# f: forked location: 1-56.7. origin: Spontaneous. discoverer: Bridges, 12k19. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 58 (fig.). phenotype: Macrochaetae, microchaetae, and trichomes affected to various degrees depending on allele-short, gnarled, and bent with ends split or sharply bent. Extreme effect of f36a on trichomes makes it the most useful allele as a cell marker in cuticular spots produced by somatic exchange. Treatment with methylurea causes normal bristle formation (De Marinis). Developmental studies [Lees and Waddington, 1942, Proc. Roy. Soc. (London) Ser. B 131: 87-110 (fig.); Lees and Picken, 1945, Proc. Roy. Soc. (London), Ser. B 132: 396-423 (fig.)] show nature of pupal bristle secretion is affected. Suppres- sion by su(f) and su(Hw)2 allele specific. f1 and f5 suppressed by su(Hw), e(we), su(f), and su(pr), enhanced by su(s) and su(wa) (Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97). RK1. alleles: Can be classed as weak with macrochaetae slightly bent, moderate with both macrochaetae and microchaetae clearly affected, strong with macrochaetae and microchateae strongly gnarled, and extreme with chaetae and trichomes strongly affected. Descriptions of phenotypes are such as to make clas- sification highly subjective. Bridges (1938, DIS 9: 46-47; see also CP552) lists 14 lost alleles of diverse origin not included here, and Belgovsky (1940, DIS 13: 47-48) lists 35 fB alleles induced by X rays in In(1)sc8 or In(1)BM2, of which 33 are lost and not included here. Included in the table are deficiencies which have been erroneously given allelic designations in the past. allele origin discoverer ref ( phenotype _______________________________________________________________________________________ f1 | gypsy Bridges, 12k19 5, 12, 13 moderate; spont suppressed by su(f) and su(Hw)2 f3 | spont Bridges, 14k14 4, 5, 6 weak; not suppressed by su(f) f3N | / spont | Green 5, 6, 8, 11 not suppressed by su(f) f5 | gypsy Bridges, 21b 4, 5, 12 strong; suppressed by su(f) and su(Hw)2 *f34b X ray Stone, 34b 5, 20 moderate *f34e X ray Oliver, 34e4 5, 17 subliminal f36a | Ives, 36a27 5 extreme; not suppressed by su(Hw)2 *f42 spont Anderson, 42c30 5, 18 strong *f51a X ray Green, 51a 5, 11 extreme; not suppressed by su(f) f56e | spont Williams, 56e 5, 22 moderate f67a X ray Becker 1 strong; suppressed by su(f) and su(Hw)2 f68e EMS Maddern, 68e11 8 moderate f68i EMS Maddern, 68i30 8 moderate f70 f71i spont 21 f257-4 X ray Demerec, 33j 5 strong f257-15 X ray Demerec, 35a 5 lethal f257-19 X ray Hoover, 35h 5 lethal *f257-22 X ray Demerec, 36c 5 lethal *f257-24 X ray Demerec, 36e 5 lethal *f257-29 X ray Bishop, 40l 5 slight *f257-30 X ray Bishop, 41a 5 moderate f+ih | X ray Muller 5, 14, 15, 16, 19 fB15 | / X ray Belgovsky, 36l 2, 3 variegated fB27 | / X ray Belgovsky, 36l 2, 3 variegated *fH spont Hexter 5, 7 moderate; not suppressed by su(f) fK gypsy Kuhn 12 suppressed by Su(Hw)2 fs ` fs1 spont Schalet ftuh spont Kuhn 10 fu fX | X ray Muller 5, 14, 15, 16, 19 moderate; gypsy suppressed by su(f) *fX1 X ray Green 5, 7 moderate; not suppressed by su(f) *fX2 X ray Green 5, 7 moderate; not suppressed by su(f) *fX3 X ray Green 5, 7 moderate; not suppressed by su(f) *fX4 X ray Green 5, 7 moderate; not suppressed by su(f) ( 1 = Becker, 1968, DIS 43: 59; 2 = Belgovsky, 1938, Isv. Akad. Nauk; 3 = Belgovsky, 1940, DIS 13: 47-48; 4 = Bridges, 1938, DIS 9: 46-47; 5 = CP627; 6 = Green, 1955, Proc. Nat. Acad. Sci. USA 41: 375-79; 7 = Green, 1956, Proc. Nat. Acad. Sci. USA 42: 73-77; 8 = Green, 1959, Proc. Nat. Acad. Sci. USA 45: 16-18; 9 = Hayman and Maddern, 1969, DIS 44: 50; 10 = Kuhn, 1973, DIS 50: 24; 11 = Lefevre and Green, 1959, Genetics 44: 769-76; 12 = Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. USA 80: 1678-82; 13 = Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. 