fl: fluted Edith M. Wallace, unpublished. # fl: fluted location: 3-59.7+ (Kuhn, Woods and Andrew, 1984, DIS 60: 134- 35). origin: Spontaneous. discoverer: Redfield, 21l. phenotype: Wings creased lengthwise and dark. Overlaps wild type slightly at 25 but not at 19. RK3. alleles: *fl2, spontaneous, Spencer, 36d15. # Fl: see Sxl # fl(1)302: female lethal 302 location: 1-{9} (to the right of ecl). origin: Induced by ethyl methanesulfonate. discoverer: Steinmann-Zwicky. references: 1988, EMBO J. 7: 3889-98. phenotype: Homozygous females die in larval or pupal stages. Male viable. cytology: Placed in 4C5-E1 based on its inclusion in Df(1)rb13 = Df(1)4C5-6;4D3-E1. Not included in Df(1)rb23 and Df(1)rb27 which overlap the left end of Df(1)rb13 but have not been characterized cytologically. # fla: flateye location: 1-2.4 [no evidence for such in w-spl interval (Lefevre and Green, 1972, Chromosoma 36: 391-412)]. origin: Induced by L-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3025). discoverer: Fahmy, 1953. references: 1958, DIS 32: 70. phenotype: Smaller fly with smaller and less curved eyes. Wings extremely variable, from normal through incised margins to crumpled vestigial stumps. Not easily classified. Viabil- ity and fertility good in males but reduced in females. # flap wing: see flw # flare: see flr # flateye: see fla # flb: see Egfr # fle: femaleless location: 3-45 (mapped with respect to mwh and red). origin: Spontaneous. synonym: file(3)100. references: Inouchi, Okuno, Oishi, and Watanabe, 1983, Jpn. J. Genet. 58: 525-30. Okuno, Satou, and Oishi, 1984, Jpn. J. Genet. 59: 237-47. phenotype: Homozygous females die; males survive. Lethal effect late. Dosage compensation normal as determined by tri- tiated uridine labeling of polytene chromosomes. No interac- tion with tra in fle/tra heterozygotes. # fli-385: flightless-385 (J.C. Hall) location: 1-ca. 0. origin: Induced by ethyl methanesulfonate. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. phenotype: Adults cannot fly or even beat wings; induced simul- taneously with a fliI allele; not allelic to fliA or fliB. # fli: flightless (J.C. Hall) A series of ethyl-methanesulfonate-induced, sex-linked muta- tions selected by Homyk et al.. All were crudely mapped; com- plementation tests were performed among fli, flrd, and other behavioral mutants recovered in the screens and mapping to the same interval. In this way eleven fli loci, designated fliA through fliK, were identified. Allelism tests with flt mutants not carried out. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553- 65. Homyk and Grigliatti, 1983, Dev. Genet. 4: 77-97. Homyk and Emerson, 1988, Genetics 119: 105-21. # fliA: see Actn # fliB location: 1-0.0. phenotype: Flightless and beats wings poorly after rearing at 17; weak flier after rearing at 22; jumps abnormally short distances when raised at restrictive temperature. TSP late larval early pupal. # fliC location: 1-19.9. phenotype: Flight and other behaviors impaired; for one allele (fliC1), raising at 22 leads to weak flight though normal appearance; rearing at 29 causes drooped wing position (often bilaterally asymmetrical), poor flying, weak locomotion, inadequate wing display of courting males; TSP for flightless- ness in first half of pupal stage. fliC2 allele nearly lethal at 29; rearing at 22 leads to good survival but weak flight; both alleles have lethal maternal effect. fliC1 females sterile. alleles: Two mutant alleles: fliC1 and fliC2. ERG normal (Homyk and Pye, 1989, J. Neurogenet. 5: 37-48). cytology: Placed in 7B2-C1; in the region of overlap of Df(1)ct-J6 = Df(1)6E1;7C1 and Df(1)ct4B1 = Df(1)7B2-4;7C3-4 (Homyk and Emerson, 1988, Genetics 119: 105-21). # fliD location: 1-25.5. phenotype: When raised at 17, adults are weak fliers; when raised at 22, bristles are small and adults cannot fly and cannot jump normally; lethal when raised at 29. ERG normal (Homyk and Pye, 1989, J. Neurogenet. 5: 37-48). TSP a res- tricted period in early pupa. cytology: Placed in 8C-9B1; not deleted by Df(1)KA14 = Df(1)7F1-2;8C6 or Df(1)v-L15 = Df(1)9B1-2;10A1-2. Females carrying fliD in heterozygous combination with Df(1)C52 = Df(1)8E;9C-D and raised at 29 exhibit partially impaired fly- ing and hopping ability which could indicate location of the gene at the 8E breakpoint; however, Df(1)C52/_ females also show abnormal movement after development at 29. # fliE location: 1-26.8. phenotype: Flightless when raised at 17; weak flight after rearing at 22; jumping ability poor after rearing at restric- tive temperature. TSP first half of pupal stage. ERG normal (Homyk and Pye, 1989, J. Neurogenet. 