FlyBase Allele Report: Dmel\D[r72]

General Information

Symbol

Dmel\D^r72

Species

D. melanogaster

Name

FlyBase ID

FBal0086878

Feature type

allele

Associated gene

Dmel\D

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Russell, 1998.3.2)

Mutagen

ethyl methanesulfonate

(Russell, 1999.1.25)

Progenitor genotype

Cytology

Description

Point mutant.

(Russell, 1999.1.25)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

Detailed Description

Statement

Reference

D^r72/Df(3L)fz-GS1a animals show strong embryonic CNS defects. These are made worse when D^{ΔHMG.Scer\UAS} or D^{Scer\UAS.T:Rep-en} are expressed via Scer\GAL4^sim.P3.7 in this background.

(Shen et al., 2013)

No loss of CQ neurons is seen in D^r72 embryos. 3% of hemisegments show loss of RP2 neurons, while duplication of RP2 is seen in 8% of hemisegments. Expansion of the eve lateral cluster (ELC) is seen in 1% of hemisegments. 16% of hemisegments show duplication of cells at the position of the aCC/pCC neurons. Neuroblast NB5-3 is missing in 2% of hemisegments.

(Overton et al., 2002)

Shows null embryonic segmentation defect.

(Russell, 1998.3.2)

80% of hemizygous embryos have severe defects throughout the nerve cord, showing thinning of longitudinal connectives and fusion of commissures. The number of midline glia cells per segment is reduced compared to wild-type embryos. The remaining midline glia cells are more frequently located anterior to the anterior commissure than in wild-type embryos. The cell bodies of the midline glia lie along the ventral surface of the commissures and do not migrate and ensheath the commissures. The axonal defects of D^r72/Df(3L)fz-GS1a embryos are rescued in the majority of cases if the embryos are expressing D^Scer\UAS.cSa under the control of Scer\GAL4^sim.PS. The number and location of the midline glia cells is also rescued.

(Sanchez Soriano and Russell, 1998)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

D^r72/Df(3L)fz-GS1a has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by Scer\GAL4^sim.P3.7/Mmus\Sox2^{ΔHMG.UAS.EYFP,Tag:MYC}

(Shen et al., 2013)

D^r72/Df(3L)fz-GS1a has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by Mmus\Sox2^{EnR.UAS.Tag:MYC}/Scer\GAL4^sim.P3.7

(Shen et al., 2013)

D^r72 has abnormal neuroanatomy phenotype, enhanceable by SoxN^U6-35

(Overton et al., 2002)

Suppressed by

Statement

Reference

D^r72/Df(3L)fz-GS1a has abnormal neuroanatomy | embryonic stage phenotype, suppressible by Mmus\Sox2^UAS.EYFP/Scer\GAL4^sim.P3.7

(Shen et al., 2013)

Enhancer of

Statement

Reference

D^r72 is an enhancer of abnormal neuroanatomy phenotype of SoxN^U6-35

(Overton et al., 2002)

Phenotype Manifest In

Enhanced by

Statement

Reference

D^r72/Df(3L)fz-GS1a has larval central nervous system phenotype, enhanceable by Scer\GAL4^sim.P3.7/Mmus\Sox2^{ΔHMG.UAS.EYFP,Tag:MYC}

(Shen et al., 2013)

D^r72/Df(3L)fz-GS1a has larval central nervous system phenotype, enhanceable by Mmus\Sox2^{EnR.UAS.Tag:MYC}/Scer\GAL4^sim.P3.7

(Shen et al., 2013)

D^r72 has neuroblast NB5-3 phenotype, enhanceable by SoxN^U6-35

(Overton et al., 2002)

Suppressed by

Statement

Reference

D^r72/Df(3L)fz-GS1a has larval central nervous system phenotype, suppressible by Mmus\Sox2^UAS.EYFP/Scer\GAL4^sim.P3.7

(Shen et al., 2013)

D^r72/Df(3L)fz-GS1a has larval ventral nerve cord commissure phenotype, suppressible by Mmus\Sox2^UAS.cSa/Scer\GAL4^sim.PS

(Sanchez Soriano and Russell, 1998)

D^r72/Df(3L)fz-GS1a has larval longitudinal connective phenotype, suppressible by Mmus\Sox2^UAS.cSa/Scer\GAL4^sim.PS

(Sanchez Soriano and Russell, 1998)

Enhancer of

Statement

Reference

D^r72/D[+] is an enhancer of denticle phenotype of SoxN^U6-35

(Overton et al., 2007)

D^r72 is an enhancer of neuroblast NB5-3 phenotype of SoxN^U6-35

(Overton et al., 2002)

Other

Statement

Reference

D^r72, SoxN^U6-35 has larval longitudinal connective phenotype

(Overton et al., 2002)

D^r72, SoxN^U6-35 has pCC neuron phenotype

(Overton et al., 2002)

D^r72, SoxN^U6-35 has symmetrical commissure phenotype

(Overton et al., 2002)

D^r72, SoxN^U6-35 has presumptive embryonic/larval central nervous system phenotype

(Overton et al., 2002)

D^r72, SoxN^U6-35 has U neuron phenotype

(Overton et al., 2002)

D^r72, SoxN^U6-35 has larval DA1 motor neuron phenotype

(Overton et al., 2002)

Additional Comments

Genetic Interactions

Statement

Reference

D^r72/+ strongly enhances the loss of denticle phenotype seen in SoxN^U6-35 embryos, such that denticle formation is almost completely abolished.

(Overton et al., 2007)

D^r72 SoxN^U6-35 double mutant embryos show severe disruption in the organisation and structure of the central nervous system. There is a complete loss of longitudinal axons in many segments and frequent gaps in the neuropil. Commissures are often absent, and those that do form are virtually never separated. The aCC/pCC and CQ neurons are missing in at least 15% of hemisegments. RP2 neurons are missing in 94% of hemisegments and eve lateral cluster neurons are missing in 99% of hemisegments. Neuroblast NB5-3 is missing in 79% of hemisegments.

(Overton et al., 2002)

Xenogenetic Interactions

Statement

Reference

Scer\GAL4^sim.P3.7-mediated expression of Mmus\Sox2^{Scer\UAS.T:Avic\GFP-EYFP} suppresses, whereas expression of Mmus\Sox2^{ΔHMG.Scer\UAS.T:Avic\GFP-EYFP,T:Hsap\MYC} or Mmus\Sox2^{Scer\UAS.T:Rep-en,T:Hsap\MYC} enhances the embryonic CNS defects of D^r72/Df(3L)fz-GS1a animals.

(Shen et al., 2013)

The axonal defects seen in D^r72/Df(3L)fz-GS1a embryos are rescued in many cases if the embryos are expressing Mmus\Sox2^Scer\UAS.cSa under the control of Scer\GAL4^sim.PS.

(Sanchez Soriano and Russell, 1998)

Complementation and Rescue Data

Fails to complement

D⁴

(Russell, 1999.1.25)

D⁷

(Russell, 1999.1.25)

D⁶

(Russell, 1999.1.25)

D¹⁰

(Russell, 1999.1.25)

D^r8