Allele Dmel\Sxl^f1

General Information
Symbol	Dmel\Sxl^f1	Species	D. melanogaster
Name		FlyBase ID	FBal0016680
Feature type	allele	Associated gene	Dmel\Sxl
Also Known As	Sxl^f#1, Sxl^fl

Allele class	loss of function allele, amorphic allele - genetic evidence
Mutagen	spontaneous
Recent Updates
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (Maine et al., 1985, Cronmiller and Cline, 1986, Salz et al., 1987, Gorman et al., 1993, Bernstein and Cline, 1994, Palmer et al., 1994, Kelley et al., 1995) loss of function allele (Cline, 1983, Steinmann-Zwicky, 1988, Nothiger et al., 1989, Anand and Chandra, 1994, Granadino et al., 1997)
Mutagen	spontaneous (Maine et al., 1985)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Probably point mutation (no gross alteration in DNA). (Maine et al., 1985)
Carried on aberration	Binscop (FlyBase Curators, 2006-, Green, 2005.2.15)
Cytology
Phenotypic Data
Phenotypic Class
	female sterile \| recessive (Schutt et al., 1998) lethal \| embryonic stage (Cline, 1983) lethal \| female (Uenoyama et al., 1982, Nothiger et al., 1989) lethal \| female (with Sxl^fhv1) (Bhadra et al., 1997) lethal \| female \| recessive (Skripsky and Lucchesi, 1982, Granadino et al., 1991) partially lethal - majority die \| dominant \| female (Cline et al., 2010) viable \| female \| reduced (Gorman et al., 1993)
Phenotype Manifest In
	egg (Schutt et al., 1998) gonad (Nothiger et al., 1989) intercalary heterochromatin & polytene chromosome \| female (with Sxl^fhv1) (Alekseyenko et al., 2002) ovary (Steinmann-Zwicky, 1994)
Detailed Description
	Statement Reference Female viability is not compromised in a cross between wild-type females and Sxl[f1] males. (Li et al., 2011) The salivary gland cells of Sxl^f1/Sxl^fhv1 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. (Alekseyenko et al., 2002) 30% of ovaries of Sxl^f4/Sxl^f1 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 Sxl^f5/Sxl^f1 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 Sxl^fs3/Sxl^f1 females that are infected with Wolbachia have no eggs and 5% of ovaries have 1-2 eggs. (Starr and Cline, 2002) A few percent of the Sxl^f1/Sxl^fhv1 female progeny survive to the third larval instar stage. (Bhadra et al., 2000) Females with homozygous germ line clones do not lay any eggs. (Schutt et al., 1998) Females of the genotype Sxl^f1/Sxl^fhv1 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. (Lyman et al., 1997) Sxl⁺/Sxl⁺;vir^-/vir^ts and Sxl^f1/Sxl⁺;vir^-/vir⁺ are viable but doubly heterozygous Sxl^f1/Sxl⁺;vir^-/vir^ts females are lethal. (Hilfiker et al., 1995) Sxl^f1/Sxl^f1 shows no dosage compensation in run²⁵ phenotype assay. (Bernstein and Cline, 1994) Heterozygous Sxl^f1/Sxl^fhv1 female larvae are mosaics of male and female cells. (Bone et al., 1994) 50% females heteroallelic for Sxl^f1 and Sxl^fhv1 survive to the third instar larval stage and are mosaic for Sxl expression. (Palmer et al., 1994) 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 Sxl^f1/+ and Sxl^f1/Df(1)RA2 female progeny derived from a cross between Df(1)RA2/+ females and Sxl^f1/Y males is severely reduced. Viability is recovered if the Sxl^f1/+ or Sxl^f1/Df(1)RA2 female progeny also carry Dp(1;3)sn^13a1 or if the Df(1)RA2/+ mothers also carry Dp(1;3)sn^13a1. (Sanchez et al., 1994) Sxl^f1/Sxl^f4 and Sxl^f1/Sxl^f5 female larvae have gonads that are female-like in size and morphology, although Sxl^f1/Sxl^f4 and Sxl^f1/Sxl^f5 adult females have ovaries filled with male-like multicellular cysts. (Steinmann-Zwicky, 1994) Sxl^K1274-1/Sxl^f1 individuals are lethal. (Sugimura et al., 1994) Viability of Sxl^f1/Sxl^fhv1 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. Sxl^f1/Sxl^fhv1 females that are also homozygous for mutants at msl-1, msl-2 or msl-3 develop as intersexes of the mosaic type. (Gorman et al., 1993) Heterozygotes with Df(1)HF396 have drastically reduced viability. (Torres and Sanchez, 1992) Restores 100% viability to males carrying a duplication of sc⁺ and heterozygous for dpn⁺, that would