# lab: see ANTC # labial: see ANTC # Labore: see Fs(3)Sz18 # lac: lacquered location: 1-7.3. phenotype: Pale fly with chitin glistening as though polished. Bristles long and scraggly, frequently duplicated. Eyes smaller and slightly bright. Wings often longitudinally pleated. Slightly delayed eclosion; viability and fertility reduced in both sexes. RK2. allele origin ( discoverer synonym ref | comments ___________________________________________________________ lac1 CB1506 Fahmy 2 lac2 EMS Fahmy 2 lac3 EMS Fahmy 2 lac4 EMS Fahmy 2 lac5 EMS Fahmy 2 lac6 EMS Fahmy 2 lac7 EMS Fahmy 2 lac8 EMS 1 lac9 MMS Fahmy 2 lac10 MMS Fahmy 2 lac11 CB2511 Fahmy 2 lac12 CB3025 Fahmy 2 lac13 CB3026 Fahmy 2 lac14 CB3034 Fahmy 2 lac15 CB3034 Fahmy 2 lac16 X ray Fahmy 2 lac17 X ray Fahmy 2 ( CB = Chester Beatty mutagen number; CB1506 = 2-chloroethyl methanesulfonate; CB2511 = D-1:6-dimethanesulfonyul manni- tol; CB3025 = L-p-N,N-di-(2-chloroethyl)aminophenylalanine; CB3026 = D-p-N,N-di-(2-chloroethyl)aminophenylalanine; CB3034 = p-N,N-di-(2-chloroethyl)aminophenylethylamine. | 1 = Banga, Bloomquist, Brodberg, Pye, Larrivee, Mason, Boyd, and Pak, 1986, Chromosoma 93: 341-46; 2 = Fahmy, 1959, DIS 33: 87. cytology: Placed in 4C5-6 based on its inclusion in Df(1)rb13 = Df(1)4C5-6;4D3-E1 but not Df(1)GA56 = Df(1)4C5-6;4D1 and the failure of two translocations, T(1;2)biD2 and T(1;3)biD1, with breakpoints in 4C5-6 to complement lac (Banga et al.). # lace location: 2- {51.4}. synonym: l(2)br36; l(2)35Dc. phenotype: Strong alleles lethal; weak alleles viable with supernumerary fragments of wing veins. alleles: allele origin discoverer synonym comments _______________________________________________________________ lace1 spont Ashburner AM1 chromosome with Su(H)2 lace2 EMS Harrington HQ34 lace3 X ray Ashburner TB8 with T(Y;2)B8 lace4 EMS Simpson P42 lace5 EMS El Messal VM1 lace6 EMS El Messal VM2 lace7 EMS Simpson VT1 lace8 EMS Simpson VT2 lace9 EMS Simpson VT3 lace10 EMS Simpson VT4 lace11 EMS Simpson VT5 lace12 EMS Simpson VT6 lace13 EMS Simpson VT7 lace14 EMS Simpson VT8 lace15 EMS Simpson VT9 lace16 EMS Carteret VT10 viable lace17 EMS Simpson VT11 cytology: Placed in 35D3-4 by Ashburner. # lacquered: see lac # Lam: Lamin location: 2-{17}. origin: Gene identified by screening a /-gt11 cDNA expression library, constructed from early embryonic mRNA, with mono- clonal antibodies against Drosophila lamin. references: Gruenbaum, Landesman, Drees, Bare, Saumweber, Paddy, Sedat, Smith, Benton, and Fisher, 1988, J. Cell Biol. 106: 585-96. phenotype: The structural gene for nuclear lamin. Translated as a prolamin of apparent molecular mass of 76-kd, which is quickly processed to a 74-kd species, presumably by proteo- lysis. The processed polypeptide is assembled into the nuclear envelope, where it becomes phosphorylated and again attains a mass of 76 kd (Smith, Gruenbaum, Berrios, and Fisher, 1987, J. Cell Biol. 105: 771-90). molecular biology: Original cDNA clone identified two tran- scripts of 2.8 and 3.0 kb; although they encode identical polypeptides, they display differential expression profiles on developmental Northerns. They are equally abundant during oogenesis, but in the early embryo the 2.8-kb species is four times more abundant than the 3.0-kb species; the latter increases in intensity until the two are again equally abun- dant at mid gastrulation; by 7.5 h, only the 3.0-kb molecule persists. Full length cDNA clones of both have been recovered and sequenced; their differences reside in the lengths of their untranslated 3' regions. The gene encodes a polypeptide of 621 amino acids and calculated molecular mass of 70,974. Amino-acid sequence shows approximately 35% identity with human lamin; shows secondary structural features characteris- tic of intermediate filament proteins; contains a segment with 49% sequence identity with hamster vimentin. # Lam-: Laminin Three genes encode the three subunits of Drosophila laminin, which associate to form a cruciform molecule in which the carboxy-terminal ends are alpha helical and associate with one another and whose amino-terminal ends are free to form three short arms of the cross. genetic cytological molecular locus location location ( weight ______________________________________________ Lam-A 3- {20} 65A10-11 400 kd Lam-B1 2- {33} 28D 220 kd Lam-B2 3- {34} 67C 180 kd ( localized by in situ hybridization. references: Fessler, Campbell, Duncan, and