Allele Dmel\snf¹

General Information
Symbol	Dmel\snf¹	Species	D. melanogaster
Name		FlyBase ID	FBal0015908
Feature type	allele	Created / Updated	2006-08-22/2006-08-22
Associated gene	Dmel\snf

Allele class	antimorph, hypomorph
Mutagen	ethyl methanesulfonate
Nature of the Allele
Allele class	antimorph (Flickinger and Salz, 1994, Deshpande et al., 1996) hypomorph (Oliver et al., 1993)
Mutagen	ethyl methanesulfonate
Mapped Features and Mutations
Type Symbol & 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 Amino acid replacement: R49H. Nucleotide substitution: G209A. H49 falls in the amino terminal RRM. (Flickinger and Salz, 1994) Missense mutation. (Salz and Flickinger, 1996)
Assay mode
Cytology
Phenotypic Data
Phenotypic Class
	viable (Deshpande et al., 1996) lethal (Steinmann-Zwicky, 1988) lethal \| dominant \| maternal effect (Steinmann-Zwicky, 1988) lethal \| male (Albrecht and Salz, 1994) female sterile (Bae et al., 1994, Flickinger and Salz, 1994, Salz, 1992, Hager and Cline, 1997, Salz and Flickinger, 1996, Gawande et al., 2006) female sterile \| recessive (Wieschaus et al., 1981, Bopp et al., 1993) female sterile germ-line-dependent (Perrimon and Gans, 1983)
Phenotype Manifest In
	ovary (Bae et al., 1994, Oliver et al., 1990, Oliver et al., 1993, Wei et al., 1994, Bopp et al., 1993, Starr and Cline, 2002)
Detailed Description
	Statement Reference 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. 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. (Steinmann-Zwicky, 1988) snf¹/Sxl^- double heterozygotes are always female sterile as expression of Sxl⁺ in the germline is required for female fertility. At 29^oC the ovarian tumours of Sxl^-/snf¹ heterozygotes are snf-like (egg chambers have no nurse-like cells) and at 20^oC 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. (Oliver et al., 1988) Homozygous females have ovarian tumours. (Oliver et al., 1990) Female sterility can be suppressed by Sxl^M1 or Sxl^M4. Mutant females appear to be missing the two germline-dependent Sxl RNAs. (Salz, 1992) Abnormalities in Sxl expression are evident in the germ line. (Bopp et al., 1993) Tumorous ovaries. (Oliver et al., 1993) 2X:2A germ cells are transformed to spermatocytes. (Pauli et al., 1993) At room temperature snf¹ Sxl^M1 males are seldom recovered, at 18^oC 30% males are viable. (Albrecht and Salz, 1994) 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. (Wei et al., 1994) Heterozygotes with snf^J210 (in the presence of the transgene P{dhd4.8}) produce ovarian tumours. Strong lethal synergistic interaction with Sxl. (Flickinger and Salz, 1994) Tumorous ovaries. (Bae et al., 1994) The ovary phenotypes of homozygous females are not suppressed by Wolbachia infection; 100% of ovaries of homozygous infected females have no eggs. (Starr and Cline, 2002)
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference snf¹ has female sterile phenotype, suppressible by Sxl^cF1.otu (Hager and Cline, 1997, Gawande et al., 2006)
Suppressor of
Statement Reference snf¹ is a suppressor \| conditional - heat sensitive of lethal \| male phenotype of Sxl^M1 (Cline, 2001) snf¹ is a suppressor of lethal phenotype of Sxl^M1 (Steinmann-Zwicky, 1988) snf¹ is a suppressor of lethal \| male limited \| dominant phenotype of Sxl^M6 (Cline et al., 1999)
Other
Statement Reference Sxl^{N.Hsp83.T:Ecol\lacZ}, snf¹ has lethal \| partially \| female \| dominant phenotype (Deshpande et al., 1999) Sxl^{N.Hsp83.T:Ecol\lacZ}, snf¹ has lethal \| female phenotype (Deshpande et al., 1999)
Phenotype Manifest In
Enhancer of
Statement Reference snf¹ is an enhancer of phenotype of ovo^D2 (Pauli et al., 1995)
Suppressor of
Statement Reference snf¹ is a suppressor of phenotype of Sxl^M1 (Salz and Flickinger, 1996, Cline et al., 1999) snf¹ is a suppressor of phenotype of Sxl^F1.hs (Salz and Flickinger, 1996)
NOT Suppressor of
Statement Reference snf¹ is a non-suppressor of phenotype of tra2^B (Andrews and Oliver, 2002)
Additional Comments
Genetic Interactions
Statement Reference Males carrying Sxl^M1 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. (Steinmann-Zwicky, 1988) snf¹ enhances the mutant phenotype of ovo^D2/+ heterozygous ovaries. (Pauli et al., 1995) Displays a stronger female-lethal synergistic interaction with loss of function Sxl mutations (Sxl^f1 and Sxl^fP7B0) than snf^J210 (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. (Salz and Flickinger, 1996) Expression of Sxl^cF1.otu suppressed the germline-autonomous female sterility of mutants. (Hager and Cline, 1997) Heterozygous females are fully viable. This viability is reduced if the females also carry Sxl^{N.Hsp83.T:Ecol\lacZ}, the viability decreasing as the number of copies of Sxl^{N.Hsp83.T:Ecol\lacZ} increase. (Deshpande et al., 1999) snf¹ partially suppresses Sxl^M1 male lethality; snf¹ Sxl^M1 double mutant males are viable at 18^oC but are not recovered at 25^oC. The temperature sensitive lethality of snf¹ Sxl^M1 males is still seen if they are also mutant for bb^flex-2; triple mutant males are recovered at 18^oC, but not at 25^oC. (Cline, 2001) The frequency of germline development (including spermatogenesis) in 2X tra2^B/Df(2R)trix males is unaffected by snf¹. (Andrews and Oliver, 2002) The ovary phenotype of snf¹ mutant flies is not rescued by reducing the gene dosage of Oda. (Vied et al., 2003) Expression of Sxl[cF1.otu] restores fertility in snf[1] female flies. (Gawande et al., 2006)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments	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 Sxl^M1. Transheterozygotes of snf or Df(1)HC244 with Sxl^f1 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 Sxl^f1/+ daughters; survival is cold-sensitive. The presense of Sxl^M1 rescues snf/Sxl^f1 females; Df(1)HC244, Sxl^M1/Sxl^f1 are viable and fertile without male transformations. Sxl^M1 is also able to rescue Sxl^f1/+ from the maternal effect of snf/+ and snf is able to rescue male viability and fertility of Sxl^M1 in snf Sxl^M1 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 ovo^D1, ovo^D2, or ovo^D3 have ovarian tumors (Oliver, Pauli and Mahowald, 1990).
Stocks ( 2 )
Bloomington	4316 snf¹ v²⁴/FM3
Kyoto	107685 snf¹ v²⁴/FM3
Notes on Origin
Discoverer