237: 58 (fig.); 14 = Muller, 1946, DIS 20: 88-89; 15 = Muller, 1947, DIS 21: 71; 16 = Muller and Oster, 1957, DIS 31: 141-44; 17 = Oliver, 1939, DIS 12: 8; 18 = Oliver, 1942, DIS 16: 53; 19 = Oster, Erlich, and Muller, 1958, DIS 32: 144-45; 20 = Stone, 1934, DIS 4: 63; 21 = Thompson and Purnell, 1972, DIS 48: 16; 22 = Williams, 1956, DIS 30: 79. | Further descriptions below. / Spontaneous derivative of f. ` Forked-suppressible, presumably = f1 (Dudick, Wright, and Brothers, 1974, Genetics 76: 487-510. allele cytology _____________________________________________ f67a Tp(1;1)12E;15E;18B;20 f257-15 T(1;2)13E9-10;15E2-3;24F *f257-19 + *f257-22 T(1;2)4D2-3;8F;15E4-F1;39E;41F-42A *f257-24 + *f257-29 T(1;3)15F5-16A1;64 *f257-30 + f+ih + fX + cytology: Localized to 15F1-3 on the basis of Df(1)f257-5 = Df(1)15E7-F1;15F2-4. Polytene analysis completed on some alleles. molecular biology: Region cloned using gypsy insertion into the f1 allele (Parkhurst and Corces, 1985, Cell 41: 429-37) and f5 (McLachlan, 1988, J. Mol. Cell. Biol. 6:1-6). f alleles from the right pseudoallelic series of Green (f, f5, f36a) have DNA inserts within a 5.4 kb segment of DNA. The forked phenotype as well as the accummulation of RNAs can be rescued by P-element mediated germline transformation with a 6.1 kb Sa1I-XhoI fragment. There are four transcripts encoded within this DNA region: polyadenylated 4.3 kb, 2.4 kb, 1.9 kb, and 1.4 kb RNAs present only during mid to late pupal stages. Transcripts are reduced or missing in mutants. Transcripts in the f1 mutant return to wild-type levels when combined with the su(Hw) or su(f) mutations (see McLachlan). other information: Green (1955, Proc. Nat. Acad. Sci. USA 41: 375-79; 1956, Proc. Nat. Acad. Sci. USA 42: 73-77) showed the forked mutants can be assigned to either of two pseudoallelic series, f is a member of the right series. Back mutations to f+ occur spontaneously, and their incidence is not increased by X rays (Green, 1959, Proc. Nat. Acad. Sci. USA 45: 16-18; Lefevre and Green, 1959, Genetics 44: 769- 76). f: forked Edith M. Wallace, unpublished. # f1 molecular biology: A member of the right hand group of alleles. Contains a gypsy insert in a 3.8 kb EcoRI restriction fragment (Parkhurst and Corces) and 3.2 kb from a particular SalI res- triction site (McLachlan, 1986, J. Mol. Cell. Biol. 6: 1-6). Orientation of gypsy element opposite that of the gene. # f3 molecular biology: A member of the left hand group of alleles shown to contain an insert of 6 kb, but to the right of f1, according to the orientation on the chromosome as determined by Parkhurst and Corces (McLachlan, 1986, J. Mol. Cell. Biol. 6: 1-6). # f3N phenotype: Expression similar to f but unlike f, does not respond to su(f). Characterized by a high spontaneous rever- sion rate (~2 x 10-5); rate may be further increased by a closely linked cis-dominant mutator allele, Mu(f3N), (5 x; Woodruff, 1975, Genet. Res. 25: 163-77), by X rays (20 x; Green, 1977, Mutat. Res. 43: 305-08), and by mustard gas (Woodruff, Bowman, and Simmons, 1972, Mut. Res. 15: 86-89). RK1. molecular biology: A member of the left hand group of alleles. Shown to contain a 2.8 kb tandem repeat, but to the right of f1 according to the orientation on the chromosome as deter- mined by Parkhurst and Corces (McLachlan). A revertant of f3N retains the repeated sequence. # f5 molecular biology: A member of the right hand group of alleles; contains two gypsy inserts, one which is similar or identical to that of f1 and the other