FB2025_01 , released February 20, 2025
Allele: Dmel\sas15
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General Information
Symbol
Dmel\sas15
Species
D. melanogaster
Name
FlyBase ID
FBal0015134
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
EdR16
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid replacement: ?643term.

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

C7178718T

Amino acid change:

R643term | sas-PA; R643term | sas-PB; R643term | sas-PC; R643term | sas-PD

Reported amino acid change:

?643term

Comment:

Mutation reported as having a stop codon at residue 643. Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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

sas15/Df(3R)ED5221 transheterozygotes appear normal at embryonic stage 14, but display weak longitudinal axon defects at stage 16. The outer Fas2-positive axon bundle is interrupted and the other bundles appear slightly irregular. Complete breaks of a longitudinal tract are rare, but do occasionally occur. Fas2 positive axons ectopically cross the midline in ~15% of segments. Defects in the anterior commissure are also seen.

sas15 homozygotes appear normal at embryonic stage 14, but display weak longitudinal axon defects at stage 16. The outer Fas2 positive axon bundle is interrupted and the other bundles appear slightly irregular. Complete breaks of a longitudinal tract are rare, but do occasionally occur. Fas2-positive axons ectopically cross the midline in ~15% of segments. Defects in the anterior commissure are also seen.

Larvae die during the first instar moult or as small second instar larvae.

Lethality occurs during embryonic and larval stages.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
NOT Enhancer of
Statement
Reference

sas15/sas[+] is a non-enhancer of visible | dominant phenotype of sogEP7

sas15/sas[+] is a non-enhancer of visible | dominant phenotype of sogEP11

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

sas15/sas[+] is a non-suppressor of visible | dominant phenotype of sogEP11

sas15/sas[+] is a non-suppressor of visible | dominant phenotype of sogEP7

Phenotype Manifest In
Enhanced by
Suppressed by
NOT Enhancer of
Statement
Reference

sas15/sas[+] is a non-enhancer of wing vein phenotype of sogEP7

sas15/sas[+] is a non-enhancer of wing vein phenotype of sogEP11

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

sas15/sas[+] is a non-suppressor of wing vein phenotype of sogEP11

sas15/sas[+] is a non-suppressor of wing vein phenotype of sogEP7

Additional Comments
Genetic Interactions
Statement
Reference

Salivary glands in sas15 mutant embryos expressing Cad99CScer\UAS.fl under the control of Scer\GAL4fkh.PH are largely normal.

A sas15 mutant background does not affect the Cad99CEXTRA.Scer\UAS.T:Ivir\HA1 overexpression phenotype.

Ptp10D1 enhances the ectopic midline crossing phenotype that is seen in sas15/Df(3R)ED5221 mutant stage 16 embryos. Multiple Fas2-positive axon bundles cross the midline in each segment, and these are perpendicular to the longitudinal tracts. The inner Fas2-positive bundle is intact, but one or both of the outer longitudinal bundles are missing.

Ptp10D1 enhances the ectopic midline crossing phenotype seen in homozygous sas15 mutant stage 16 embryos.

Ptp69D1/Df(3L)8ex25 enhances the ectopic midline crossing phenotype seen in sas15/Df(3R)ED5221 mutant stage 16 embryos.

Ptp69D1/Df(3L)8ex25 enhances the ectopic midline crossing phenotype seen in homozygous sas15 mutant stage 16 embryos. Segments of the outer longitudinal tract are missing. Multiple Fas2-positive axon bundles cross the midline in each segment, and these are perpendicular to the longitudinal tracts. The inner Fas2-positive bundle is intact, but one or both of the outer longitudinal bundles are missing. Complete breaks in the Fas2-positive longitudinal tract are seen. The anterior and posterior commissures are fused into a single commissural tract.

Expression of sasScer\UAS.cLa under the control of Scer\GAL4Fas2-Mz507 almost completely rescues the CNS defects seen in sas15/Df(3R)ED5221, Ptp69D1/Df(3L)8ex25 double mutant embryos.

Expression of sasScer\UAS.cLa under the control of Scer\GAL4Fas2-Mz507 almost completely rescues the CNS defects seen in sas15, Ptp69D1/Df(3L)8ex25 double mutant embryos.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

R. Lewis.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (9)