Comments
	Germ line clonal analysis shows that snf function may be germ line autonomous, although the data is not conclusive. (Wieschaus et al., 1981) Interacts synergistically with ovo^D1, ovo^D2 and ovo^D3. (Oliver et al., 1990) 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. (Bopp et al., 1993) Some male-like cysts in 2X snf¹ mutant ovaries fail to show hybridization with the Sxl⁺ specific probe. (Oliver et al., 1993) 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. (Pauli et al., 1993) snf^e8H and snf¹ fail to complement each other and snf^JA2 partially complements snf^e8H and snf¹. snf¹ blocks the function of the wild-ype Sxl protein. (Salz and Flickinger, 1996) Mutation greatly reduces the ability of Sxl^cF1.otu to induce female Sxl⁺ RNA splicing in the male germline: number of autoregulatory cysts in testes is much reduced. (Hager and Cline, 1997)
Synonyms & Secondary IDs ( 6 )
Reported As
Symbol Synonym	fs(1)1621 (Perrimon et al., 1986, Perrimon and Gans, 1983, Wieschaus et al., 1981, ) fs(1)G1621 snf¹ (Christensen et al., 2008.6.11) snf¹⁶²¹ (Nagengast et al., 2003, Vied et al., 2003, Starr and Cline, 2002, Cline, 2001, Cline et al., 1999, Hager and Cline, 1997, Wang et al., 1997, Cline and Meyer, 1996, Salz and Flickinger, 1996, Deshpande et al., 1996, Horabin et al., 1995, Pauli et al., 1995, Bae et al., 1994, Oliver et al., 1994, Flickinger and Salz, 1994, Albrecht and Salz, 1994, Pauli et al., 1993, Oliver et al., 1993, Granadino et al., 1992, Salz, 1992, Oliver et al., 1990, Oliver et al., 1988, Gawande et al., 2006) Snf¹⁶²¹ (Deshpande et al., 1999) snf^fs1621 (Horabin and Schedl, 1996)
Name Synonym
Secondary FlyBase IDs

References ( 35 )

Generate a list of	All references relating to this allele ( 35 )

List References by type	Research paper ( 32 ) Review ( 1 ) Personal communication to FlyBase ( 1 ) Abstract ( 1 )
Recent research papers ( 1 )
	Gawande et al., 2006, EMBO J. 25(6): 1263--1272 Drosophila Sex-lethal protein mediates polyadenylation switching in the female germline. [FBrf0190359] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2006 Show reviews ...

Allele Dmel\snf1

Allele Dmel\snf¹