5: 37-48). # fliF location: 1-29.1. phenotype: Flightless, jumping ability poor; mosaic analysis suggests primary defect could be in muscles (Homyk, 1977, Genetics 87: 105-28). In fliF2 and fliF3, indirect flight muscles have relatively mild abnormalities of z bands and myo- fibrils. Reduced amounts of at least two high-molecular- weight proteins from indirect flight muscles [Deak, Rahmi, Bellamy, Bienz, Blumer, Fenner, Golin, Ramp, Reinhardt, Duben- dorfer, and Cotton, 1980, Development and Neurobiology of Drosphila (Siddiqi, Babu, Hall, and Hall, ed.). Plenum Press, New York and London, pp. 183-92; Deak, Bellamy, Bienz, Dubuis, Fenner, Gollin, Rahmi, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81]. alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________ fliF1 EMS Homyk 2 fliF2 EMS 696 = gmp1 1 fliF3 EMS 628 = gmp2 1 ( 1 = Deak, Rahmi, Bellamy, Bienz, Blumer, Fenner, Golin, Ramp, Reinhardt, Dubendorfer, and Cotton, 1980, Development and Neurobiology of Drosphila (Siddiqi, Babu, Hall, and Hall, ed.). Plenum Press, New York and London, pp. 183-92; 2 = Homyk and Sheppard, 1977, Genetics 87: 95-104. # fliG location: 1-32.67. references: Zhimulev, Belyaeva, Pokolkova, Kotchneva, Fomina, Bgatov, Khudyakov, Patzevich, Semeshin, Baricheva, Aizenzon, Kramers, and Eeken, 1981, DIS 56: 192-96. 1982, DIS 58: 210-14. Zhimulev, Pokholkova, Bgatov, Umbetova, Solovjeva, Khudyakov, and Belyaeva, 1987, Biol. Zentralbl. 106: 699-720; 1987, DIS 66: 194-97. phenotype: Flight and other behaviors impaired. One allele, fliG1, allows for weak flight; another, fliG2, leads to almost no flight ability and weak running or climbing (Homyk, 1977, Genetics 87: 105-28); wings abnormal in appearance (intrinsi- cally and in terms of positions in which they are held); male fertility reduced; sex combs reduced. All alleles are nearly lethal when reared at 18 and cause poor viability when raised at 25. Not allelic to fltC, fltD, fltE, fltF, or fltG, or to sdby. cytology: Placed in the 9F11-12 interband or in the left edge of 9F12 based on its being uncovered by Df(1)v-L3 = Df(1)9F10;10A7-8 but not by Df(1)v-M6 = Df(1)9F11-12;10A1-2 and mapping to the left of v (Zhimulev et al., 1981, 1987). alleles: Four mutant alleles: fliG1, fliG2, fliG3 (= fliGB186), and fliG4 (= fliGdp324), all cold-sensitive lethals or semilethals. The first two described by Homyk and Sheppard, the latter two by Zhimulev et al.; fliG4 induced in v+Yy+. # fliH: see hdp-a # fliI location: 1-66.5. phenotype: Both viable and lethal alleles isolated. Viable alleles are recessive and flightless; wing position normal; jumping abilities variously impaired depending on allele. Temperature-sensitive alleles show temperature-sensitive period to be during first half of pupal stage. Rearing fliI1 and fliI2 at 17 leads to weak flight and at 22 to flightless- ness. Indirect-flight-muscle fibers wavy with amorphous internal structures; myofilaments disorganized; z bands and myofibrils abnormal; thin filaments often aggregated into bun- dles with striations (not seen in wild type). Mosaic analysis with fliI5 suggests primary defect in thoracic muscles (Koana and Hotta, 1978, J. Embryol. Exp. Morphol. 45: 123-43). Trans heterozygotes with sdby are flightless. Lethal alleles die in larval or pupal stages. Maternal effect lethal; pro- geny produced from homozygous female germline clones of severe alleles (e.g., fliI14) are not rescuable by normal allele of paternal origin; abnormal folding during gastrulation; meso- derm invagination abnormal; only patches of epidermis present at later stages; embryos from clones homozygous for weaker alleles (e.g. fliI22) were more nearly normal in appearance. alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________________ fliI1 EMS Homyk 2 temperature sensitive fliI2 EMS Homyk 2 temperature sensitive fliI3 EMS Homyk 2, 9 nonconditional fliI4 EMS Koana fltO1 3 strong allele fliI5 EMS Koana fltO2 3, 9 moderate allele fliI6 EMS Koana fltO3 3 moderate allele fliI7 EMS Koana fltO4 3 moderate allele fliI8 P l(1)D44 1, 9 fliI9 Kaplan l(1)DCA3-19 fliI10 X ray Novitski l(1)EN3 9, 10, 11 larval lethal; maternal-effect lethal fliI11 EMS Lifschytz l(1)M90 8 on y+Ymal+ fliI12 EMS Lifschytz l(1)R-9-6 7 fliI13 EMS Lifschytz l(1)R-10-9 7 fliI14 EMS Lifschytz l(1)W2 4, 6, 7, larval lethal; 8, 9, 11 maternal-effect lethal fliI15 X ray Lefevre l(1)A3 4 fliI16 X ray Lefevre l(1)A141 4 fliI17 X ray Lefevre l(1)GA105 4 fliI18 X ray Lefevre l(1)HC183 4, 9 pupal lethal; maternal-effect lethal fliI19 X ray Lefevre l(1)HF338 4 fliI20 X ray Lefevre l(1)RA70 4 fliI21 EMS Lefevre l(1)DA534 5, 9 pupal/adult lethal; maternal- effect lethal fliI22 EMS Lefevre l(1)EF498 5, 9 pupal lethal; maternal-effect lethal fliI23 EMS Lefevre l(1)VE924 5 ( 1 = Eeken, Sobels, Hyland, and Schalet, 1985, Mutat. Res. 150: 261-75; 2 = Homyk and Sheppard, 1977, Genetics 87: 95-104; 3 = Koana and Hotta, 1978, J. Embryol. Exp. Morphol. 45: 123-43; 4 = Lefevre, 1981, Genetics 99: 461- 80; 5 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 6 = Lifschytz and Falk, 1968, Mutat. Res. 6: 235-44; 7 = Lifschytz and Falk, 1969, Mutat. Res. 8: 147-55; 8 = Lifschytz and Yakobovitz, l978, Mol. Gen. Genet. 161: 275-84; 9 = Perrimon, Smouse, and Miklos, 1989, Genet- ics 121: 313-31; 10 = Schalet and Lefevre, l971, Chromosoma 44: 183-202; 11 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902; cytology: Placed in the distal half of 19F based on deficiency mapping with deficiencies of unknown polytene breakpoints (Perrimon, Smouse, and Miklos, 1989, Genetics 121: 313-31. # fliJ: see elav # fliK location: 1-30.1. synonym: l(1)9Fc. phenotype: Flying and jumping ability poor or absent; mutants tend to be generally inactive, including poor courtship; both alleles lead to stress-sensitive paralysis and are temperature sensitive, in that rearing at 29 leads to severe weakness and early death. Temperature sensitive throughout most of development. ERG normal (Homyk and Pye, 1989, J. Neurogenet. 5: 37-48). alleles: allele origin discoverer synonym ref ( comments ________________________________________________________________ fliK1 EMS Homyk 1 fliK2 EMS Homyk 1 fliK3 X ray Lefevre l(1)A147 2 In(1)9F9;20 fliK4 X ray Lefevre l(1)L49 2 lethal fliK5 X ray Lefevre l(1)N51 2 lethal fliK6 EMS Lefevre l(1)EM15 2, 3 PA/NME fliK7 EMS Lefevre l(1)VE686 3 lethal fliK8 EMS Lefevre l(1)VE828 3 E/L fliK9 HMS Kramers l(1)HM25 4, 5 lethal ( 1 = Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65; 2 = Lefevre, 1981, Genetics 99: 461-80; 3 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 4 = Zhimulev, Belyaeva, Pokolkova, Kotchneva, Fomina, Bga- tov, Khudyakov, Patzevich, Semeshin, Baritcheva, Aizenzon, Kramers, and Eeken, 1981, DIS 56: 192-96; 5 = Zhimulev, Pokholkova, Bgatov, Semeshin, and Belyaeva, 1981, Chromosoma 82: 25-40. cytology: Placed in 9F3-5 based on inclusion in Df(1)HC133 = Df(1)9B9-10;9F2-5 but not Df(1)ras-P14 = Df(1)9E1-2;9F3-4 (Zhimulev, Pokholkova, Bgatov, Umbetova, Solovjeva, Khudyakov, and Belyaeva, 1987, Biol. Zentralbl. 106: 699-720; 1987, DIS 66: 194-97). # flightless: see fli # flight defective: see flt # flight reduced: see flrd # flipper: see flp #*fll: flyless location: 3- (not located). origin: Spontaneous. discoverer: Cercos, 41g15. references: Andres, 1943, DIS 17: 48. phenotype: Wings apparently normal, but fly cannot keep them spread and cannot fly more than a few inches. RK3. # flo: fiber loop (J.C. Hall) location: 2-58 (1% recombination with cn). origin: Induced by ethyl methanesulfonate. discoverer: Heisenberg and Fishbach. synonym: floN115. phenotype: Looped axon fiber present in axonal columns in distal part of medulla (second order optic lobe); nearly full penetrance (Heisenberg). # flp: see flw #*flp: flipper location: 2-27 (based on location of flphd). origin: Spontaneous. discoverer: Mohr, 18h5. references: Bridges and Mohr, 1919, Genetics 4: 304. phenotype: Wings fail to expand, remain compact, very dark, extended, and curved slightly downward. Fly a wizened dwarf. Body surface dull and dark. Both sexes sterile. RK3. # flphd: flipper-hood origin: X ray induced. discoverer: M. Simmons, 1972. references: Craymer, 1980, DIS 55: 198. phenotype: Like flp but fertile in both sexes. flphd/+ tends to have dusky, corregated wings. RK3 as dominant; RK1 as recessive. other information: Allelism inferred from location (27 vs 30) and phenotype. # flr: flare location: 3-38.8 (with respect to h and th). origin: Induced by ethyl methanesulfonate. references: Garcia-Bellido and Dapena, 1974, Mol. Gen. Genet. 