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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
snf1621, fs(1)1621
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Nucleotide change:


Reported nucleotide change:


Amino acid change:

R49H | snf-PA

Reported amino acid change:


Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Missense mutation.

Amino acid replacement: R49H. Nucleotide substitution: G209A. H49 falls in the amino terminal RRM.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

The ovary phenotypes of homozygous females are not suppressed by Wolbachia infection; 100% of ovaries of homozygous infected females have no eggs.

At room temperature snf1 SxlM1 males are seldom recovered, at 18oC 30% males are viable.

Heterozygotes with snfJ210 (in the presence of the transgene P{dhd4.8}) produce ovarian tumours. Strong lethal synergistic interaction with Sxl.

Many more germ cells in ovarian tumors are positive for expression of male germline markers than in wild type testes, suggesting a relaxation of growth control, or accumulation of apical cells due to a developmental block.

Abnormalities in Sxl expression are evident in the germ line.

2X:2A germ cells are transformed to spermatocytes.

Female sterility can be suppressed by SxlM1 or SxlM4. Mutant females appear to be missing the two germline-dependent Sxl RNAs.

Homozygous females have ovarian tumours.

snf1/Sxl- double heterozygotes are always female sterile as expression of Sxl+ in the germline is required for female fertility. At 29oC the ovarian tumours of Sxl-/snf1 heterozygotes are snf-like (egg chambers have no nurse-like cells) and at 20oC they are Sxl-like (egg chambers have an excessive number of nurse cells). Sxl-/snf1 flies showed some somatic sexual transformation: male sex combs among normal female bristles.

A dominant maternal female lethal effect that becomes apparent in hemizygous daughters. Maternal lethality, zygotic lethality and some male transformations are due to lack of snf activity.

female semi-sterile. Females produce few if any eggs; males normal. Young females homozygous female viable produce ova which can be fertilized and develop normally into adults. Older females cease production of oocytes, producing at first only pseudo nurse cells and subsequently tumorous germaria containing hundreds or thousands of cells of apparently germinal origin. Tumorogenesis takes place earlier at higher temperatures. snf/Df(1)C159 hemizygous for mutant; more temperature-sensitive; the germ-line phenotype more severe than in homozygote but viability seems unaffected (Gollin and King). Mosaic studies suggest that gene function is germ line autonomous (Wieschaus et al.; Perrimon and Gans); however, the leakiness of the mutant phenotype introduced an element of ambiguity, raising the possibility of a somatic contribution to oogenesis as well.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by

snf1 has lethal | female phenotype, suppressible by SxlM1

Suppressor of

snf1 is a suppressor | cold sensitive of lethal | male phenotype of SxlM1

snf1 is a suppressor | heat sensitive of lethal | male phenotype of SxlM1

snf1 is a suppressor of lethal | dominant | male limited phenotype of SxlM6

snf1 is a suppressor of lethal phenotype of SxlM1

Phenotype Manifest In
Enhancer of

snf1 is an enhancer of phenotype of ovoD2

Suppressor of

snf1 is a suppressor of phenotype of SxlM1

snf1 is a suppressor of phenotype of SxlF1.hs

NOT Suppressor of

snf1 is a non-suppressor of phenotype of tra2B

Additional Comments
Genetic Interactions

SxlM1 suppresses snf1 female sterility at 18[o] and 25[o]C, while snf1 suppresses male lethality only at 18[o]C.

Expression of SxlcF1.otu restores fertility in snf1 female flies.

The ovary phenotype of snf1 mutant flies is not rescued by reducing the gene dosage of Oda.

The frequency of germline development (including spermatogenesis) in 2X tra2B/Df(2R)trix males is unaffected by snf1.

snf1 partially suppresses SxlM1 male lethality; snf1 SxlM1 double mutant males are viable at 18oC but are not recovered at 25oC. The temperature sensitive lethality of snf1 SxlM1 males is still seen if they are also mutant for bbflex-2; triple mutant males are recovered at 18oC, but not at 25oC.