Fessler, 1987, J. Cell Biol. 105: 2383-91. Montell and Goodman, 1988, Cell 53: 463-73. phenotype: The three genes are coordinately expressed with lit- tle or no transcript detectable prior to germ-band elongation. At eight hr, expression detected in the mesoderm and to a lesser extent in a subset of the ectoderm, including the epi- dermis. In the developing CNS grains associated with certain glial elements; no transcript seen after 18 hr. Immunocyto- chemical observations in embryos show laminin to be localized to basement membranes surrounding internal organs and muscles, in the underlying hypodermal epithelium and in the nervous system; also in basement membranes of larvae and adults. In the developing CNS, high levels are seen in the mesectodermal strand, in a pair of mesodermal cells near the segment border, in and around axon pathways, and in glial cells. Neurons and glia of the PNS also show abundant laminin immunoreactivity [Montell and Goodman, 1989, J. Cell Biol. 109: 2441-53 (fig.)]. # Lam-B1 molecular biology: All three genes cloned. LamB1 sequenced; conceptual amino acid sequence of 1784 residues comprises six domains: starting from the C-terminus, domains I and II separated by a short stretch termed ( comprise 67 kd are largely ( helical, show 25% and 22% homology with mouse B1 subunit, respectively, and comprise the segment of the chain that associates with the A and B2 subunits. The ( region has 27 amino acids including six cysteines and eight glycines; it shows 36% homology with the mouse ( sequence; five of the six cysteines and five of the eight glycines are conserved. Domains III (44 kd) and V (30 kd) contain eight and five cysteine-rich repeats that exhibit homology with epidermal growth factor; they are 54% and 53% homologous with the mouse polypeptide, respectively. Domains IV (25 kd) and VI (28 kd) show 58% and 26% homology with mouse, respectively and have been postulated to be collagen-binding domains. # Lam-B2 molecular biology: Sequence determined (Chi and Hui, 1989, J. Biol. Chem. 264: 1543-50; Montell and Goodman, 1989, J. Cell Biol. 109: 2441-53). Conceptual amino acid sequence contains 1639 residues. Domain structure similar to that of LAM-B1, except that LAM-B2 lacks the 27 amino acid cystein-rich ( domain that separates domains I and II in LAM-B1. There is also a large deletion in domain V and seven rather than eight EGF repeats in domain III; five more EGF repeats reside in domain V. Shows higher homology to mouse LAM-B2 than to Dro- sophila LAM-B1. # lame: see lme # Lamin: see Lam # Laminin: see Lam- # lance B: see lanceolate # lance: see nw2 # lance-b: see ll # lanceolate: see ll # lao: see Aldox # Lap-A: Leucine aminopeptidase A location: 3-98 (near Lap-D; no recombination yet observed). references: Beckman and Johnson, 1964, Hereditas 51: 221-30. Walker and Williamson, 1980, Insect Biochem. 10: 535-41. Walker, Williamson, and Church, 1981, Biochem. Genet. 19: 47-60. phenotype: Structural gene for leucine aminopeptidase A [LAP- A(E.C.3.4.1.1)], one of six such enzymes revealed by starch- gel electrophoresis. More anodally migrating than LAP-D; molecular weight 280,000 daltons; pH optimum 6.7. Enzyme apparently monomeric; no hybrid molecules formed in heterozygotes for electrophoretic variants. Appears 12 hrs after ovoposition; found in larvae and pupae but not adults. Localized in larval hemolymph; not induced by substrate feed- ing. alleles: Naturally occuring alleles: LapAF, LapAS, LapA0; fast, slow, and null alleles respectively. # Lap-D: Leucine aminopeptidase D location: 3-98.3 (Falke and MacIntyre). references: Beckman and Johnson, 1964, Hereditas 51: 221-30 (fig.). Falke and MacIntyre, 1966, DIS 41: 165-66. Muh, 1973, DIS 50: 200. Walker and Williamson, 1980, Insect Biochem. 10: 535-41. Walker, Geer, and Williamson, 1980, Insect Biochem. 10: 543- 46. Walker, Williamson, and Church, 1981, Biochem. Genet. 