FB2021_03, released June 15, 2021

Allele: Dmel\Sxlf9

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General Information
Symbol
Dmel\Sxlf9
Species
D. melanogaster
Name
FlyBase ID
FBal0016686
Feature type
allele
Associated gene
Dmel\Sxl
Associated Insertion(s)
Carried in Construct
Key Links
Allele class

loss of function allele

hypomorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

hypomorphic allele - genetic evidence

(Bernstein and Cline, 1994, Lindsley and Zimm, 1992)

loss of function allele

(Maine et al., 1985)
Mutagen
ethyl methanesulfonate
(Lindsley and Zimm, 1992, Maine et al., 1985)
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
       
      Progenitor genotype
      Cytology
      Nature of the lesion
      Statement
      Reference

      Not associated with any gross DNA change. Based on recombination mapping and conversion factor of 1μMorgan=47bp (based on FBrf0042060), the Sxlf9 lesion maps approximately 3.3kb downstream of the SxlM1 lesion.

      (Bernstein and Cline, 1994)

      Probably point mutation (no gross alteration in DNA).

      (Maine et al., 1985)
      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

      Survival of her1/hermat-1 and her1/her2 daughters is severely affected in the presence of Sxlf9.

      (Pultz and Baker, 1995)

      Sxlf9/Sxlf1 shows incomplete dosage compensation in run25 phenotype assay.

      (Bernstein and Cline, 1994)

      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).

      (Lindsley and Zimm, 1992)

      Fully complements SxlfLS.

      (Granadino et al., 1991)
      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

      (Oliver et al., 1990)
      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.

      (Gladstein et al., 2010)

      The viability of Sxlf9 in female double heterozygous combination with fl(1)3535, fl(1)3546 or l(1)4343 is reduced.

      (Anand et al., 1998)

      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.

      (Albrecht and Salz, 1993)

      The number of vitellogenic eggs produced by ovoD2 heterozygous females is is not increased by Sxlf9.

      (Oliver et al., 1990)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Complements

      Sxldlf

      (Anand et al., 1998)

      Sxlf2593

      (Lindsley and Zimm, 1992)

      SxlfLS

      (Lindsley and Zimm, 1992)

      SxlM1,fPa-ra

      (Lindsley and Zimm, 1992)
      Comments

      SxlF1.hs can rescue 40% female lethality and the survivors are fertile.

      (Bell et al., 1991)
      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.

      (Bernstein and Cline, 1994)

      Defective in the initiation of Sxl function.

      (Pultz and Baker, 1995)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (1)
      Reported As
      Symbol Synonym
      Sxlf9
      (Gladstein et al., 2010)
      Name Synonyms
      Secondary FlyBase IDs
        References (13)