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General Information
Symbol
Dmel\Sxlf1
Species
D. melanogaster
Name
FlyBase ID
FBal0016680
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Sxlf#1, Sxlfl
Key Links
Mutagen
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

Probably point mutation (no gross alteration in DNA).

Carried on aberration
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

intercalary heterochromatin & polytene chromosome | female (with Sxlfhv1)

Detailed Description
Statement
Reference

Expression of SxlScer\UAS.cRa in a Sxlf1 mutant background results in full male lethality. Female viability is unaffected.

Female viability is not compromised in a cross between wild-type females and Sxlf1 males.

The salivary gland cells of Sxlf1/Sxlfhv1 females show somatic mosaicism; some cells are of "male" type (Sxl is not expressed), while others are of "female" type (Sxl is expressed). The frequency of weak spots in the intercalary heterochromatin regions of the X chromosomes is much lower in the "male" cells compared to in the "female" cells and bands of intercalary heterochromatin in the X chromosome look solid, dense and non-broken in the "male" cells, as occurs in normal males.

30% of ovaries of Sxlf4/Sxlf1 females that are infected with Wolbachia have no eggs, 20% of ovaries have 1-2 eggs, 35% of ovaries have 3-9 eggs and 15% of ovaries have more than 10 eggs. 70% of ovaries of Sxlf5/Sxlf1 females that are infected with Wolbachia have no eggs, 5% of ovaries have 1-2 eggs, 15% of ovaries have 3-9 eggs and 10% 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.

A few percent of the Sxlf1/Sxlfhv1 female progeny survive to the third larval instar stage.

Females with homozygous germ line clones do not lay any eggs.

Females of the genotype Sxlf1/Sxlfhv1 fail to activate the Sxl locus in a subset of their cells and thus are mosaic for cells that follow either the male of female pathway for dosage compensation. In XX cells that have adopted the male fate msl-2 interacts in a full male-like pattern. Mosaics lacking mle or msl-3 show partial immunostaining patterns for msl-2. msl-1 and msl-2 precisely colocalise at the msl-3 and mle independent sites. msl-2 localisation is completely abolished in the absence of msl-1.

Sxl+/Sxl+;vir-/virts and Sxlf1/Sxl+;vir-/vir+ are viable but doubly heterozygous Sxlf1/Sxl+;vir-/virts females are lethal.

Sxlf1/Sxlf1 shows no dosage compensation in run25 phenotype assay.

Heterozygous Sxlf1/Sxlfhv1 female larvae are mosaics of male and female cells.

50% females heteroallelic for Sxlf1 and Sxlfhv1 survive to the third instar larval stage and are mosaic for Sxl expression.

Causes female lethality in double heterozygous combination with Df(1)svr, Df(1)N71, Df(1)HF396, Df(1)N19, Df(1)HC244 and Df(1)RA2. The viability of Sxlf1/+ and Sxlf1/Df(1)RA2 female progeny derived from a cross between Df(1)RA2/+ females and Sxlf1/Y males is severely reduced. Viability is recovered if the Sxlf1/+ or Sxlf1/Df(1)RA2 female progeny also carry Dp(1;3)sn13a1 or if the Df(1)RA2/+ mothers also carry Dp(1;3)sn13a1.

Sxlf1/Sxlf4 and Sxlf1/Sxlf5 female larvae have gonads that are female-like in size and morphology, although Sxlf1/Sxlf4 and Sxlf1/Sxlf5 adult females have ovaries filled with male-like multicellular cysts.

SxlK1274-1/Sxlf1 individuals are lethal.

Viability of Sxlf1/Sxlfhv1 females reduced compared to wild type, but some individuals survive into larvae and a few survive to adult hood. The larvae are mosaic for Sxl function: Sxl protein is bound to X chromosomes in approximately half of the cells in the salivary glands, mle protein is bound to X chromosomes in those cells where Sxl is not. Sxlf1/Sxlfhv1 females that are also homozygous for mutants at msl-1, msl-2 or msl-3 develop as intersexes of the mosaic type.

Heterozygotes with Df(1)HF396 have drastically reduced viability.

Restores 100% viability to males carrying a duplication of sc+ and heterozygous for dpn+, that would otherwise have only 50% viability.

Lethal in heterozygous combination with Df(1)N71 or Df(1)svr.

80% of female scsisB-1/sc10-1 embryos die. All female scsisB-1/sc10-1 embryos heterozygous for Sxlf1 die. Female embryos heterozygous for scsisB-1 and Sxlf1, and deficient for one copy of sisA show 75% lethality.

The germ cell death associated with ovoD1rv23 during early gastrulation is suppressed in Sxlf1 homozygotes.

Triploid intersexes with a chromosome ratio of 2X:3A are transformed to pseudomales in Sxlf1 heterozygotes which are also tra mutants. The gonads form well developed and nicely coiled testes, which are mostly filled with spermatogenic germ cells which were usually arrested at the spermatocyte stage.