otherwise have only 50% viability. (Younger-Shepherd et al., 1992) Lethal in heterozygous combination with Df(1)N71 or Df(1)svr. (Granadino et al., 1991) 80% of female sc^sisB-1/sc^10-1 embryos die. All female sc^sisB-1/sc^10-1 embryos heterozygous for Sxl^f1 die. Female embryos heterozygous for sc^sisB-1 and Sxl^f1, and deficient for one copy of sisA show 75% lethality. (Torres and Sanchez, 1991) The germ cell death associated with ovo^D1rv23 during early gastrulation is suppressed in Sxl^f1 homozygotes. (Oliver et al., 1990) Triploid intersexes with a chromosome ratio of 2X:3A are transformed to pseudomales in Sxl^f1 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. (Nothiger et al., 1989) Sxl^f1 heterozygous female progeny derived from heterozygous da¹ mothers have reduced viability. The viability is increased if the Sxl^f1/+ progeny are also carrying msl-3¹, and is decreased if the da¹/+ mothers are also carrying msl-3¹. The frequency of sex transformation in Sxl^f1/+ 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 Sxl^f1/+ female progeny derived from da¹/+ mothers is greatly reduced if the progeny are also homozygous for msl-3¹. (Uenoyama, 1984) Homozygotes die as embryos. The viability of triploid intersexes homozygous for Sxl^f1 is almost as high as that of triploid intersexes with wild-type Sxl function. Triploid intersexes that are carrying Sxl^f1 are masculinised. (Cline, 1983) Homozygous females do not survive. Some females heterozygous for Sxl^f1 and homozygous for mle¹, mle⁴, msl-1^unspecified, or msl-2¹ have sex combs on the basitarsi of their forelegs. (Skripsky and Lucchesi, 1982) 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 Sxl^f1 lethality, but it does partially masculinize Sxl^f1/+ 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, Sxl^f1/Sxl^f1 clones induced in Sxl^f1/+ females can be phenotypically male and reduced in size. 2X:3A animals homozygous or heterozygous for Sxl^f1 are viable but masculinized. In genetic mosaics and chimeras, Sxl^f1 homozygous germ cells develop abnormally and fail to generate functional gametes. In some situations, the mutant female tissue displays masculine traits. Sxl^f1 rescues males from the otherwise lethal effects of a simultaneous duplication of sis-a⁺ and sis-b⁺. canonical amorph
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference Sxl^f1, da[+]/da² has partially lethal - majority die \| dominant phenotype, enhanceable by Df(3R)pps¹/+ (Johnson et al., 2010) Sxl^f1, da[+]/da² has partially lethal - majority die \| dominant phenotype, enhanceable by pps^+tJa/Df(3R)pps¹/+ (Johnson et al., 2010)
NOT Enhanced by
Statement Reference Sxl^F1.hs, Sxl^f1, tra¹ has sex-determination defective phenotype, non-enhanceable by snf^+t5.5 (Cline et al., 1999) Sxl^f1 has partially lethal - majority die \| dominant \| female phenotype, non-enhanceable by ssx⁵⁵/ssx⁵⁵ (Cline et al., 2010)
Suppressed by
Statement Reference Sxl^f1, fl(1)35³⁵ has viable \| female \| reduced phenotype, suppressible \| partially by Dp(1;3)sn^13a1 (Anand et al., 1998) Sxl^f1, fl(1)35⁴⁶ has viable \| female \| reduced phenotype, suppressible \| partially by Dp(1;3)sn^13a1 (Anand et al., 1998) Sxl^f1, l(1)43⁴³ has viable \| female \| reduced phenotype, suppressible \| partially by Dp(1;3)sn^13a1 (Anand et al., 1998) Sxl^f1/Sxl^f5 has female sterile phenotype, suppressible \| partially by Oda[+]/Oda^k11803 (Vied et al., 2003) Sxl^f4/Sxl^f1 has female sterile phenotype, suppressible \| partially by Oda[+]/Oda^k11803 (Vied et al., 2003)
NOT suppressed by
Statement Reference Sxl^fhv1/Sxl^f1 has lethal \| female phenotype, non-suppressible by Low¹ (Bhadra et al., 1997)
NOT Enhancer of
Statement Reference Sxl^F1.hs, tra¹, Sxl^f1, snf^+t5.5 is a non-enhancer of lethal \| male phenotype of snf^+t5.5 (Cline et al., 1999) Sxl^F1.hs, tra¹, Sxl^f1, snf^+t5.5 is a non-enhancer of sex-determination defective phenotype of snf^+t5.5 (Cline et al., 1999)
Suppressor of