which is closer to the SalI res- triction site (1.2 kb); orientation is the same. In addition f5 contains a 4.4 kb insert in a restriction fragment to the left of that carrying the f1 gypsy insert; it is located approximately 4.7 kb to the left of the reference SalI site (McLachlan). # f36a molecular biology: A member of the right-hand group of alleles. Contains a 3.0 kb insertion 2.5 kb to the right of the refer- ence SalI site (McLachlan). # f56e molecular biology: A molecular deletion detected by Parkhurst and Corces but not by McLachlan; in the 3.8 EcoRI fragment studied by Parkhurst and McLachlan. # f+ih: forked-wild type in heterochromatin origin: X ray induced simultaneously with fX. synonym: fm: forked-mottled = fX f+ih. phenotype: f+ih with any f allele has normalizing effect. Patches of bristles and occasionally whole fly is wild type. An extra Y chromosome enhances the normalizing effect. RK2A. cytology: Salivary chromosomes appear normal (J.I. Valencia). molecular biology: The inserted segment contains the entire 40 kb walk of McLachlan. other information: Apparently, f+ih is all or part of the nor- mal allele of f transposed to the proximal heterochromatin of the X chromosome, where it variegates. The sequences remain- ing in the original position behave as a hypomorphic allele of f, fX. Oster, Erlich, and Muller (1957, DIS 31: 141-44) argue that the sum of sequences inserted in the heterochroma- tin plus those remaining behind exceeds the normal sequential content of f+. # fB15 origin: X ray induced in BM2 male. phenotype: Shows variegated expression of f. More extreme in combination with E(f). RK2A. cytology: Genetic data indicate that the mutation is associated with a reinversion of the BM2 inversion. BM2 phenotype reverted. # fB27 origin: X ray induced in BM2 male. phenotype: Males have mostly normal bristles, a few reduced like a Minute, rarely forked. fB27/f are mosaic for forked. fB27/fB27 females rarely survive; those that do sometimes have reduced bristles or notched wings, or both, and are sterile. More extreme in combination with E(f). RK3A. # fX: forked from X irradiation origin: X ray induced, simultaneously with f+ih. synonym: fm: forked-mottled = fX f+ih. discoverer: Muller. phenotype: A medium f. Suppressed by su(f). Behaves as a hypomorphic allele (Oster, Erlich, and Muller, 1958, DIS 32: 144-45). RK1. molecular biology: Restriction map indistinguishable from that of f1 (McLachlan). # F2: see Ef1 ( 2 # fa: see N # faswb-h: see e(faswb) # facetious: see rgP # factor for male fertility: see fmf # fai: faint location: 2-61. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.) Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Homozygous larval lethal. Unpigmented cuticle and mouth parts. alleles: Six, two of which are weak; fai1 and fai2 (isolated as IIA and IIV) retained. # faint little ball: see Egfr # faint sausage: see fas # faintoid: see gs # fap: female abdomen pattern location: 3-0.5 (to the left of mwh; Robertson and Riviera, 1972, DIS 48: 21). origin: Spontaneous. references: Robertson and Louw, 1966, DIS 41: 154-55 (fig.). Robertson, Briscoe, and Louw, 1977, Genetica 47: 73-77. phenotype: Female-specific recessive that removes black pigment from the sixth and seventh tergites when homozygous; heterozy- gotes exhibit intermediate phenotype at 18. alleles: Natural populations highly polymorphic at this locus with at least six alleles (Robertson and Riviera, 1972). cytology: Polytene chromosomes normal (Slyzinska). # Farkas: see Fs(3)Sz8 # fas: see rgP # fas: faint sausage location: 2-68. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82 (fig.) Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Embryonic lethal; embryos have poorly developed cuticle with necrotic patches and an abnormal head. First visible in extended-germ-band stage. alleles: Four, out of which two are retained, fas1 and fas2 (isolated as IC and IIA). # Fas1: Fasciclin I location: 3-{58}. origin: Isolated from Drosophila embryonic cDNA libraries using a fasciclin I probe from grasshopper. references: Zinn, McAllister, and Goodman, 1988, Cell 53: 577-87 (fig.). phenotype: Expression confined to neurons. In 12-14 h embryos high levels of fasciclin I are detectable in two commissural axon bundles (fascicles) per segment, a thick one in the pos- terior commissure and a thin one in the anterior commissure. In addition high expression is seen in two clusters of neu- ronal cell bodies per hemisegment as well as in the interseg- mental and segmental nerve axons. Finally, fasciclin I is detected on the surface of all peripheral neurons. Postulated to be involved in neuron recognition during growth cone gui- dance. Flies deficient in FasI function are fully viable and CNS development apparently is normal. cytology: Placed in 89D by in situ hybridization to polytene chromosomes. Deleted by Df(3R)Ubx109 = Df(3R)89D1-2;89E1-2. molecular biology: Apparently full-length cDNA clone of 3.0 kb isolated and sequenced. Conceptual amino-acid sequence indi- cates a protein similar in size to the 638-amino-acid, 70 kd fasciclin I from grasshoppers; it is 48% homologous to the grasshopper protein. Contains a putative signal sequence, but no convincing transmembrane domain. Concluded to be an extrinsic membrane protein since it is isolated with the mem- brane fraction. Mature protein composed of four homologous domains of approximately 150 amino acids each, followed by 20-25 C-terminal residues. # Fas3: Fasciclin III location: 2-{53}. origin: Identified by screening a cDNA expression library with monoclonal antibodies directed against embryonic CNS and shown to identfy proteins expressed on the cell surface of a res- tricted subset of cells of the embryo, including specific cells of the developing central nervous system. references: Gauger, Glicksman, Saltino, Condie, Schubiger, and Brower, 1987, Development 100: 237-44. Patel, Snow, and Goodman, 1987, Cell 48: 975-88 (fig.). Snow, Bieber, and Goodman, 1989, Cell 59: 313-23. phenotype: Monoclonal-antibody staining reveals a complex sequence of temporal and spatial expression of Fas3. It is expressed on segmentally repeated patches of cells during neu- rogenesis and outside the developing CNS on segmentally repeated stripes in the epidermis at the segmental grooves, on patches of epithelial cells near the stomodeal and proctodeal invaginations, on the visceral but not the somatic mesoderm, and on the luminal surface of the salivary gland epithelium; expression is highest where fasciclin-III-positive cells con- tact one another. After germ-band extension transiently expressed on segmentally repeated patches of neuroepithelial cells and specific underlying neuronal lineages; by the end of germ band retraction fasciclin-III is expressed in repeated stripes across all body segments. At hour 12 fasciclin is detected on a subset of three axon bundles (fascicles) in the anterior commissure and two in the posterior commissure of each segment; generally, however it's not expressed on the axons of these neurons that exit CNS, specifically on the longitudinal fascicles. Expression of Fas3 in transfected cultured cells promotes their adhesion to each other, but not to nonexpressing cells (Snow, et al.). The monoclonal antibo- dies used in the isolation of fasciclin identify four closely related membrane glycoproteins of 80, 66, 