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General Information
Symbol
Dmel\Sxlf9
Species
D. melanogaster
Name
FlyBase ID
FBal0016686
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
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
Not associated with any gross DNA change. Based on recombination mapping and conversion factor of 1╬╝Morgan=47bp (based on FBrf0042060), the Sxlf9 lesion maps approximately 3.3kb downstream of the SxlM1 lesion.
Probably point mutation (no gross alteration in DNA).
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
Survival of her1/hermat-1 and her1/her2 daughters is severely affected in the presence of Sxlf9.
Sxlf9/Sxlf1 shows incomplete dosage compensation in run25 phenotype assay.
Defective in some very early steps in the sex-determination process, but which has no adverse effect on the growth or sexual development of homozygous mutant diplo-X clones induced by mitotic recombination. Rare escapers at 18oC are phenotypically female; nevertheless, it has a dominant masculinizing effect on the phenotype of triploid intersexes ( 2X:3A ) and interacts in a dominant-lethal fashion with mutations in da or sisA, both early acting positive regulators of Sxl. Fully complements "SxlfPR" class (partial deletions of Sxl information that impair later functions of the gene more than earlier).
Fully complements SxlfLS.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Suppressor of
Statement
Reference
Sxlf9 is a non-suppressor of decreased fecundity | dominant | female phenotype of ovoD2
Other
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
The viability of Sxlf9/+ females is significantly reduced if they also carry one maternally-derived copy of msl-31.
The viability of Sxlf9 in female double heterozygous combination with fl(1)3535, fl(1)3546 or l(1)4343 is reduced.
Whereas female progeny heterozygous for Sxlf9 from snfe8H mothers are recovered less frequently than expected (65% relative viability), female progeny heterozygous for SxlfLS (defective in a later, maintenance/expression function) are fully viable.
The number of vitellogenic eggs produced by ovoD2 heterozygous females is is not increased by Sxlf9.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
SxlF1.hs can rescue 40% female lethality and the survivors are fertile.
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments
Sxlf9 fully complements SxlM1,f3. Complements SxlfLS and Sxlf2, and partially complements Sxlf7,M1 for female viability. Recombination distance between Sxlf9 and 'f3' of SxlM1,f3 is 0.015cM. Recombination distance between Sxlf9 and SxlM1 is 0.007cM.
Defective in the initiation of Sxl function.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (13)