Statement Reference Sxl^f1 is a suppressor of partially lethal - majority die \| dominant \| male limited phenotype of cav²²⁴⁸ (Li et al., 2011)
NOT Suppressor of
Statement Reference Sxl^f1 is a non-suppressor of lethal \| embryonic stage phenotype of Scer\GAL4^nos.PG, run^Scer\UAS.cLa (Tracey et al., 2000) Sxl^f1 is a non-suppressor of lethal \| first instar larval stage \| male \| recessive phenotype of bon^S024108 (Beckstead et al., 2005) Sxl^f1 is a non-suppressor of lethal \| first instar larval stage \| male limited \| recessive phenotype of bon^S043420 (Beckstead et al., 2005)
Other
Statement Reference Df(1)HC244, Sxl^f1 has lethal phenotype (Steinmann-Zwicky, 1988) Df(1)HC244, Sxl^M1/Sxl^f1 has viable phenotype (Steinmann-Zwicky, 1988) Sir2^ex10, Sxl[+]/Sxl^f1 has viable phenotype (Astrom et al., 2003) Sir2^ex10, Sxl^f1 has viable phenotype (Astrom et al., 2003) Spf45^J23, Sxl[+]/Sxl^f1 has lethal \| female \| maternal effect phenotype (Chaouki and Salz, 2006) Su(var)205², Sxl^f1 has partially lethal - majority die \| dominant \| maternal effect phenotype (Li et al., 2011) Su(var)205⁴, Sxl^f1 has partially lethal - majority die \| dominant \| maternal effect phenotype (Li et al., 2011) Su(var)205⁵, Sxl^f1 has partially lethal - majority die \| dominant \| maternal effect phenotype (Li et al., 2011) Sxl^f1, da[+]/da² has partially lethal - majority die \| dominant phenotype (Johnson et al., 2010) Sxl^f1, fl(1)35³⁵ has lethal \| dominant \| female \| maternal effect phenotype (Anand et al., 1998, Anand et al., 1998) Sxl^f1, fl(1)35⁴⁶ has lethal \| dominant \| female phenotype (Anand et al., 1998, Anand et al., 1998) Sxl^f1, l(1)43⁴³ has lethal \| dominant \| female phenotype (Anand et al., 1998, Anand et al., 1998) Sxl^f1, mle¹ has sex-determination defective \| dominant \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, mle¹ has sex-determination defective \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, mle¹ has visible \| dominant \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, mle¹ has visible \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, mle⁴ has sex-determination defective \| dominant \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, mle⁴ has sex-determination defective \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, mle⁴ has visible \| dominant \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, mle⁴ has visible \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, msl-1^unspecified has sex-determination defective \| dominant \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, msl-1^unspecified has sex-determination defective \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, msl-1^unspecified has visible \| dominant \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, msl-1^unspecified has visible \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, msl-2¹ has sex-determination defective \| dominant \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, msl-2¹ has sex-determination defective \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, msl-2¹ has visible \| dominant \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, msl-2¹ has visible \| female phenotype (Skripsky and Lucchesi, 1982) Sxl^f1, snf^e8H has lethal \| dominant \| female phenotype (Albrecht and Salz, 1993) Sxl^f1, snf^e8H has lethal \| recessive \| female \| maternal effect phenotype (Albrecht and Salz, 1993) Sxl^f1, vir⁶ has viable \| reduced phenotype (Bopp et al., 1999, Bopp et al., 1999) Sxl^fhv1/Sxl^f1, mle⁴ has sex-determination defective \| female phenotype (Skripsky and Lucchesi, 1982)
Phenotype Manifest In
Suppressed by
Statement Reference Sxl^f1/Sxl^f5 has ovary phenotype, suppressible \| partially by Oda[+]/Oda^k11803 (Vied et al., 2003) Sxl^f4/Sxl^f1 has ovary phenotype, suppressible \| partially by Oda[+]/Oda^k11803 (Vied et al., 2003)
Other