59, and 46 kd molec- ular weight; all depend on the presence of Fas3+ for their presence. cytology: Placed in 36E1 by in situ hybridization to polytene chromosomes. In the region of overlap of Df(2L)H20 = Df(2L)36A7-10;36E4-F1 and Df(2L)V18 = Df(2L)36C4-D1;37C2-5. alleles: A null mutation, Fas3n1, has been isolated (Elkins). molecular biology: cDNA's cloned and sequenced; conceptual amino acid sequence indicates a mature polypeptide, following cleavage of a 20-amino-acid signal sequence, of 488 amino acids of calculated molecular mass of 53.6 kd. It comprises a putative 326-amino-acid extracellular domain, a 24-amino-acid transmembrane domain, and a 138-amino-acid intracellular domain. The extracellular domain contains four potential N- linked glycosylation sites, and the intracellular domain con- tains a single tyrosine residue, two potential phosphorylation sites, and an opa-repeat sequence (a second such sequence found in the 3' untranslated region). # fat: see ft # Fat body protein: see Fbp # faulty chaetae: see fc #*fb: fine bristle location: 1-1.0. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1954. references: 1958, DIS 32: 70. phenotype: Thin, slightly shortened bristles. Occasional scal- loping of wing margins. Delayed emergence. Good viability and fertility in both sexes. RK3. # fbr: fine bristles location: 1-3.3. origin: Spontaneous (appears to be unstable). references: Golubovsky, 1978, DIS 53: 122. phenotype: Bristles reduced in length and diameter. other information: Transmission in crosses irregular; possibly associated with a transposable element. Possibly allelic to dm or slc. # Fbp1: Fat body protein 1 location: 3-{41}. synonym: P1. references: Lepesant, Kejzlarova-Lepesant, and Garen, 1978, Proc. Nat. Acad. Sci. USA 75: 5570-74. Lepesant, Levine, Garen, Kejzlarova-Lepesant, Rat, and Somme- Martin, 1982, J. Appl. Mol. Genet. 1: 371-83. Paco-Larson, Nakanishi, Levine, and Garen, 1986, Dev. Genet. 7: 197-203. Deutsch, Laval, Lepesant, Maschat, Pourrain, and Rat, 1989, Dev. Genet. 10: 220-31. phenotype: Encodes P1 polypeptide, which accumulates in the fat body of third-instar larvae; not detectable at earlier stages or in other tissues. Expression stimulated by the increased ecdysone level characteristic of third-instar larvae; function of the protein product uncertain (Deutch et al., 1989). cytology: Located in 70D1-2 by in situ hybridization to the salivary chromosomes. molecular biology: Fbp1 cloned and its nucleotide sequence determined (Lepesant, et al., 1982); gene shows a simple molecular structure and organization, with very short introns interrupting transcribed sequences coding for unique mRNA. The putative P1 polypeptide of 1,030 amino acids has a presumptive N-terminal signal peptide; since no extracellular P1 product is detectable in the hemolymph, the signal peptide may serve to compartmentalize the protein within the fat-body cell. The sequence also contains two aspartic + asparagine stretches of 11 or 12 amino acids (Deutch et al., 1989). A transcript is not detected until the second larval molt; at this time, it is restricted to the fat body (Lepesant et al., 1982; Paco-Larson et al., 1986). A peak in the accumulation of transcript occurs at the time of puparium formation and is followed by its disappearance after the early pupal stage; the rise and fall follows by several hours that of the larval serum proteins, which are also fat-body specific in their expression. Fbp1 expression completely inhibited in ecd-1ts flies shifted to restrictive temperature following the second larval molt or in dorlt187 third-instar larvae; expression rescued by administration of 20-hydroxyecdysone. Germ-line transformation experiments demonstrate that 138 but not 80 base pairs upstream from the transcription start site are suf- ficient to impart complete temporal, spatial, and hormonal regulatory control of transcription. # Fbp2: Fat body protein 2 location: 2-{35}. synonym: P6. references: Langer-Safer, Levine, and Ward, 1982, Proc. Nat. Acad. Sci. USA 79: 4381-85. Lepesant, Levine, Garen, Lepesant-Kejzalrova, Rat, and Somme- Martin, 1982, J. Appl. Mol. Genet. 