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General Information
Symbol
Dmel\binR22
Species
D. melanogaster
Name
FlyBase ID
FBal0043738
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
bin22
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C6991704T

Reported nucleotide change:

C?T

Amino acid change:

Q292term | bin-PA

Reported amino acid change:

Q292term

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

Amino acid replacement: Q292term.

Nucleotide substitution: C?T.

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

In embryos homozygous mutant for binR22 longitudinal visceral muscle (LVM) founder cell migration initiates similarly to the wild type, but the tracks become progressively irregular during germ band retraction at stage 12. By the end of germ band retraction none of the cells have reached the anterior of the trunk visceral mesoderm (TVM).

binR22 mutants show a salivary gland phenotype. At stage 14, mutant salivary glands remain associated with the inner circular muscle layer, while in wild type, these structures become separate. After stage 15, cells from the distal tips of the binR22 salivary glands spread into the region of the undifferentiated midgut that forms the gastric caecae in the wild-type embryos. The mutant glands become mispositioned and/or elongated and maintain contact with the area of the midgut immediately adjacent to the proventriculus.

The salivary glands in mutant embryos have no defects in turning or posterior migration.

The presumptive trunk visceral mesoderm primordia segregate towards the interior and coalesce into a band as in mutant embryos (as in wild type), but there are irregularities in their arrangement, which become much more pronounced after stage 11. At stage 13, these cells fail to become columnar, are not tightly attached to the endoderm and become clustered segmentally (in wild type they remain a continuous band). During stages 14-17 the cells are mostly scattered in areas within or underneath the somatic mesoderm. Midgut constrictions are not formed. Cells which originate from trunk visceral mesoderm primordia fuse into syncytia of somatic muscles.

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

Expression of BacA\p35Scer\UAS.cHa under the control of Scer\GAL4tey-5053A partially suppresses the longitudinal visceral muscle (LVM) founder cell migration defects seen in homozygous binR22 embryos. LVM founder cells regain much of the ability to migrate, however their tracks are less regular. The migrating cell occupy a broader lateral area without being subdivided into a dorsal and a ventral stream and fewer cells reach the very anterior end of the trunk visceral mesoderm (TVM) compared to wild type.

Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (8)