Statement Reference Sxl^f1, mle¹ has abdominal sternite 6 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, mle¹ has abdominal tergite 5 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, mle¹ has abdominal tergite 6 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, mle¹ has oviprotector phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, mle¹ has prothoracic metatarsus \| female phenotype (Uenoyama et al., 1982, Skripsky and Lucchesi, 1982, Uenoyama et al., 1982, Skripsky and Lucchesi, 1982) Sxl^f1, mle⁴ has prothoracic metatarsus \| female phenotype (Skripsky and Lucchesi, 1982, Skripsky and Lucchesi, 1982) Sxl^f1, msl-1^unspecified has prothoracic metatarsus \| female phenotype (Skripsky and Lucchesi, 1982, Skripsky and Lucchesi, 1982) Sxl^f1, msl-2¹ has prothoracic metatarsus \| female phenotype (Skripsky and Lucchesi, 1982, Skripsky and Lucchesi, 1982) Sxl^f1, msl-2² has abdominal sternite 6 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-2² has abdominal tergite 5 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-2² has abdominal tergite 6 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-2² has oviprotector phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-2² has prothoracic metatarsus \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-3¹ has abdominal sternite 6 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-3¹ has abdominal tergite 5 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-3¹ has abdominal tergite 6 \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-3¹ has oviprotector phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982) Sxl^f1, msl-3¹ has prothoracic metatarsus \| female phenotype (Uenoyama et al., 1982, Uenoyama et al., 1982)
Additional Comments
Genetic Interactions
Statement Reference Sxl[f1] suppresses the semi-lethality of homozygous cav[2248] males. In progeny from Su(var)205[5] heterozygous females crossed to Sxl[f1]/Y males, female viability is dramatically reduced. The effect of Su(var)205[5] is strictly maternal; no significant reduction in female viability is observed in the reciprocal cross. In progeny from Su(var)205[4] heterozygous females crossed to Sxl[f1]/Y males, female viability is dramatically reduced. In progeny from Su(var)205[2] heterozygous females crossed to Sxl[f1]/Y males, female viability is reduced. (Li et al., 2011) The weak dominant female-lethal effect of Sxl[f1] is not enhanced by ssx[55]/ssx[55]. (Cline et al., 2010) Only 57% of the expected Sxl[f1]/+ daughters from da[2]/+ mothers survive to adulthood. When mothers are heterozygous for both Df(3R)pps[1] and da[2], there is a significant reduction in viability. (Johnson et al., 2010) The lethality of bon^S043420 homozygous males is not rescued if they are also carrying Sxl^f1; almost no escapers are seen. The lethality of bon^S024108 homozygous males is not rescued if they are also carrying Sxl^f1; no Sxl^f1/Y ; bon^S024108/bon^S024108 male animals survive beyond the first larval instar. (Beckstead et al., 2005) Oda^k11803/+ partially suppresses the ovary phenotype and female sterility of Sxl^f5/Sxl^f1. Oda^k11803/+ partially suppresses the ovary phenotype and female sterility of Sxl^f4/Sxl^f1. (Vied et al., 2003) Sxl^f1 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. (Acharyya and Chatterjee, 2002) Addition of two copies of sisA^+t12 and two copies of os^t10 has no effect on the viability of Sxl^f1/Y males. (Sefton et al., 2000) The preferential sensitivity of males to the lethal effects of expression of run^Scer\UAS.cLa under the control of Scer\GAL4^nos.PG is not suppressed by Sxl^f1. (Tracey et al., 2000) 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 Sxl^f1, and the frequency of non-disjunction is further increased. The viability of Sxl^f1/+ ; vir⁶/vir⁶ females is severely reduced and escapers rarely produce eggs. (Bopp et al., 1999) The addition of up to three copies of P{snf⁺,dhd⁺} to Sxl^f1/Y;Sxl^F1.hs, tra¹ partially feminized males does not enhance the feminisation or lethality phenotypes seen in these flies. (Cline et al., 1999) Lethal in female double heterozygous combination with fl(1)35³⁵. The lethality of fl(1)35³⁵/Sxl^f1 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)sn^13a1. Females