Probably point mutation (no gross alteration in DNA).
intercalary heterochromatin & polytene chromosome | female (with Sxlfhv1)
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.
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.
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.
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.
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.
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
Sxlf1, da[+]/da2 has partially lethal - majority die | dominant phenotype, enhanceable by Df(3R)pps1/+
Sxlf1, da[+]/da2 has partially lethal - majority die | dominant phenotype, enhanceable by pps+tJa/Df(3R)pps1/+
Sxlf1/Sxlf5 has female sterile phenotype, suppressible | partially by Oda[+]/Odak11803
Sxlf4/Sxlf1 has female sterile phenotype, suppressible | partially by Oda[+]/Odak11803
Sxl[+]/Sxlf1, fl(1)3546 has partially lethal | female phenotype, suppressible | partially by Dp(1;3)sn13a1
Sxl[+]/Sxlf1, l(1)4343 has partially lethal | female phenotype, suppressible | partially by Dp(1;3)sn13a1
Sxl[+]/Sxlf1, fl(1)3535 has partially lethal | female phenotype, suppressible | partially by Dp(1;3)sn13a1
Sxlf1 is a suppressor of partially lethal - majority die | dominant | male limited phenotype of cav2248
Sxlf1 is a non-suppressor of lethal | recessive | male | first instar larval stage phenotype of bonS024108
Sxlf1 is a non-suppressor of lethal | recessive | male limited | first instar larval stage phenotype of bonS043420
Sxlf1 is a non-suppressor of lethal | embryonic stage phenotype of Scer\GAL4nos.PG, runUAS.cLa
Scer\GAL4arm.PS, Sxlf1, Soce\SxlUAS.cRa/Zzzz\Soce-SxlScer\UAS.cRa has viable phenotype
Scer\GAL4arm.PS, Sxl::Soce\Soce-SxlUAS.SX17, Sxlf1 has viable phenotype
Scer\GAL4arm.PS, Sxl::Soce\Soce-SxlUAS.SX28, Sxlf1 has viable phenotype
Su(var)2054, Sxlf1 has partially lethal - majority die | dominant | maternal effect phenotype
Su(var)2055, Sxlf1 has partially lethal - majority die | dominant | maternal effect phenotype
Su(var)2052, Sxlf1 has partially lethal - majority die | dominant | maternal effect phenotype
Sxlf1, da[+]/da2 has partially lethal - majority die | dominant phenotype
Spf45J23, Sxl[+]/Sxlf1 has lethal | female | maternal effect phenotype
Sxlf1, vir6 has partially lethal phenotype
Df(1)HC244, SxlM1/Sxlf1 has viable phenotype
Df(1)HC244, Sxlf1 has lethal phenotype
Sxlf1, mle1 has sex-determination defective | female phenotype
Sxlf1, mle1 has sex-determination defective | dominant | female phenotype
Sxlf1, msl-21 has sex-determination defective | female phenotype
Sxlf1, msl-21 has sex-determination defective | dominant | female phenotype
Sxlf1, mle4 has sex-determination defective | female phenotype
Sxlf1, mle4 has sex-determination defective | dominant | female phenotype
Sxlfhv1/Sxlf1, mle4 has sex-determination defective | female phenotype
Sxlf1, msl-1unspecified has visible | dominant | female phenotype
Sxlf1, msl-1unspecified has sex-determination defective | dominant | female phenotype
Sxlf1, msl-1unspecified has visible | female phenotype
Sxlf1, msl-1unspecified has sex-determination defective | female phenotype
Sxlf1, msl-21 has prothoracic metatarsus | female phenotype
Sxlf1, mle4 has prothoracic metatarsus | female phenotype
Sxlf1, msl-1unspecified has prothoracic metatarsus | female phenotype
Sxlf1, mle1 has abdominal tergite 6 | female phenotype
Sxlf1, mle1 has prothoracic metatarsus | female phenotype
Sxlf1, msl-31 has abdominal sternite 6 | female phenotype
Sxlf1, msl-31 has oviprotector phenotype
Sxlf1, msl-31 has abdominal tergite 5 | female phenotype
Sxlf1, msl-31 has abdominal tergite 6 | female phenotype
Sxlf1, msl-31 has prothoracic metatarsus | female phenotype
Sxlf1, msl-22 has abdominal sternite 6 | female phenotype
Sxlf1, msl-22 has oviprotector phenotype
Sxlf1, msl-22 has abdominal tergite 5 | female phenotype
Sxlf1, msl-22 has abdominal tergite 6 | female phenotype
Sxlf1, msl-22 has prothoracic metatarsus | female phenotype
Sxlf1, mle1 has abdominal sternite 6 | female phenotype
Sxlf1, mle1 has oviprotector phenotype
Sxlf1, mle1 has abdominal tergite 5 | female phenotype
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 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.
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.
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.
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+.
Muller and Zimmering, 1960.
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.