FlyBase Allele Report: Dmel\gsb-n[D-19A]

General Information

Symbol

Dmel\gsb-n^D-19A

Species

D. melanogaster

Name

FlyBase ID

FBal0295034

Feature type

allele

Associated gene

Dmel\gsb-n

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

amorphic allele - molecular evidence

Mutagen

ends-in gene targeting

Nature of the Allele

Allele class

amorphic allele - molecular evidence

(He and Noll, 2013)

Mutagen

ends-in gene targeting

(He and Noll, 2013)

Progenitor genotype

Cytology

Description

The following mutations have been introduced into exon 4 of gsb-n : a single base pair deletion (resulting in a frameshift), an additional point mutation (generating a SpeI site) and two closely spaced in-frame amber and ochre stop codons. The mutations truncate the gsb-n protein after Asp164, the first amino acid of the extended homeodomain.

(He and Noll, 2013)

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

partially lethal - majority die (with gsb-n^del)

(He and Noll, 2013)

partially lethal - majority live (with gsb-n^f06670)

(He and Noll, 2013)

partially lethal - majority live | recessive

(He and Noll, 2013)

Phenotype Manifest In

Detailed Description

Statement

Reference

Homozygous embryos show no obvious abnormalities in the SNa, ISN or ISNb motor axons.

(He and Noll, 2013)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Other

Statement

Reference

Df(2R)gsb/+, gsb-n^D-19A has lethal phenotype

(He and Noll, 2013)

Df(2R)gsb/+, gsb-n^D-19A has abnormal neuroanatomy | embryonic stage phenotype

(He and Noll, 2013)

Df(2R)GGG^d13/+, gsb-n^D-19A has lethal phenotype

(He and Noll, 2013)

Df(2R)GGG^d13/+, gsb-n^D-19A has abnormal neuroanatomy | embryonic stage phenotype

(He and Noll, 2013)

Df(2R)gsb^db/+, gsb-n^D-19A has lethal phenotype

(He and Noll, 2013)

Df(2R)gsb^db/+, gsb-n^D-19A has abnormal neuroanatomy | embryonic stage phenotype

(He and Noll, 2013)

Phenotype Manifest In

Other

Statement

Reference

Df(2R)gsb/+, gsb-n^D-19A has larval segmental nerve branch SNa of A1-7 phenotype

(He and Noll, 2013)

Df(2R)GGG^d13/+, gsb-n^D-19A has larval segmental nerve branch SNa of A1-7 phenotype

(He and Noll, 2013)

Df(2R)gsb^db/+, gsb-n^D-19A has larval segmental nerve branch SNa of A1-7 phenotype

(He and Noll, 2013)

Additional Comments

Genetic Interactions

Statement

Reference

Two types of SNa axon defect are seen in embryos which carry gsb-n^D-19A and are also transheterozygous for a deficiency removing both gsb-n and gsb (either Df(2R)gsb, Df(2R)GGG^d13 or Df(2R)gsb^db respectively): a 'thin' SNa phenotype, where the axons appear thinner but the normal bifurcation of the SNa is retained (72%, 75% and 80% respectively) and a 'bifurcation missing' phenotype where the SNa axons lack the normal bifurcation and instead project inappropriately into the lateral muscle field (14%, 11% and 10% respectively).

Analysis of marked NB5-4 SNa motor neuron clones in gsb-n^D-19A/Df(2R)GGG^d13 embryos indicates that they show ectopic innervation of ventral muscles 27 and 29 in 90% of cases (these muscles are targeted by the SNc in wild-type embryos). In 92% of the clones that show these ectopic SNc innervations, the SNa projection is ether partially or completely missing. The recognisable SNa motor axons sometimes form only one of the normal two branches, or stall before reaching the lateral muscle field.

The shape of muscles and the location of their attachment to the epidermis appears normal in gsb-n^D-19A/Df(2R)GGG^d13 embryos.

(He and Noll, 2013)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

gsb-n^D-19A/Df(2R)GGG^d13 is rescued by Scer\GAL4^elav-C155/gsb-n^UAS.cHa

(He and Noll, 2013)

Partially rescued by

gsb-n^D-19A/Df(2R)gsb is partially rescued by gsb-n^{+mRes-deltaIN3}

(He and Noll, 2013)

Comments

Two copies of gsb-n^{+mRes-deltaIN3} rescue 70-80% of gsb-n^D-19A/Df(2R)gsb animals to fertile adults.

gsb-n^{+mRes-deltaIN3} completely rescues the SNa axon defects of gsb-n^D-19A/Df(2R)gsb embryos.

Expression of gsb-n^Scer\UAS.cHa under the control of Scer\GAL4^elav-C155 almost completely rescues the SNa axon defects of gsb-n^D-19A/Df(2R)GGG^d13 embryos.

(He and Noll, 2013)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

gsb-n^D-19A

gsbn^D-19A

(He and Noll, 2013)

Name Synonyms

Secondary FlyBase IDs

References (1)

Report Sections

Open Close