FB2024_03 , released June 25, 2024
Allele: Dmel\NrtM2
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General Information
Symbol
Dmel\NrtM2
Species
D. melanogaster
Name
FlyBase ID
FBal0002234
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dabM2
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Nucleotide substitution: T?A.

Amino acid replacement: L464term.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

T16775210A

Reported nucleotide change:

T?A

Amino acid change:

L464term | Nrt-PA; L464term | Nrt-PB; L464term | Nrt-PC

Reported amino acid change:

L464term

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

63% of segments have commissure defects in the central nervous system of Abl1 NrtM54/NrtM2 Df(3L)st-j7 embryos.

The lethality of Abl1/NrtM2 Df(3L)st-j7 is partially rescued by AblScer\UAS.cFa or AblK417N.Scer\UAS, expressed under the control of Scer\GAL431.

faxM7 Abl1/In(3L)std11 and faxM12 Abl1/In(3L)std11 individuals are lethal due to disruptions in the CNS longitudinal and commissural axons. The presence of NrtM2 does not affect the lethality. Dosage sensitive interactions exist between NrtM2, faxM7 and faxM12. Abl+mTnabl is unable to rescue the lethality of fax- Nrt- individuals.

Abl1/Df(3L)st-j7 NrtM2 double mutant causes absence of most intersegmental longitudinal axon bundles and most commissural axon bundles. The lethality of NrtM2 Df(3L)st-j7/Abl1 animals is rescued by four copies of P{Dab.G} to almost full viability.

NrtM2 Df(3L)st-j7/In(3L)std11 double mutant embryos show muscle absences and detachments.

Enhances the Abl1 and Abl2 mutant phenotype from pupal lethal to embryonic or larval lethality by an haploinsufficiency dependent on Abl (HDA).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

Induced on: Df(3L)st-j7. The NrtM2 mutant allele was originally thought to be a mutation in the Dab gene (see FBrf0058531 and FBrf0084025), but sequencing of the chromosome indicates that it is a lesion in the Nrt gene.

Comments
Comments

Haploinsufficiency dependent upon an Abl mutant background (HDA).

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (7)