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General Information
Symbol
Dmel\pyr18
Species
D. melanogaster
Name
FlyBase ID
FBal0239104
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of the progenitor insertion which removes the entire pyr gene.

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

pyr18/Df(2R)BSC25 mutant embryos exhibit random loss of cardioblasts (both generic cardioblasts and ostial cardioblasts), as compared to controls.

pyr18 embryos show a mild defect in the migration of ventral astrocytes, while the infiltration of astrocyte processes into the neuropil is not significantly different from that of controls.

pyr18 mutant embryos show a mild reduction in the number of longitudinal visceral muscle (LVM) fibres around the midgut, particularly in the anterior portion where LVM fibre spacing is wider and the first midgut constriction is either absent or reduced.

pyrS0439/pyr18 mutant larval guts contain 5-8 longitudinal visceral muscle fibres per half side compared to 9-11 in wild type.

Adult homozygotes eclose at a rate of 0.71%.

Unequal spreading of mesoderm cells can be seen in stage 8 homozygous embryos. Subtle defects in mesoderm monolayer formation are seen.

Cells at the dorsal edge of the mesoderm form only short filopodial protrusions during dorsolateral migration in homozygous and pyr18/Df(2R)ED2238 embryos, in contrast to wild-type cells which form thin, long protrusions. The mutant cells fail to extend along the dorsal ventral axis.

Homozygous and pyr18/Df(2R)ED2238 embryos have disrupted dorsal vessel and dorsal somatic muscle development. In some cases, both cardioblasts and dorsal muscles are lacking in the same hemisegment, while in other cases a lack of cardioblasts does not correlate with a corresponding lack of dorsal muscles in the same hemisegment.

Homozygous and pyr18/Df(2R)ED2238 embryos have defects in the ventral oblique muscles VO4, VO5 and VO6. Duplications and loss of the segment border muscle are seen in homozygous embryos.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)