128: 117-30. phenotype: Chaetae and trichomes in thorax and abdomen abnor- mally shaped. Chaetae have rudimentary sockets, and shaft is frequently crooked and branched. Trichomes transformed into multiple short outgrowths which appear as swellings on wing cells and as rosettes in abdominal cuticle cells. Homozygotes are zygotic lethals but cell viable; homozygous clones may have reduced survival in thorax but not in abdomen. Excellent marker for homozygous 3L clones. alleles: Three alleles: flr1, flr2, and flr3. Lethal in all pairwise combinations. # flrd: flight reduced (J.C. Hall) A series of ethyl-methanesulfonate-induced, sex-linked mutants with reduced flying ability recovered by Homyk et al.. All were crudely mapped; complementation tests were performed among fli, flrd, and other behavioral mutants recovered in the same screens and mapping to the same interval. In this way 17 flrd loci, designated flrdA through flrdR (no K or Q) were identified; two others were not mappable. Allelism tests with flt mutants were not performed. references: Homyk and Sheppard, 1978, Genetics 87: 95-104. Homyk, Szidonya, and Suzuki, 1980, Mol. Gen. Genet. 177: 553-65. # flrdA location: 1- 1.2. phenotype: Flight weak; small amplitude of wing beats. Not allelic to flrdB or flrdC. # flrdB location: 1- 1.1. phenotype: Flight weak; females may be more impaired than males; small amplitude of wing beats; jumping ability subnor- mal. # flrdC location: 1- 4.0. phenotype: Flight weak; adults seem generally feeble, including poor jumping ability; 10-30% of adults fail to inflate wings normally; even when wings inflated, males seldom extend them fully when courting. # flrdD location: 1- 28.1. phenotype: Weak flight when raised at 29; flightless when raised at 22; wing beats have small amplitude and wing behavior of courting males is aberrant; impaired jumping abil- ity when raised at either temperature; mosaic analysis sug- gests primary defect could be in muscles (Homyk, 1977, Genet- ics 87: 105-28). # flrdE location: 1- 39.9. phenotype: Weak flight; adults often fail to retract wings properly and walk holding one or both wings at 90 angle to body axis. # flrdF location: 1- 42.2. phenotype: Flightless; jumping ability poor; mosaic analysis suggests primary defect could be in muscles (Homyk and Shep- pard, 1977). # flrdG location: 1- 44.6. phenotype: Weak flight; males may be more impaired than females; no wing beats; general locomotor activity weak, including poor jumping ability; adults begin dying around 10 days post eclosion; homozygous mutant females do not lay eggs (which is not necessarily due to same variant as that causing behavioral defects). # flrdH location: 1-51.0. phenotype: Weak to very weak flight; small amplitude of wing beats in flight; weak jumping ability; all alleles lead to decreased viability, flying ability, or both when raised at higher temperatures; mutations are heat-sensitive male steriles, and at least one allele, flrdH3, causes abnormali- ties of wing movements in courtship after rearing at 29. TSP of flrdH3 second and third larval instars (Homyk and Grigli- atti, 1983, Dev. Genet. 4: 77-97). alleles: Four mutant alleles: flrdH1, flrdH2, flrdH3, and flrdH4; flrdH2 (flrdH2xk) originally designated flrdK. # flrdJ location: 1- 51.0. phenotype: Very weak flight. Mosaic analysis suggests primary defect in thoracic muscles [Homyk, 1977, Genetics 87: 105-28 (described these as flrdI rather than flrdJ)]. # flrdI: see l(1)adl16 # flrdK: see flrdH2 # flrdL location: 1- 62.5. phenotype: Weak flight; generally somewhat inactive. # flrdM location: 1- 23.6. phenotype: Weak flight and jumping; adults generally somewhat inactive; some such individuals have poor landing response. # flrdN location: 1-38.0. phenotype: Weak flight and jumping ability; more severe pheno- type, including poor wing usage in male courtship, after rear- ing at 29. Wings held up and out when raised at 29. TSP for wing posture restricted to late third instar; that for flight- lessness begins in second instar and extends until near end of pupal stage. # flrdO location: 1- 45.3. phenotype: Weak to poor flying ability; fliO1 is most severe of three alleles; wings tend to be held in aberrant positions, including by courting males (all alleles). alleles: Three mutant alleles: flrdO1, flrdO2, and flrdO3. # flrdP location: 1- 44.6. phenotype: Flight and jumping ability weak; adults become uncoordinated briefly after mechanical shock. other information: Complements flrdG although mapping to the same position. # flrdQ location: 1- 56.7. phenotype: Weak flying and jumping ability; wing beating in flight has small amplitude; adults generally somewhat inac- tive. # flrd-R location: 1- 58.6. phenotype: Flight weak; generally somewhat inactive; some of the mutant individuals have melanotic spot under cuticle, near wing (not known to be due to same genetic change as that affecting flight). # flrd-393: flight reduced-393 (J.C. Hall) location: 1- not localized. origin: Induced by ethyl methanesulfonate. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. phenotype: Very weak flight; small amplitude of wing beats in flight; usage of wings by courting males abnormal. other information: Position of mutation or mutations responsi- ble for aberrant phenotypes said not to be resolvable. # flrd-397 (J.C. Hall) location: 1- not localized. origin: Induced by ethyl methanesulfonate. references: Homyk and Sheppard, 1977, Genetics 87: 95-104. phenotype: Weak flight; usage of wings by courting males abnor- mal. other information: Position of mutation or mutations responsi- ble for aberrant phenotypes said not to be resolvable. # flt: flight defective (J.C. Hall) A series of ethyl-methanesulfonate-induced X-chromosome mutants isolated by Koana and Hotta (1978, J. Embryol. Exp. Morphol. 45: 123-43). All were crudely mapped and complemen- tation tests performed among those mapping in the same inter- val. In this way 15 loci were identified and designated fltA through fltO. They were not tested for allelism with other collections of sex-linked flightless mutants such as fli or flrd; many cases of allelism between these series are likely. # fltA location: 1- between y and cho. phenotype: Impaired flight; jumping ability nearly normal. # fltB location: 1- between cho and cv. phenotype: Impaired flight; jumping ability nearly normal. # fltC location: 1- between cv and v. phenotype: Impaired flight, but when raised at 24, some indivi- duals fly normally; when raised at 29, all are completely flightless; jumping ability nearly normal. # fltD location: 1- between cv and v. phenotype: Completely flightless; reduced jumping ability. Mosaic analysis suggests primary focus in thoracic muscles. other information: Complements flrdD, gmp, and sdby. # fltE location: 1- between cv and v. phenotype: Impaired flight; jumping ability normal. # fltF location: 1- between cv and v. phenotype: Impaired flight; unable to take off from a surface; severely impaired jumping ability. # fltG location: 1- between cv and v. phenotype: Impaired flight; fltG has near-normal jumping abil- ity; fltG2 is normal in this behavior. alleles: Two mutant alleles: fltG1 and fltG2. # fltH location: 1- between v and f. phenotype: Completely flightless; normal jumping ability; wavy myofibrils in flight muscles, with larger than normal diame- ter; thick and thin filaments sometimes disorganized with deficient Z bands; sarcomere length abnormal; mosaic analysis suggests primary defect in thoracic muscles. # fltI location: 1- between v and f. phenotype: Impaired flight; jumping ability nearly normal. # fltJ location: 1- between v and f. phenotype: Impaired flight; unable to take off from a surface; normal jumping ability. alleles: Three mutant alleles: fltJ1, fltJ2, and fltJ3, the latter two weaker than the first. # fltK location: 1- between v and f. phenotype: Completely flightless; reduced jumping ability. # fltL location: 1- between v and f. phenotype: Completely flightless; normal jumping ability. # fltM location: 1- between f and centromere. phenotype: Impaired flight; jumping ability nearly normal. # fltN location: 1- between f and centromere. phenotype: Impaired flight; jumping ability nearly normal. # fltO: see fliI # flu: fluorouracil response location: 3- not mapped. origin: Naturally occurring polymorphism. references: Duke and Glassman, 1968, Nature 220: 588-89. O'Byrne-Ring and Duke, 1980, Biochem. Genet. 