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General Information
Symbol
Dmel\Sxlf18
Species
D. melanogaster
Name
FlyBase ID
FBal0034090
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
sxlfs3, Sxlfs#3
Key Links
Mutagen
    Nature of the Allele
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Nucleotide change:

    G7084598A

    Amino acid change:

    G292D | Sxl-PA; G300D | Sxl-PAB; G309D | Sxl-PAC; G322D | Sxl-PC; G332D | Sxl-PD; G292D | Sxl-PE; G324D | Sxl-PG; G324D | Sxl-PJ; G332D | Sxl-PL; G322D | Sxl-PN; G332D | Sxl-PT

    Reported amino acid change:

    G?D

    Comment:

    The Sxlf18 point mutation blocks the alternative splicing necessary to generate exon-10-encoded C-terminal versions of Sxl female transcripts and substitutes aspartic acid for glycine in the exon-8-encoded C-terminal isoforms.

    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    Point mutation.

    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

    Sxlf18 mutant female germline stem cells are rapidly lost from the niche by two weeks after clone induction.

    Approximately 8% of Sxlf18 mutant germaria contain cystoblasts with defects in differentiation.

    Sxlf18,f32 is a dominant intragenic suppressor of recessive Sxlfs3 female sterility. Sxlf18,f32/Sxlfs3 females are fully viable and fertile.

    Recombination across the y-sn interval on the X chromosome of SxlM1,f3/Sxlfs3 females is reduced compared to wild type.

    77% of ovaries of homozygous females that are not infected with Wolbachia have no eggs, 20% of ovaries have 1-2 eggs and 3% of ovaries have 3-9 eggs. These oogenesis defects are partly rescued by Wolbachia infection; 20% of the ovaries of infected homozygous females have no eggs, 28% of ovaries have 1-2 eggs, 40% of ovaries have 3-9 eggs and 12% of ovaries have more than 10 eggs. 95% of ovaries of Sxlfs3/Sxlf1 females that are infected with Wolbachia have no eggs and 5% of ovaries have 1-2 eggs.

    Sxlf4/Sxlfs3; Su(Sxlfs)X2X2/+ females show severely reduced recombination (no recombinant progeny are produced). The reduction in recombination is caused by the lack of wild-type Sxl activity rather than the presence of Su(Sxlfs)X2X2 (recombination is restored to almost wild-type values in Sxlfs3/+ ; Su(Sxlfs)4646/+ females). A high frequency of non-disjunction is also seen in Sxlf4/Sxlfs3 ; Su(Sxlfs)X2X2/+ females. Sxlf4/Sxlfs3; Su(Sxlfs)X2X2/+ vitellogenic cysts show the same defects as Sxlf4/Sxlf4; Su(Sxlfs)4646/+ cysts. No chiasmata are present in stage 13-14 oocytes of Sxlf4/Sxlfs3 ; Su(Sxlfs)X2X2/+ females. Consequently, chromosomes are usually seen in an anaphase-like arrangement in the first division spindle. In many instances, chromosomes are arranged in two or three spindles instead of one.

    Tumorous ovaries.

    Many more germ cells in ovarian tumors are positive for expression of male germline markers than in wild type testes, suggesting a relaxation of growth control, or accumulation of apical cells due to a developmental block.

    Homozygous females have ovarian tumours.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    NOT Enhancer of
    NOT Suppressor of
    Statement
    Reference
    Phenotype Manifest In
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    The phenotype of a reduction in recombination across the y-sn interval on the X chromosome that is seen in SxlM1,f3/Sxlfs3 females is enhanced by otu17/+ ; there is a further reduction in map distance in the double mutants. In addition, the rate of X chromosome nondisjunction is increased eightfold.

    The number of vitellogenic eggs produced by ovoD2 heterozygous females is not increased by Sxlf18.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Comments

    Sxlf18,f32 is a dominant intragenic suppressor of recessive Sxlfs3 female sterility. Sxlf18,f32/Sxlfs3 females are fully viable and fertile.

    Images (0)
    Mutant
    Wild-type
    Stocks (3)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (5)
    References (16)