Sxl^f7,M1/Sxl^M1,fΔ33 females display masculinized external and internal somatic morphology and body size. The only hints of somatic femininity are a few small sixth-sternite bristles and about 25% fewer sexcomb teeth than seen in true males.

Sxl^f7,M1 and Sxl^M1,fΔ33 fail to complement for female viability if exosed to 18[o]C during early embryogenesis or if exposed to 30[o] during the pupal period.

Sxl^f7,M1/Y males are phenotypically wild-type. The addition of Dp(1;1)jnR1-A which contains a duplication of Sxl⁺ also leads to phenotypically wild-type flies.

Homozygous females survive at a low frequency suggesting some residual ability to regulate the dosage compensation system. Females are transformed to phenotypic males. Females rescued by Sxl^NΔ.Hsp83 have male morphology.

Moderate hypomorph for somatic dosage compensation and autoregulation; null for somatic sex determination while germline functions are wild-type.

50% of Sxl^M1,f3/Sxl^f7,M1 females survive indicating some capacity for dosage compensation. Animals have very male-like morphology and have to small body size, and pseudotestes.

Sxl^M1,f3/Sxl^f7,M1 males behave like normal males. Sxl^M1,f3/Sxl^f7,M1 females elicit less courtship than normal females and produce large quantities of the inhibitory pheromones that normal males synthesize. Mutant females also produce very little or none of the female-predominant aphrodisiac pheromone.

Homozygous females survive at a frequency of 35-15%, though their cuticle is masculinized. Sxl^f7,M1 shows incomplete dosage compensation in run²⁵ phenotype assay.

Sxl^f7,M1/Sxl^fc females do not develop ovaries, though germ cells of this genotype transplanted into wild-type hosts produce functional oocytes, suggesting that it is in the somatic cells of this genotype that the ovaries are affected.

Sxl^f7,M1/Sxl^M1,f3 female heterozygotes exhibit segment spanning muscles in the fifth abdominal segment indicative of a transformation to the male specific phenotype. Somatic development of males is unaffected.

There is sufficient female dosage compensation for some homozygous females to survive but their somatic tissue is completely masculinized.

Homozygous XX flies show a high degree of lethality, the survivors are male. Sxl^f7,M1/Sxl^fb or Sxl^f7,M1/Sxl^fc flies occasionally have a male spot on the fifth and sixth tergites.

Sxl^M1,f3/Sxl^f7,M1 transheterozygotes that are chromosomally female (XX) are transformed into "pseudomales". The gonads form testes which are generally non-gametogenic, containing degenerated germ cells and debris or gonial cells whose sex could not be determined. The few gametogenic testes seen (9%) contained only spermatogenic stages.

Partial loss-of-function allele. Only partially complements Sxl^fPb.

selected as an intragenic suppressor of Sxl^M1 male lethality; maps 0.0099 cM

to the left of Sxl^M1. Only characterized in cis

combination with Sxl^M1. The double mutant is male

viable and semi-viable in homozygous females. Escaper

females are phenotypically male and sterile.

Hemizygous females are inviable. Double heterozygote

with snf is sterile, like Sxl^f1 but unlike

Sxl^M1,f3. The double-mutant allele retains some

ability to rescue daughters from the otherwise lethal

maternal-effect of da; however, lowering maternal

da⁺ activity appears to decrease Sxl^f7,M1

functioning, consistent with other evidence that the

parental allele, Sxl^M1, is not fully constitutive.

In the absence of a wild-type Sxl allele, Sxl^f7,M1

daughters that survive the da maternal effect are

phenotypically male and sterile; in contrast, the

addition to this genotype of a wild-type Sxl allele in

trans renders survivors phenotypically female, but

still sterile with masculinized gonads. The latter

genotype of female is fertile provided mothers carry

at least one da⁺ allele. The ability of Sxl^f7,M1

to rescue daughters is greatly enhanced by mutations

in the autosomal, male-specific-lethal loci, genes

involved in hyperactivation of X-linked genes in

males. The basis for this enhancement is related to

the ability of these same mutations to enhance the

survival of Sxl^f7,M1 hemizygous females. Although

Sxl^f7,M1 was used to demonstrate the ability of Sxl

gene products to activate Sxl⁺ alleles in trans, it

can be inferred that this allele is far below wild

type in this activity. Sxl^f7,M1 is a dominant

suppressor of sis-a female-specific lethality,

generating sterile females remarkably similar to those

described above rescued from the da maternal effect.

Unlike Sxl^M1,f3, fails to complement Sxl^f2593; yet

partially complements Sxl^M1,f3 and Sxl^fPb,

generating sterile phenotypic males. Allele supports

oogenesis in homozygous mutant germ-line clones

induced by mitotic recombination. In males, mutant

allele suppresses the otherwise lethal effect of a

duplication of region 3C2-5A2; addition of Sxl⁺ to

this aneuploid genotype generates mosaic intersexes

indicating that the positive autoregulatory activity

of Sxl products can bypass the X/A signal. Double

heterozygote with snf is sterile (like Sxl^f1

and unlike Sxl^M1,f3).

male-viable

female-semi-lethal

Sxl^M1,fΔ33/Sxl^f7,M1 has abnormal sex-determination | female limited phenotype, suppressible | partially by tra^F.U2af50

Sxl^M1,fΔ33/Sxl^f7,M1, tra^F.U2af50 has abnormal sex-determination | female limited phenotype, suppressible by Dp(1;3)sn^13a1

Sxl^M1,f3/Sxl^f7,M1 has abnormal sex-determination | female phenotype, suppressible by tra^F.Hsp83

Sxl^f7,M1 has abnormal sex-determination | recessive | female phenotype, suppressible by tra^F.Hsp83

Sxl^f7,M1, snf^+t5.5 has wild-type | male phenotype

Sxl^f7,M1, Tp(1;3)sn^13a1, snf^+t5.5 has lethal | male phenotype

Sxl^f7,M1, fl(1)35³⁵ has partially lethal | female phenotype

Sxl^f7,M1, fl(1)35⁴⁶ has partially lethal | female phenotype

Sxl^f7,M1, l(1)43⁴³ has partially lethal | female phenotype

Sxl^M1,f3/Sxl^f7,M1 has gonad phenotype, suppressible | partially by tra^F.Hsp83

Sxl^f7,M1 has gonad phenotype, suppressible by tra^F.Hsp83