18: 717-26. phenotype: Resistant strain, flur, resistant to at least 0.0035% FU and shows resistance to FUDR as well. Sensitive strain, flus exhibits over 90% mortality following exposure to 0.0008% FU (6 x 10-5 M). Thymidilate synthetase levels of resistant strains four times those of sensitive strains. alleles: Two alleles described: flur and flu2 designating resistant and sensitive alleles. # Flu: Flutter (J.C. Hall) location: 1-37. origin: Induced by ethyl methanesulfonate. references: Deak, Bellamy, Bienz, Dubuis, Fenner, Gollin, Rahmi, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81. phenotype: Flies heterozygous for one of the mutant alleles, Flu1, have reduced flight ability, impaired jump response, and relatively slight disturbances in morphology of Z bands and myofibrils of indirect flight muscles; these Flu/+ flies are also like Hyperkinetic (Hk) mutants in terms of agitated behavior after etherization; Flu1/Flu1 flies are more severely affected with respect to flight and Hk-like phenotype; Flu2 is recessive in regard to flight and shaking defects; Flu1 stu- died for indirect flight muscle proteins and has reduced amounts of at least two high-molecular-weight materials. alleles: Two mutant alleles: Flu1 and Flu2. # fluff: see ff # fluorouracil response: see flu # fluted: see fl # Flutter: see Flu # flw: flap wing (J.C. Hall) location: 1-31. references: Deak, 1977, J. Embryol. Exp. Morphol. 40: 35-63. Deak, Rahmi, Bellamy, Bienz, Blumer, Fenner, Gollin, Ramp, Reinhardt, Dubendorfer, and Cotton, 1980, Development and Neurobiology of Drosophila, (Siddiqui, Babu, Hall, and Hall, eds.). Plenum Press, New York and London, pp. 183-92. phenotype: Wings held in lateral position, instead of dorsally, and parallel to substrate as in wild type; thorax has darkened longitudinal stripe; anterior scutellar bristles sometimes missing or doubled; eyes bulging and slightly roughened; head compressed; third antennal joint shortened; unable to fly; jumping ability poor; fibrillar muscles of thorax (dorsoven- trals, dorsolongitudinals) are variably abnormal, ranging from disorganized to missing; tergal depressor of trochanter jump muscle is normal in light microscope; behavioral and muscular phenotypes affected by flw2 may be due to primary defect in muscle primordia, concluded from mosaic experiment (Deak, 1977); at least two flw alleles (flw3 and flw4) cause reduced amount of a particular protein from indirect flight muscles (same molecule as that affected by hdp, int, rsd, and up muta- tions) (Deak, Bellamy, Bienz, Dubuis, Fenner, Gollin, Rahmi, Ramp, Reinhardt, and Cotton, 1982, J. Embryol. Exp. Morphol. 69: 61-81). flw is not allelic to gmp. alleles: allele origin discoverer synonym __________________________________________ flw1 Waletsky, 1937 flp flw2 Hanratty flw3 EMS flw671 flw4 EMS flw725 flw5 EMS flw942 cytology: Placed in 9C on the basis of its inclusion in Df(1)N110 = Df(1)9B3-4;9D1-2 but not Df(1)C52 = Df(1)8E;9C-D (Craymer and Roy, 1980, DIS 55: 200-04). # flyless: see fll # flz: filzig location: 2-59. 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; denticles and hairs of larvae have abnormal fuzzy texture. Mouth hooks poorly developed. alleles: Five, flz1 and flz2 (isolated as IP and IIG) retained. cytology: Placed in 44F-46D by segmental aneuploidy. #*fm: fine macros location: 1-66.1. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1959, DIS 33: 86. phenotype: Small fly with narrow abdomen and extremely short, thin bristles. Males fertile; viability about 50% wild type. RK3. other information: Possibly allelic to lf or lfl. # fmf: factor for male fertility location: 1- 0.5 (more than 0.008 but less than 0.189 cM to right of dor). origin: Locus inferred from infertility of males deficient for 2B7-12, i.e., Df(1)st472/y2Y67g = Df(1)2B6-8;2B11- 12/Dp(1;Y)1A1;2B6-7. references: Aizenzon and Belyaeva, 1982, DIS 58: 3-7. Belyaeva, Aizenzon, Kiss, Gorelova, Pak, Umbetova, Kramers, and Zhimulev, 1982, DIS 58: 190. phenotype: Males poorly viable and sterile. cytology: Inferred position 2B7-12. # Fmrf: FMRF amide homologue precursor location: 2-{59}. references: Nambu, Murphy-Erdosh, Andrews, Feistner, and Scheller, 1988, Neuron 1: 55-61. phenotype: Encodes the precursor polypeptide that is processed to generate a nonapeptide, DPKQDFMRFamide, that shares homol- ogy with the FMRFamide neuropeptide from molluscs. Gene appears to be expressed from late embryogenesis through the adult stage (see also White, Hurteau, and Punsal, 1986, J. Comp. Neurol. 