1: 371-83. Paco-Larson, Nakanishi, Levine, and Garen, 1986, Dev. Genet. 7: 197-203. Deutsch, Laval, Lepesant, Maschat, Pourrain, and Rat, 1989, Dev. Genet. 10: 220-31. phenotype: Gene detected in the larval fat body of Drosophila melanogaster. Function of the protein product uncertain (Deutch et al., 1989). cytology: Located in 30B by in situ hybridization to the salivary chromosomes. molecular biology: Fbp2 cloned, and its nucleotide sequence determined (Lepesant, 1982). The gene has an unusually high methionine content (20%); conceptual amino acid sequence shows significant similarity to that of Drosophila alcohol dehydro- genase, which lacks methionine. A transcript is not detected until the second larval molt, when it is restricted to the fat body (Lepesant et al., 1982; Paco-Larson et al., 1986). As in Fbp1, a peak in the accumulation of transcript occurs at the time of puparium formation and is followed by its disappear- ance after the early pupal stage; apparently not sensitive to the removal or addition of ecdysone during the third larval instar. # Fat body protein: see Fbp #*fc: faulty chaetae location: 1-0.9. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1958, DIS 32: 70. phenotype: Short, thin bristles. About one-third of flies show either absence or duplication of one scutellar bristle. Via- bility and fertility good in both sexes. RK2. other information: Possibly allelic to kz. # fch: fragile chorion location: 3-55. origin: Induced by ethyl methanesulfonate. references: Tearle and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal effect; chorion very thin or nonexistent. alleles: Two, fch1 and fch2 (isolated as 055 and 267). # fcl: foreclosed location: 1-(between 57.8 and 59.1). origin: Induced by ethyl methanesulfonate. references: Eberl and Hilliker, 1988, Genetics 118: 109-20. phenotype: Embryonic lethal; no internal organogenesis; prom- inent central yolk plug; dorsal closure may be incomplete; head involution partial; germ band contraction incomplete. No cuticle evident in cuticle preparations, but mouth parts and spiracles visible. Embryos exhibit considerable movement. alleles: Two putative alleles fcl1 and fcl2 (isolated as l(1)EH244b and l(1)EH523. cytology: Placed in 16C2-18B11 based on the failure of Dp(1;3)f+71b = Dp(1;3)15A4;16C2-3;80-81 and XPYDB5O = XPYD18B4-11 to cover it. #*fd: furled location: 1- (rearrangement). origin: Induced by 32P. discoverer: Bateman, 1949. references: 1950, DIS 24: 54. 1951, DIS 25: 77. phenotype: Like vestigial but with immovable mouth parts and fully extended proboscis. Dies early, perhaps owing to failure to ingest. Viability at eclosion good. RK3A. cytology: Associated with T(1;3)fd = T(1;3)7A;86E + In(3R)89C;96A (Darby). # fdg: fibrillar dysgenesis location: 1-55.0 origin: Induced by ethyl methanesulfonate. synonym: l(1)fdg. references: Newman, and Wright, 1983, Dev. Genet. 3: 329-45 (fig.). phenotype: Embryonic lethal at 32-30; larval-pupal lethal at lower temperatures. Mutant embryos exhibit abnormal distribu- tion of muscle fiber elements and organelles. Also abnormal Z-body alignment. # female abdomen pattern: see fap # female lethal 302: see fl(1)302 # Female lethal: see Sxl # female sterile: see fs( ) # Female sterile: see Fs( ) # femaleless: see fle # fes: see fs(2)B # fes(2)K: see fs(2)K # ff: fluff location: 1-57.7. