild type.

    Homozygotes do not show a change in sleep need after exposure to social enrichment, in contrast to control flies which show an increase in sleep requirement after exposure to social enrichment.

    The response of norpA39 flies to a 12 hour:12 hour 25<up>o</ up>C:18<up>o< /up>C temperature cycle in LL is similar to wild-type flies, except that the increase in locomotor levels after transition to the warm phase and resulting activity peak are not as pronounced in the norpA39 mutants. However, norpA39 flies fail to entrain to two consecutive warm:cold cycles in LL where the second cycle is phase advanced by 6 hours, instead they abruptly change their activity level at the time of temperature transition.

    norpA39 flies exhibit a decrease in trehalose and sucrose consumption.

    The onset of the evening activity peak in mutant flies in 12 hour light:12 hour dark conditions is advanced compared to wild-type flies at both 18[o]C and 29[o]C.

    Mutant flies show photoreceptor degeneration and disruption of the rhabdomeres 3 days after eclosion.

    norpA39 flies need on average 3 more days than wild-type flies do to adjust their evening peak to a new LD regime.

    Homozygotes exhibit light-dependent loss of the deep pseudopupil (apparent 13 days after a 12 hour light:dark cycle). One copy of norpA39 in rdgE1/Df(2R)vg135 transheterozygous males or females has only a slight effect at slowing the rdgE1-induced retinal degeneration.

    The amplitude response to vapours of all odorants tested in the maxillary palp is significantly reduced. The antennal response is unaffected. Maxillary palps have no gross anatomical defects and the electrical conduction properties are normal.

    Double mutants with CdsA1 confer protection from light-dependent degeneration of photoreceptor cells (mutant phenotype exhibited by CdsA1 homozygotes).

    Flies are blind.

    no ERG

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    Additional Comments
    Genetic Interactions

    norpA39, Rh70 and norpA39, cry01 double-homozygous adults reared under 12h:12h white light:dark cycles exhibit a significant delay in resynchronizing to a 6h delay in 12h:12h white light:dark cycle compared to controls; these phenotypes are not enhanced by additional cry01 and Rh70 homozygosity, respectively.

    Following a 6 hour delay in their light-dark cycle, cryb norpA39 flies show a longer delay in resynchronizing their evening activity peak (5-7 days) compared to cryb flies. The addition of Rh52 or Rh61 to this background extends the time required for resynchronization to beyond 7 days. The addition of both Rh52 and Rh61 to the cryb norpA39 background results in minimal (if any) tendency to resynchronize circadian behaviour.

    Following a 6 hour advancement in their light-dark cycle, cryb norpA39 flies show a longer delay in resynchronizing their circadian behaviour (several days) compared to either single mutant. Introducing either Rh52 or Rh61 to this background interferes more strongly with resynchronization, while the quadruple cryb norpA39 Rh52 Rh61 mutant shows the strongest phenotype.

    Expression of CDaseScer\UAS.cAa under the control of Scer\GAL4GMR.PF suppresses the retinal degeneration seen in norpA39 flies. One copy of lacek05305 suppresses the retinal degeneration seen in norpA39 flies.

    norpA39; cryb double mutants take very long to entrain to a new LD regime, some flies do not even reach a new phase by the eleventh day after the shift.

    Double mutants of cryb with norpA39, neither of which cause entrainment problems alone, exhibit entrainment problems in the initial LD regime. Only 50% of those that entrain to the initial LD cycle were able to synchronize to a new light regime that applies 16-lux blue light. At lower light intensities nearly all of the double mutants fail to entrain to the new LD cycles.

    Xenogenetic Interactions
    Complementation and Rescue Data
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    Notes on Origin



    The basic expression and daily oscillation pattern of per protein in light-dark cycles is normal in norpA39 mutant flies.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (4)
    References (26)