Sxlf1 heterozygous female progeny derived from heterozygous da1 mothers have reduced viability. The viability is increased if the Sxlf1/+ progeny are also carrying msl-31, and is decreased if the da1/+ mothers are also carrying msl-31. The frequency of sex transformation in Sxlf1/+ female progeny derived from da1/+ mothers is increased if either the mothers or the progeny are homozygous for msl-31. The frequency of morphological abnormalities seen in Sxlf1/+ female progeny derived from da1/+ mothers is greatly reduced if the progeny are also homozygous for msl-31.

Homozygotes die as embryos. The viability of triploid intersexes homozygous for Sxlf1 is almost as high as that of triploid intersexes with wild-type Sxl function. Triploid intersexes that are carrying Sxlf1 are masculinised.

Homozygous females do not survive. Some females heterozygous for Sxlf1 and homozygous for mle1, mle4, msl-1unspecified, or msl-21 have sex combs on the basitarsi of their forelegs.

Homozygous females invariably die as embryos but hemizygous males are fully viable and fertile. In most wild-type genetic backgrounds, heterozygous females exhibit normal viability and fertility, although occasionally display morphological defects characteristic of early cell death; however, can be dominant semi-lethal for females in some wild-type genetic backgrounds and under suboptimal growth conditions. In doubly heterozygous combination with otherwise recessive mutations in positive regulators of Sxl, this allele can behave as a dominant: heterozygote viability is reduced for daughters of da/+ females, as well as for females that are also heterozygotes for either sis-a, sis-b or snf. In some such doubly heterozygous situations, escaper females may be incompletely masculinized (mosaic intersex). Homozygosity for mutations in the autosomal male-specific lethal loci does not suppress recessive Sxlf1 lethality, but it does partially masculinize Sxlf1/+ females (generating mosaic intersexes) and suppresses cell-death-related morphological defects. Homozygous moribund embryos show sex-specific alterations in the phenotypic expression of hypomorphic X-linked alleles such as run25, a reflection of upsets in dosage compensation (female hyperactivation). Depending on the time of induction, Sxlf1/Sxlf1 clones induced in Sxlf1/+ females can be phenotypically male and reduced in size. 2X:3A animals homozygous or heterozygous for Sxlf1 are viable but masculinized. In genetic mosaics and chimeras, Sxlf1 homozygous germ cells develop abnormally and fail to generate functional gametes. In some situations, the mutant female tissue displays masculine traits. Sxlf1 rescues males from the otherwise lethal effects of a simultaneous duplication of sis-a+ and sis-b+. canonical amorph

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

Sxlf1/Sxlf5 has female sterile phenotype, suppressible | partially by Oda[+]/Odak11803

Sxlf4/Sxlf1 has female sterile phenotype, suppressible | partially by Oda[+]/Odak11803

Sxl[+]/Sxlf1, l(1)4343 has partially lethal | female phenotype, suppressible | partially by Dp(1;3)sn13a1

NOT suppressed by
Statement
Reference

Sxlfhv1/Sxlf1 has lethal | female phenotype, non-suppressible by Low1

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Statement
Reference

Sirt1ex10, Sxl[+]/Sxlf1 has viable phenotype

Phenotype Manifest In
Suppressed by
Statement
Reference

Sxlf1/Sxlf5 has ovary phenotype, suppressible | partially by Oda[+]/Odak11803

Sxlf4/Sxlf1 has ovary phenotype, suppressible | partially by Oda[+]/Odak11803

Other
Additional Comments
Genetic Interactions
Statement
Reference

Sxlf1 suppresses the semi-lethality of homozygous cav2248 males.

In progeny from Su(var)2055 heterozygous females crossed to Sxlf1/Y males, female viability is dramatically reduced. The effect of Su(var)2055 is strictly maternal; no significant reduction in female viability is observed in the reciprocal cross.

In progeny from Su(var)2054 heterozygous females crossed to Sxlf1/Y males, female viability is dramatically reduced.

In progeny from Su(var)2052 heterozygous females crossed to Sxlf1/Y males, female viability is reduced.

The weak dominant female-lethal effect of Sxlf1 is not enhanced by ssx55/ssx55.

Only 57% of the expected Sxlf1/+ daughters from da2/+ mothers survive to adulthood.

When mothers are heterozygous for both Df(3R)pps[1] and da2, there is a significant reduction in viability.

The lethality of bonS043420 homozygous males is not rescued if they are also carrying Sxlf1; almost no escapers are seen. The lethality of bonS024108 homozygous males is not rescued if they are also carrying Sxlf1; no Sxlf1/Y ; bonS024108/bonS024108 male animals survive beyond the first larval instar.

Odak11803/+ partially suppresses the ovary phenotype and female sterility of Sxlf5/Sxlf1. Odak11803/+ partially suppresses the ovary phenotype and female sterility of Sxlf4/Sxlf1.

