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General Information
Symbol
Dmel\Six4289
Species
D. melanogaster
Name
FlyBase ID
FBal0125277
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:
C20791016T
Reported nucleotide change:
C1753T
Amino acid change:
Q87term | Six4-PA; Q87term | Six4-PB
Reported amino acid change:
Q87term
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Nucleotide substitution: C1753T.
Amino acid replacement: Q87term.
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
Six4108 homozygotes and Six4108/Six4289 transheterozygotes are lethal.
Homozygous follicle cell clones can induce neighbouring anterior follicle cells to form ectopic, migratory border cell clusters.
Embryos homozygous for Six4289 exhibit very few srp-positive cells in the trunk at stage 14, as oppose to wild-type embryos, in which these cells form a continuous layer in the lateral mesoderm. There appears a defect in initial specification of the primary fat body precursors in stage 10-12 mutant embryos. Many of the somatic gonadal precursors that initially appear in Six4289 mutants appear to die subsequently. The number of cells expressing eya decreases markedly during stage 12, while a greater number of apoptotic cells is observed in the region normally occupied by somatic gonadal precursors. Six4289 mutants exhibit a characteristic pattern of muscle defects. The cardioblasts appear normal, as do the dorsal somatic muscles while lateral and ventral somatic muscles are severely disrupted. The lateral body wall muscles are severely affected, with many muscles absent. In the ventral region, the ventral acute muscle, VA3, and segment border muscle, are absent in most segments, while some ventral oblique muscles and most of the ventral longitudinal muscles are usually present.
Homozygotes fail to hatch. Embryos have gonadal coalescence defects. The embryonic muscle pattern is disrupted. Muscles appear disorganised in their arrangement and attachment. Some muscles appear to be entirely missing, although the number and location of such muscles varies between segments and embryos. The primary defect appears to be in the fusion process.
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 (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (4)