Heterozygous females are fully viable. This viability is reduced if the females also carry SxlN.Hsp83.T:Ecol\lacZ, the viability decreasing as the number of copies of SxlN.Hsp83.T:Ecol\lacZ increase.

Expression of SxlcF1.otu suppressed the germline-autonomous female sterility of mutants.

Displays a stronger female-lethal synergistic interaction with loss of function Sxl mutations (Sxlf1 and SxlfP7B0) than snfJ210 (amorphic). One copy of P{SxlcF1} in wild type males, even under nonheat shock conditions, recovers only 2% of expected males. 75% of expected males are recovered from snf1; P{SxlcF1} males.

snf1 enhances the mutant phenotype of ovoD2/+ heterozygous ovaries.

Males carrying SxlM1 can survive if they are also mutant for snf.They have several abnormalities: sex combs are a mosaic of male and female bristles, reduced and rotated genitalia, sternite 6 is covered in bristles and sternite 7 is sometimes present.

Xenogenetic Interactions
Complementation and Rescue Data

Interactions with Sxl alleles studied by Cline (1989), Steinmann-Zwicky (1988) and Oliver et al. (1988). Fertility of snf homozygotes is rescued by the presence of SxlM1. Transheterozygotes of snf or Df(1)HC244 with Sxlf1 show very low viability when snf is inherited from the female; survivors are sterile and show patchy transformations to maleness, such as sex-comb bristles and pigmentation of tergites 5 and 6. Viability of heterozygotes produced by the reciprocal cross also reduced but less so; surviving heterozygotes display reduced fertility. Viability effects appear to arise mostly from a maternal effect of the gene, whereas masculinizing and sterility effects result from decreased zygotic expression. The maternal effect of snf also reduces survival of Sxlf1/+ daughters; survival is cold-sensitive. The presense of SxlM1 rescues snf/Sxlf1 females; Df(1)HC244, SxlM1/Sxlf1 are viable and fertile without male transformations. SxlM1 is also able to rescue Sxlf1/+ from the maternal effect of snf/+ and snf is able to rescue male viability and fertility of SxlM1 in snf SxlM1 double mutants. In contrast to the sis genes, which also interact with Sxl, the zygotic dose of snf has little or no influence on the sexual phenotype of 2X;3A animals; moreover, snf interacts little if at all with sis-a. Thus although snf+ clearly has a positive involvement in Sxl+ functions, its precise placement in the sex determination hierarchy is currently unclear. It has been suggested that it is involved in the positive autoregulatory aspect of Sxl function that maintains female development. Females heterozygous for snf and either ovoD1, ovoD2, or ovoD3 have ovarian tumors (Oliver, Pauli and Mahowald, 1990).

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Stocks (3)
Notes on Origin

Mutation greatly reduces the ability of SxlcF1.otu to induce female Sxl+ RNA splicing in the male germline: number of autoregulatory cysts in testes is much reduced.

Germ line clonal analysis shows that snf function may be germ line autonomous, although the data is not conclusive.

Interacts synergistically with ovoD1, ovoD2 and ovoD3.

Sxl protein expression in the oogonial cells of larvae is severely reduced. The germ cells and gonads of the adult have little Sxl protein though the somatic follicle cells have normal levels. Substantial levels of male-type splicing can be detected in the mutant ovaries, and lower but still significant levels in the soma.

Some male-like cysts in 2X snf1 mutant ovaries fail to show hybridization with the Sxl+ specific probe.

Reverse transcription and PCR, and in situ hybridization with the male specific exon, showed that the Sxl transcripts are spliced in the male-specific mode in transformed germ cells.

snfe8H and snf1 fail to complement each other and snfJA2 partially complements snfe8H and snf1. snf1 blocks the function of the wild-ype Sxl protein.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (37)