247: 430-38). cytology: Placed in 46C by in situ hybridization; proximal to Df(2R)eve1.27 = Df(2R)46C3-4;46C9-11. molecular biology: Clones isolated from library using an oli- gonucleotide probe based on the putative amino-acid sequence of the nonapeptide, which had been isolated. Gene encodes a single 1.7 kb message; cDNA clones sequenced; conceptual amino-acid sequence indicates a precursor protein of 347 amino acids; the sequence contains a putative signal sequence, five copies of DPKQDFMRF as well as ten additional peptides exhi- biting various degrees of relatedness. Each peptide is flanked by single arginine cleavage sites and ends contain a carboxy-terminal glycine that can serve as the substrate for amidation. #*fnc: fine chaetae location: 1-34.9. origin: Induced by S-2-chloroethylcysteine (CB. 1592). discoverer: Fahmy, 1957. references: 1959, DIS 33: 86. phenotype: Extremely fine, short bristles. Body parts dispro- portionately reduced; reduction least marked on head and most marked on abdomen. Wings broad and slightly rounded at tips, occasionally with incisions of margin. Eyes slightly brighter red than normal. Males viable but sterile. RK3. # fo: folded location: 1-63. discoverer: Grossman, 1932. references: 1934, DIS 1: 30. phenotype: Wings remain unexpanded in a varying percentage of flies. Balancers shriveled; postscutellars bent forward. Overlaps wild type. RK3. # Fo: Forkoid location: 2-107 (between or and sp). origin: X ray induced. discoverer: Mohler, 58c18. references: 1960, DIS 34: 52. phenotype: Heterozygote shows reduction in size of bristles and weak forking of head and posterior thoracic bristles. Using Dp(2;3)P, it may be shown that the expression of +/+/Fo < +/Fo < +/Fo/Fo; +/Fo/Fo shows extreme forking of all bristles and is sterile. Homozygous lethal. Fo interacts with f alleles to produce extreme f bristles. RK1. alleles: Fo1 and Fo2; the latter induced by Angel with ethyl methanesulfonate; allelism based on phenotype and map position (1.4% to right of bw). cytology: Located between 58E3 and 60B10, on basis of its inclusion in Dp(2;3)P = Dp(2;3)58E3-F2;60D14-E2;96B5-C1 but not in Df(2R)Px = Df(2R)60B8-10;60D1-2 (Mohler) or in the deficiency for the tip of 2R derived from T(1;2)Bld = T(1;2)1C3-4;60B12-13 (Armentrout). # focal melanosis: see me # fog: folded gastrulation location: 1-65. references: Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. Zusman and Wieschaus, 1985, Dev. Biol. 111: 359-71. Perrimon, Smouse, and Miklos, 1989, 121: 313-31. phenotype: Hemizygous lethal; the cellular blastoderm apparently normal and gastrulation begins at normal time. No posterior midgut formed; germ band does not elongate onto dor- sal side of embryo but it is thrown into a series of transverse ventral folds. Older embryos often twist around the longitudinal axis for one complete turn; many exhibit an anterodorsal hole through which the brain protrudes and a split in the posterior CNS and protrusion of the midgut. Hem- izygous deficiency gives same phenotype. No effect of mater- nal genotype; homozygous germ line clones make eggs capable of supporting normal embryonic development. Fate mapping local- izes fog lethal focus to the posterior pole most likely in presumptive posterior-midgut or proctodaeum cells. alleles: allele origin discoverer synonym ref ( comments __________________________________________________________________________ fog1 Novitski l(1)114 1, 3, 4, 5, 6, 8 fog2 EMS Lifschytz l(1)M67 2 on y+Ymal+ *fog3 X ray Lefevre l(1)C88x 1 In(1)5E4-7;20 fog4 EMS fog4A6 7, 8 fog5 EMS 7 fog6 EMS 7 fog7 EMS 7 fog8 EMS 7 fog9 EMS 7 fog10 EMS 7 fog11 EMS 7 fog12 EMS 7 ( 1 = Lefevre, l981, Genetics 99: 461-80.; 2 = Lifschytz and Yakobovitz, l978, Mol. Gen. Genet. 161: 275-84.; 3 = Perri- mon, Smouse, and Miklos, 1989, 121: 313-31; 4 = Schalet and Lefevre, l973, Chromosoma 44: 183-202; 5 = Schalet and Lefevre, 1976, The Genetics and Biology of Drosophila (Ash- burner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1b, pp. 847-902; 6 = Schalet and Singer, l971, DIS 46: 131-32; 7 = Wieschaus, Nusslein- Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 172-86; 8 = Zusman and Wieschaus, 1985, Dev. Biol. 111: 359-71; cytology: Localized to 20A-B. #*fol: folded wings location: 2-39. origin: Spontaneous. discoverer: Goldschmidt, 1937. phenotype: Expanded wing folded. Overlaps wild type. RK3. # folded: see fo # folded gastrulation: see fog # folded wings: see fol # for: foraging location: 2-10. origin: Naturally occurring variants. references: DeBelle, Hilliker, and Sokolowski, 1987, Behav. Genet. 17: 620-21. 