FB2024_03 , released June 25, 2024
Allele: Dmel\SxlfLS
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General Information
Symbol
Dmel\SxlfLS
Species
D. melanogaster
Name
FlyBase ID
FBal0016689
Feature type
allele
Associated gene
Dmel\Sxl
Associated Insertion(s)
gypsy{}SxlfLS
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
spontaneous
(Lindsley and Zimm, 1992, Maine et al., 1985)
Progenitor genotype
Associated Insertion(s)
gypsy{}SxlfLS
Cytology
Description

Transposon insertion site maps just downstream of Pm, between Pm and Pe.

(Bernstein and Cline, 1994)

gypsy insert present.

(Lindsley and Zimm, 1992)

gypsy element insertion.

(Granadino et al., 1991)

Insertion of gypsy element.

(Salz et al., 1987)

Insertion of 10kb DNA gypsy element into Sxl. Insertion site is approximately 1.5kb distal to the site of P-element insertion in SxlfPb and 1kb distal to the site of insertion in Sxlf2.

(Maine et al., 1985)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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 not affected in the presence of SxlfLS.

      (Pultz and Baker, 1995)

      SxlfLS/Sxlf1 shows wild type dosage compensation in run25 phenotype assay.

      (Bernstein and Cline, 1994)

      Able to initiate female development, but is defective in its ability to maintain the female developmental commitment and/or to elicit female sexual differentiation. It is masculinizing in homozygous mutant somatic clones induced by mitotic recombination and it causes the tissue in such clones to grow poorly; nevertheless, it has no dominant effect on the sexual phenotype of triploid intersexes, nor does it interact in a dominant fashion with mutations in da or sisA, both early acting positive regulators of Sxl. Fully complements Sxlf9, which appears to have a very different set of defects.

      (Lindsley and Zimm, 1992)

      Fully complemented by Sxlfb, Sxlfc and Sxlf9. Homozygous germ cell clones do not develop into oocytes.

      (Granadino et al., 1991)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressor of
      Statement
      Reference

      SxlfLS is a 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 SxlfLS 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 increased by SxlfLS.

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

      Sxlf9

      (Lindsley and Zimm, 1992)
      Fails to complement

      Sxldlf

      (Anand et al., 1998)
      Comments

      SxlF1.hs can rescue 94% female lethality but the females are sterile.

      (Bell et al., 1991)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      Comments
      Comments

      XO male clones generated at the larval stage in SxlfLS/+ females are only viable if they contain the SxlfLS mutation.

      (Bachiller and Sanchez, 1991)

      Complements Sxlf9, and partially complements Sxlf2 for female viability. Defective in Sxl Pm-mediated activities - the later functions governing maintenance and expression of the female-committed developmental state. Shows dominant masculinizing interactions with snf that are as strong as for a Sxl deficiency.

      (Bernstein and Cline, 1994)

      Nuclei of SxlfLS/Sxlf2593 larvae exhibit binding of the msl gene products to the paired X chromosomes but no Sxl binding.

      (Hilfiker et al., 1994)

      Defective in the maintenance of Sxl function.

      (Pultz and Baker, 1995)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (1)
      Reported As
      Symbol Synonym
      SxlfLS
      Name Synonyms
      Secondary FlyBase IDs
        References (16)