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1955. references: 1959, DIS 33: 86. phenotype: Extremely fine short bristles. Wings slightly rounded at tips. Males and females viable and fertile; eclo- sion delayed. RK3. other information: One allele induced by nitrogen-mustard. #*fft: fused filament location: Not located. origin: Spontaneous. discoverer: Robertson and Reeve. references: 1954, DIS 28: 78. phenotype: Chorionic filaments of eggs laid by fft females usu- ally fused into a single structure. A few normal eggs also laid. Hatchability reduced and variable. RK3. # fg: see spdfg #*fi: frail location: 1-53. origin: Recovered among progeny of flies treated with Janus green. discoverer: Muller, 28e20. references: 1935, DIS 3: 30. phenotype: Wings nearly as small as m, thin and frail. Bris- tles fine. Fly weak. Viability 10-30% wild type. RK3. # fiber loop: see flo # fibrillar dysgenesis: see fdg #*fil: fine lash location: 1-56.8. origin: Induced by L-p-N,N-(2-chloroethyl)amino-phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1959, DIS 33: 86. phenotype: Thin, slightly shorter bristles. Eyes reduced in size; posterior border very close to orbital bristles. Both sexes viable and fertile. RK3. other information: Two alleles induced by ethyl methanesul- fonate. # filzig: see flz # fin: finer location: 1-29.6. origin: Induced by D-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3026). discoverer: Fahmy, 1954. references: 1959, DIS 33: 86. phenotype: Fly slightly smaller than normal with shorter, thinner bristles. Delayed eclosion. Males viable but sterile. RK3. # fine bristle: see fb # fine bristles: see fbr # fine chaetae: see fnc # fine lash: see fil # fine macros: see fm # finer: see fin # fizzy: see fzy fj: four jointed Edith M. Wallace, unpublished. # fj: four jointed location: 2-81.5. origin: Spontaneous. discoverer: Schultz, 31d1. phenotype: Similar to d. Tarsi four instead of five jointed. Legs short and stocky, owing to failure of joint formation between second and third tarsal segments (Tokunaga and Gerhart, 1976, Genetics 83: s76). Femur, tibia, and tarsae foreshortened [Tokunaga and Gerhart, 1976; Mikuta, 1979, Genetika (Moscow) 15: 624-32]. Probability of joint failure proportional to degree of shortening of second tarsal segment (Tokunaga and Gerhart, 1976). Joint failure phenotype can extend into fj/+ tissue adjacent to fj/fj clones (Tokunaga and Gerhart, 1976). Leg chaetae show irregularities in the rela- tive orientation of sockets and bracts (Held, Duarte, and Derakhshanian, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 145-57). Enhanced by ssa and ssaB [Villee, 1945, Genet- ics 30: 26-27; Mglinetz and Ivanov, 1976, Genetika (Moscow) 12: 87-94] and by pb [Kaurov, Ivanov, and Mglinetz, 1978, Genetika (Moscow) 14: 306-12]; also influenced by AntpNs (Mikuta and Mglinetz). fj eyD flies have but three tarsal joints (Postlethwait and Schneiderman, 1975, Ann. Rev. Genet. 7: 381-433). Development similar to that of dachs [Wadding- ton, 1943, J. Genet. 45: 29-43 (fig.)]. Wings shorter and broader with crossveins conspicuously closer together; veins diverge at greater angle (Tokunaga, Michinomae, Sizemore, and Gerhart, 1978, Genetics 88: s98). Effect visible in pupal wing (Waddington, 1940, J. Genet. 41: 75-139). Eyes smaller, ellipsoid, coarse textured; head foreshortened. RK2. alleles: *fj40e (Ives, 1941, DIS 14: 39) showed more extreme but more variable venation anomalies than fj1. cytology: Placed in 55B-C based on its inclusion in Df(2R)11B = Df(2R)54F6-55A1;55C1-3 and Df(2R)Pcl-w5 = Df(2R)55A-B;55C (Deng and Rizki, 1988, Genome 30, Suppl. 