Sxlf1 has no great effect on the differentiation of sexually dimorphic tissues of haplo-X and diplo-X individuals carrying the ix5 mutation, although a weak genetic interaction is observed.

Addition of two copies of sisA+t12 and two copies of ost10 has no effect on the viability of Sxlf1/Y males.

The preferential sensitivity of males to the lethal effects of expression of runScer\UAS.cLa under the control of Scer\GAL4nos.PG is not suppressed by Sxlf1.

X chromosomal recombination frequencies in female germ cells homozygous for vir6 are significantly reduced compared to wild-type and there is an increased frequency of non-disjunction. The frequency of recombination is further lowered if the germ cells also carry Sxlf1, and the frequency of non-disjunction is further increased. The viability of Sxlf1/+ ; vir6/vir6 females is severely reduced and escapers rarely produce eggs.

The addition of up to three copies of P{snf+,dhd+} to Sxlf1/Y;SxlF1.hs, tra1 partially feminized males does not enhance the feminisation or lethality phenotypes seen in these flies.

Lethal in female double heterozygous combination with fl(1)3535. The lethality of fl(1)3535/Sxlf1 females is primarily embryonic and there is an effect of maternal fl(1)3535 genotype on the lethal period; most of the progeny of females homozygous for fl(1)3535 die as embryos whereas the progeny of fl(1)3535/+ females die at larval as well as embryonic stages. The lethality can be partially rescued by Dp(1;3)sn13a1. Females doubly heterozygous for fl(1)3546 and Sxlf1 show 3.5% viability. Lethality of fl(1)3546/Sxlf1 females can occur at embryonic or larval stages. The lethality can be partially rescued by Dp(1;3)sn13a1. Females doubly heterozygous for l(1)4343 and Sxlf1 show 7% viability. Lethality of l(1)4343/Sxlf1 females occurs at embryonic and larval stages. The lethality can be partially rescued by Dp(1;3)sn13a1.

Female lethal-synergistic interactions with snf- mutations.

When homozygous females for snfe8H are crossed to a male carrying a null allele for Sxl, no female progeny are recovered.

Progeny of genotype Df(1)HC244/Sxlf1 are rare suggesting a lethal zygotic effect. Survivors are sterile and show male traits: male abdomen pigmentation and a few sex comb teeth. Ovaries are present and filled with eggs that show abnormal chorion appendages which are often fused and enlarged. A maternal effect is seen in that less then half the expected number of daughters is found.

Some females heterozygous for Sxlf1 and homozygous for mle1, mle4, msl-1unspecified, or msl-21 have sex combs on the basitarsi of their forelegs.

Sxlf1/+ chromosomal females also homozygous or heterozygous for either mle1, msl-31 or msl-22 show variable transformation of sexually dimorphic structures to male characteristics. The frequency of transformation is not high, is higher in females homozygous (rather than heterozygous) for the male-specific lethal allele, and expression is incomplete. The frequency of transformation is higher in female flies with mothers homozygous for the male-specific lethal allele. Sex combs are only seen in Sxlf1/+ females homozygous for the male-specific lethal allele.

Xenogenetic Interactions
Statement
Reference

Expression of Zzzz\Soce-SxlScer\UAS.cRa under the control of Scer\GAL4arm.PS in a Sxlf1 mutant background has no effect on male viability. Female viability is unaffected. All males show normal external morphology.

Expression of Sxl::Soce\Soce-SxlScer\UAS.SX17 under the control of Scer\GAL4arm.PS in a Sxlf1 mutant background results in almost completely viability. Only 0.9% lethality is observed. Female viability is unaffected and all surviving males show normal external morphology.

Expression of Sxl::Soce\Soce-SxlScer\UAS.SX64 under the control of Scer\GAL4arm.PS in a Sxlf1 mutant background results in 60% male lethality. Female viability is unaffected and all surviving males show normal external morphology.

Expression of Sxl::Soce\Soce-SxlScer\UAS.SX35 under the control of Scer\GAL4arm.PS in a Sxlf1 mutant background results in 87% male lethality. Female viability is unaffected and all surviving males show normal external morphology.

Expression of Sxl::Soce\Soce-SxlScer\UAS.SX28 under the control of Scer\GAL4arm.PS in a Sxlf1 mutant background has no effect on male viability. Female viability is also unaffected and all males show normal external morphology.

More hybrid males (which are derived from a cross of Sxlf1/+ D.melanogaster females to D.simulans males) carrying Sxlf1 survive to the third larval instar compared to hybrids carrying Sxl+.

Complementation and Rescue Data
Fails to complement
Comments
Images (0)
Mutant
Wild-type
Stocks (21)
Notes on Origin
Discoverer

Muller and Zimmering, 1960.

Comments
Comments

Does not interfere with transcription of the locus.

Nuclei follow a female pathway, elevated H4Ac16 staining, acetylated form of His4, is not detected in the paired X chromosome.

Individuals of heteroallelic combination Sxlfhv1 and Sxlf1 have reduced Sxl levels.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (11)
References (75)