1989, Genetics 123: 157-63. phenotype: The major gene responsible for foraging strategy of feeding larvae. Larvae from so-called sitter strains move about 6.5 cm in five minutes while feeding on a yeasted sur- face, whereas those from so-called rover strains travel some 17 cm; heterozygotes are rovers. Several X-ray induced rever- sions of the dominant rover phenotype shown to be non- complementing lethals which map to 10 on chromosome 2, thus localizing a major behavioral locus. alleles: Two alleles thus defined, forR, the rover allele, and fors, the sitter allele. cytology: Placed in 24A3-C5 based on the lethality of the non- complementing lethal alleles in combination with Df(2L)ed-Sz = Df(2L)24A3-4;24D3-4 but not with Df(2L)ed = Df(2L)24C3- 5;25A1-4. # foreclosed: see fcl # fork head: see fkh # forked: see f # Forkoid: see Fo # four jointed: see fj # four wheel drive: see fwd # fr: fringed location: 2-80. origin: Spontaneous. discoverer: Bridges, 22c30. references: 1938, DIS 9: 48. phenotype: Wings often spread; wing margins snipped; bristles irregular and fringelike. Eyes small and rough. Midline of abdomen at slight angle to longitudinal axis of fly. Much variability in expression; safest criterion is wing margin irregularity. Viability and fertility variably reduced depending on allele. Character less extreme at low tempera- ture. alleles: Four spontaneous alleles recorded. allele discoverer synonym ref ( viability fertility RK ________________________________________________________________________________ *fr0 Bridges, 15a20 1, 2 3 fr1 Bridges, 22c30 2 16-90% female 3 nearly sterile fr2 Novitski, 37a22 trm: trimmed 2, 3, 5 good but female 2 erratic sterile *frdibro Bridges, 17k19 dibro 2, 4 poor sterile 3 ( 1 = Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. 278: 257 (fig.); 2 = CP627; 3 = Lewis, 1938, DIS 10: 55-56; 4 = Lynch, 1920, Genetics 4: 527-28; 5 = Novitski, 1937, DIS 8: 10, 13. # fragile chorion: see fch # frail: see fi # Frd: Freckled location: 2-102.4 (2.1 units to the left of bw). origin: X ray induced. discoverer: M. G. Davis, 1961. references: Erlich, 1963, DIS 37: 47. Barigozzi, 1963, Proc. Intern. Congr. Genet., 11th., Vol. 1: 207. 1965, DIS 40: 64. phenotype: Pupa and young fly characterized by accumulation of dark pigment; in older fly, pigment becomes concentrated in black specks scattered through body, head, and legs. Deposi- tion of electron-dense material in nucleus and cytoplasm of fat cells begins during pupal stage; pericardial cells of adult become filled with electron-opaque granules and vacuoles (Perotti and Bairati, 1968, J. Insect Path. 10: 122-38). The occasional weak manifestation of the Frd phenotype transmitted from Cy/Frd males to their Cy offspring and their descendents led Barigozzi and Girla (1968, Genet. Res. 11: 141-50) to postulate an extra chromosomal component of the Frd phenotype. Homozygous lethal. RK2. # frh: fruh (T. Schupbach) location: 2-62. origin: Induced by ethyl methanesulfonate. references: Schupbach, and Wieschaus, 1989, Genetics 121: 101-17. phenotype: Maternal-effect lethal mutant; homozygous females lay eggs which show no visible signs of development when observed under transmitted light in a stereo microscope; defective in fertilization or very early embryonic develop- ment. frh3 and frh6 sometimes give rise to embryos which form irregular blastoderms and develop very abnormally, producing fragmented pieces of cuticle. alleles: Six; frh1 through frh6 (isolated as RO, HM, PH, PM, SB, and APL respectively). # fringed: see fr # frizzled: see fz # fru: fruitless (J.C. Hall) location: 3-62.0. origin: X ray induced. synonym: fruity. references: Gill, 1963, DIS 38: 33. 1963, Am. Zool. 3: 507. Hall, 1978, Behav. Genet. 8: 125-41. Tompkins, Hall, and Hall, 1980, J. Insect. Physiol. 26: 689- 97. Hall, Siegel, Tompkins, and Kyriacou, 1980, Stadler Genet. Symp. 12: 43-82. phenotype: Males court but do not mate with females; fru males court other males (especially when such flies also are homozy- gous for fru) and stimulate vigorous courtship on the part of fru or wild-type males. Mutant males produce volatile com- pounds different from those generated by normal males, on cri- teria of gas chromatography and bioassays of behavioral effects of these compounds; females appear to be unaffected by fru, which is not allelic to sr. cytology: Placed in 90C to 91A, based on uncovering by Df(3R)P14. other information: Not allelic to sr. # Fructokinase: see Hex-C # fruh: see frh # fruhe2: see aur # fruitless: see fru # fruity: see fru