1: 192). # Fk: see Hex-C # fkh: fork head location: 3-95. references: Jurgens and Weigel, 1988, Wilhelm Roux's Arch. Dev. Biol. 197: 345-54. Weigel, Jurgens, Kuttner, Seifert, and Jackle, 1989, Cell 57: 645-58. phenotype: Embryonic lethal. fkh+ appears to be required in the most anterior and posterior regions of the embryo; in amorphic mutants homeotic transformation effects the appear- ance of post-oral head structures in these terminal domains. The ectopic head structures are sometimes associated with thoracic structures anteriorly and anterior tail structures posteriorly. Thus fkh mutations produce transformations directed to the center involving structures normally found in different parasegments. Anteriorly, esophagus and proventri- culus, derivatives of the ectodermal stomodaeum, are absent but not the pharynx or the hypopharyngeal organ, which resides on the anterior surface of the embryo; parts of the head skeleton are distorted; other parts apparently normal. Salivary glands absent. Posteriorly, anal pads and Malpighian tubules, derivatives of the ectodermal proctodaeum, are absent; replaced by anterior tail structures and post-oral head structures; supernumerary anal sensilla and dorsal hairs also present. Anterior and posterior fkh domains are beyond the regions controlled by ANTC and BXC, respectively; however ectopic expression of ANTC and BXC expression can occur in the fkh domains of fkh but not fkh+ embryos. No maternal effect. Homozygous fkh clones in adult cuticle completely normal in structure indicating no requirements for fkh+ in imaginal disk development. In situ hybridization reveals transcript in two terminal domains shortly before blastoderm cellularization occupying 5% embryonic length anteriorly and 15% posteriorly. fkh protein first detected in posterior domain at the end of syncytial blastoderm and the anterior domain at the beginning of cellularization. Expression continues in the derivatives of the ectodermal stomodaeum and proctodaeum throughout gas- trulation. In addition fkh protein is detected in the midgut, the salivary glands, the central nervous system, and the yolk cells. alleles: allele origin ref ( comments ________________________________________________________________ fkh1 EMS 1 nonsense mutation in codon 254 fkh2 EMS 2 in frame deletion of codons 233-237; 17 bp deletion + 2 bp insertion fkh3 EMS 2 nonsense mutation in codon 63 fkh4 X ray 2 weak allele; T(2;3)38;98D2-3 fkh5 X ray 2 weak allele; T(Y;3;4)98D2-3;99F;101 fkh6 X ray 2 out of frame deletion of codons 8-10 + 2 bp of codon 11 fkh7 X ray 2 deletion of ca. 90 kb fkh8 X ray 2 weak allele; In(3LR)80F;98D2-3 ( 1 = Jurgens, Wieschaus, Nusslein-Volhard and Kluding, 1984, Wilhelm Rous's Arch. Dev. Biol. 193: 283-95; 2 = Jurgens and Weigel, 1988, Wilhelm Roux's Arch. Dev. Biol. 197: 355-59. molecular biology: Region cloned in a 120 kb walk. Identity of fkh gene confirmed by P-mediated germ-line transformation. 4.2 kb transcript observed in Northern blots; 4002 base pairs of cDNA sequence determined; direction of transcription from right to left; breakpoints of fkh rearrangement located down- stream from the gene. Sequence reveals an uninterrupted open reading frame of 1530 base pairs, encoding a 510-residue polypeptide of calculated molecular weight of 54.3 kd; anti- body staining reveals the restriction of fkh protein to nuclei. No significant sequence similarity to known proteins detected in computer search of databases. A second tran- script, distal to fork head (dfk), which is transcribed from left to right, lies less than 500 base pairs to the right of fkh.