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General Information
Symbol
Dmel\SmD3k11803
Species
D. melanogaster
Name
FlyBase ID
FBal0100399
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
l(2)k118-03, 118/3
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Insertion components
P{lacW}SmD3k11803
Product class / Tool use(s)
Encoded product / tool
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

Mutant embryos show defects in the lateral chordotonal organs and the ventral nerve cord.

Smaller number of PNS neurons express 22C10 in homozygous embryos and PNS axons dispay severe defects in growth cone guidance and fasciculation. Most noticeable phenotype is splitting of the intersegmental nerve into two fascicles, the ISN 'loop' phenotype. Defects in the CNS are similar to those observed in the PNS. Numerous muscles are missing, displaced or exhibit aberrant shapes. Embryos also contain many mononucleate myoblasts that fail to fuse into muscle syncytia. Defects also in the visceral and cardiac musculature.

Homozygous embryos exhibit loss of neurons.

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
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

I. Kiss.

Comments
Comments

The P{lacW}SmD3k11803 insertion appears to affect only SmD3 function and not Oda function (despite being within an Oda intron), since the lethality of P{lacW}SmD3k11803 homozygotes is fully rescued by the P{SmD3.+t2.3} construct which contains the complete SmD3 gene. Complements: OdaEP2104.

P{lacW} insertion can be excised and revert the lethal phenotype to wild type.

Precise or near precise excision of the P{lacW} insertion reverts both the lethality and the PNS phenotype, demonstrating the insertion causes the phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (8)