FB2024_03 , released June 25, 2024
Allele: Dmel\inscP49
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General Information
Symbol
Dmel\inscP49
Species
D. melanogaster
Name
FlyBase ID
FBal0049667
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Caused by aberration
Cytology

Polytene chromosomes normal.

Description

Deletion removing about 9kb including the site of insertion of the P-element in inscAB44 and part of the transcribed region.

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

inscP49 mutant MP2 clones display wild-type morphology and development.

In mutant embryos the DA3A muscle is duplicated at the expense of DO5A in most segments.

Approximately 30% of hemisegments produce an extra DA1 muscle in homozygous embryos. There is an approximately 60% reduction in the number of eve-expressing pericardial cells. An additional dorsal oblique muscle is observed in approximately 40-50% of hemisegments, which is likely to be DO1 in many cases. The founder cell of the DA1 muscle (FDA1) and its sibling (FDA1sib) both adopt an FDA1-like identity. The founder cell of the DO1 muscle (FDO1) is duplicated at the expense of its sibling (FDO1sib). numb3 inscP49 embryos have a qualitatively similar phenotype to numb3 embryos, although they exhibit these phenotypes at higher expressivity.

Muscle and pericardial cell defects.

Phenotypically similar to Df(2R)P72.

Defective in orientation of the mitotic spindle.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Other
Statement
Reference
Phenotype Manifest In
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The proportion of hemisegments with abnormal number of neurons in the asymmetrically dividing RP2 neural lineage is significantly increased in wtsx1/+;inscP49/+ double heterozygous embryos compared to either of the single heterozygotes or wild type.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (18)