doubly heterozygous for fl(1)35⁴⁶ and Sxl^f1 show 3.5% viability. Lethality of fl(1)35⁴⁶/Sxl^f1 females can occur at embryonic or larval stages. The lethality can be partially rescued by Dp(1;3)sn^13a1. Females doubly heterozygous for l(1)43⁴³ and Sxl^f1 show 7% viability. Lethality of l(1)43⁴³/Sxl^f1 females occurs at embryonic and larval stages. The lethality can be partially rescued by Dp(1;3)sn^13a1. (Anand et al., 1998) Female lethal-synergistic interactions with snf^- mutations. (Salz and Flickinger, 1996) When homozygous females for snf^e8H are crossed to a male carrying a null allele for Sxl, no female progeny are recovered. (Albrecht and Salz, 1993) Progeny of genotype Df(1)HC244/Sxl^f1 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. (Steinmann-Zwicky, 1988) Some females heterozygous for Sxl^f1 and homozygous for mle¹, mle⁴, msl-1^unspecified, or msl-2¹ have sex combs on the basitarsi of their forelegs. (Skripsky and Lucchesi, 1982) Sxl^f1/+ 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 Sxl^f1/+ females homozygous for the male-specific lethal allele. (Uenoyama et al., 1982)
Xenogenetic Interactions
Statement Reference More hybrid males (which are derived from a cross of Sxl^f1/+ D.melanogaster females to D.simulans males) carrying Sxl^f1 survive to the third larval instar compared to hybrids carrying Sxl⁺. (Pal Bhadra et al., 2006)
Complementation & Rescue Data
Fails to complement	Sxl^dlf (Anand et al., 1998)
Comments
Stocks ( 19 )
Bloomington	3896 C(1)DX, y¹ f¹/Sxl^f1 oc¹ ptg¹ v¹ 3761 y¹ l(1)EN8¹ B¹/Binsc, Sxl^f1 oc¹ ptg¹ 3768 y¹ w¹ N^spl-1 sn¹ l(1)EN7¹/Binsc, Sxl^f1 oc¹ ptg¹ 3763 y¹ w¹ N^spl-1 l(1)EN13¹ sn¹/Binsc, Sxl^f1 oc¹ ptg¹ 3776 y¹ w¹ N^spl-1 sn¹ l(1)EN14¹/Binsc, Sxl^f1 oc¹ ptg¹ 4186 y¹ w¹ N^spl-1 sn¹ fliI¹⁰ bb^/Binsc, Sxl^f1 oc¹ ptg¹ 3764 y¹ w¹ N^spl-1 sn¹ l(1)EN1¹/Binsc, Sxl^f1 oc¹ ptg¹ B⁺ 3766 y¹ w¹ N^spl-1 sn¹ l(1)EN5¹/Binsc, Sxl^f1 oc¹ ptg¹ B⁺ 3760 y¹ l(1)EN2¹ w¹ N^spl-1 sn¹ bb^/Binsc, Sxl^f1 oc¹ ptg¹ 3765 y¹ w¹ N^spl-1 sn¹ l(1)EN4¹ bb^*/Binsc, Sxl^f1 oc¹ ptg¹
Kyoto	107256 C(1)DX, y¹ f¹/Sxl^f1 oc¹ ptg¹ v¹ 107187 y¹ cm¹ Sxl^f1 v¹ f¹/FM7a/Dp(1;2;Y)w⁺
	More stocks available...
Notes on Origin
Discoverer	Muller and Zimmering, 1960.

Comments
	Nuclei follow a female pathway, elevated H4Ac16 staining, acetylated form of His4, is not detected in the paired X chromosome. (Bone et al., 1994) Individuals of heteroallelic combination Sxl^fhv1 and Sxl^f1 have reduced Sxl levels. (Hilfiker et al., 1994) Does not interfere with transcription of the locus. (Albrecht and Salz, 1993)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 11 )
Reported As
Symbol Synonym	f#1 (Uenoyama, 1984) Fl Sxl[F#1] (Tracey et al., 2000) Sxl^F1 (Beckstead et al., 2005, Bashaw and Baker, 1995, Kelley et al., 1995) Sxl^f1 (Cline et al., 2010, Chaouki and Salz, 2006, Johnson et al., 2010, Li et al., 2011, González et al., 2008) sxl^f1 (Sofola et al., 2007) Sxl^f#1 (Pal Bhadra et al., 2005, Acharyya and Chatterjee, 2002, Bhadra et al., 2000, Bhadra et al., 1997, Pultz et al., 1994, Sheen et al., 1993, Oliver et al., 1990, Oliver et al., 1988, Salz et al., 1987, Cronmiller and Cline, 1986, Maine et al., 1985, Cline, 1983, Uenoyama et al., 1982, Skripsky and Lucchesi, 1982, Pal Bhadra et al., 2006) Sxl^F (Pal-Bhadra et al., 1996) Sxl^fl (Salz and Flickinger, 1996, Steinmann-Zwicky, 1988) Sxl^null (Starr and Cline, 2002)
Name Synonym	Female lethal
Secondary FlyBase IDs

References ( 73 )

Generate a list of	All references relating to this allele ( 73 )

List References by type	Research paper ( 66 ) Review ( 4 ) Personal communication to FlyBase ( 1 ) Abstract ( 1 ) FlyBase analysis ( 1 )
Recent research papers ( 1 )
	Li et al., 2011, PLoS Genet. 7(6): e1002122 Cooperative and antagonistic contributions of two heterochromatin proteins to transcriptional regulation of the Drosophila sex determination decision. [FBrf0213989] Show all research papers ...
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Allele Dmel\Sxlf1

Allele Dmel\Sxl^f1