19: 47- 60. phenotype: Structural gene for leucine aminopeptidase D[LAP- D(E.C.3.4.1.1)], one of six such activities revealed by starch-gel electrophoresis and a staining with L-leucil-B- napthylamide and Fast Black K salt; enzyme monomeric; molecu- lar weight = 280,000 daltons; pH optimum 7.6; may be Zn metal- loenzyme. Found in larvae and pupae, but not adults; highest in young larvae. Localized to larval midgut where levels are induced by dietary substrate. alleles: Three alleles mentioned in literature, LapDF and LapDS plus an unnamed, uncharacterized one alluded to by Sakai, Tung, and Scandalios (1968, Genetics 60: 219-20). Lap- DF/Lap-DS produce equal amounts of slowly and rapidly migrat- ing LAP D and no enzyme of intermediate mobility. # Large: see Lg # Larval cuticle protein: see Lcp # Larval serum: see Lsp # Larval visceral protein: see Lvp # late hatching: see lh # Lcp: Larval cuticle protein A series of genes encoding electrophoretically separable proteins extractable from the cuticles of third-instar larvae, but not other stages. Four immunologically related proteins are encoded by a cluster of genes on 2R and another cluster of three unrelated to the preceding four, but related to each other, located on 3L. Designated numerically in order of increasing mobility on non-denaturing gels of encoded polypep- tide, with the exception of Lcp10. genetic cytological locus location location ref ( _______________________________________________ Lcp1 2-59.4 44D 2, 3, 4 Lcp1 | 2-59.4 44D 5 Lcp2 2-59.4 44D 2, 3, 4 Lcp3 2-59.4 44D 2, 3, 4, 5 Lcp4 2-59.4 44D 3, 4, 5 Lcp5 3-11 1, 2 Lcp6 3-11 1, 2 Lcp7 2 Lcp8 3-11 1, 2 Lcp10 3-11 1 ( 1 = Chihara and Kimbrell, 1986, Genetics 114: 393-404; 2 = Fristrom, Hill and Watt; 3 = Snyder, Hirsh, and David- son, 1981, Cell 25: 165-77; 4 = Snyder, Hunkapiller, Yuen, Silvert, Fristrom, and Davidson, 1986, Cell 29: 1027-40; 5 = Snyder, Kimbrell, Hunkapiller, Hill, Fristrom, and Davidson, 1982, Proc. Nat. Acad. Sci. USA 79: 7430-34. # Lcp1-4 phenotype: Encode larval cuticle proteins CP1, CP2, CP3, and CP4 (alternatively L3CP1 to L3CP4); molecular weights 17.5, 17.5, 9 and 13 kd respectively. Each has a 15-residue signal peptide. allele origin ref ( comments ____________________________________________ Lcp1F population 1 Lcp1S population 1 Lcp2F population 1, 2 with Lcp3n1 Lcp2S population 1, 2 Lcp31 population 1, 2 Lcp3n1 population 1, 2 with Lcp2F H.M.S. Beagle Lcp41 population 1 ( 1 = Fristrom, Hill, and Watt; 2 = Snyder, Kimbrell, Hunka- piller, Hill, Fristrom, and Davidson, 1982, Proc. Nat. Acad. Sci. USA 79: 7430-34. molecular biology: These four genes and a pseudogene are clustered within 7.9 kb of DNA located in region 44D. The genes are arranged in numerical order along the chromosome, but polarity with respect to the centromere is not known. Each gene is approximately 0.5 kb in length; Lcp1 and Lcp2 are separated by 2.9 kb, Lcp2 and Lcp3 by 0.87 kb, and Lcp3 and Lcp4 by 1.6 kb. All four genes contain a short intron between the third and fourth codon of the signal peptide. Lcp1 and Lcp2 show 91% amino acid homology, Lcp3 and Lcp4 show 85%, and between these two pairs there is approximately 60% homology (Snyder, Hirsh, and Davidson). A putative pseudogene, whose sequence suggests origin via unequal crossing over between Lcp1 and Lcp2, found between these two genes, 500-600 bp from Lcp2. Transcription of Lcp1, Lcp1psi and Lcp2, takes place off of the opposite strand and divergently from that of Lcp3 and Lcp4 (Snyder, Hunkapiller, Yuen, Silvert, Fristrom, and Davidson). Lcp2F gene product has been shown to differ from that of the more common Lcp2S allele by two amino acid substi- tutions; Lcp3n1 contains a 7.3 kb DNA insertion, identified as H.M.S. Beagle, located within the TATA box (Snyder, Kimbrell, Hunkapiller, Hill, Fristrom and Davidson). # Lcp5 alleles: Lcp+ is the commonly encountered allele; the other alleles are infrequent. Electrophoretic variants, when homoz- ygous, may reveal two bands, one at the new position and one at the original position; these alleles are designated r for residual. Others leave no residual band and are designated nr. allele origin ref ( comments ________________________________________________ Lcp5+ population 1, 3 Lcp5FF population 1, 2 very fast Lcp5Fnr population 1, 3 fast, no residual Lcp5Fr population 1 fast, residual Lcp5op population 1, 2 over producer Lcp5Snr population 1, 2 slow, no residual Lcp5Sr population 1, 3 slow, residual ( 1 = Chihara and Kimbrell, 1986, Genetics 114: 393-404; 2 = del Puerto, 1985, Thesis, University of San Francisco; 3 = Fristrom, Hill, and Watt, 1978, Biochemistry 17: 3917- 24. # Lcp6 location: 3-11 (not separated from Lcp5 among 487 F1). allele: Lcp6+ is the common allele; the remainder rare or rela- tively so. allele origin ref ( comments ________________________________________________ Lcp6+ population 1, 3 Lcp6f population 1, 2 faint, polymorphic Lcp6n population 1, 2 null allele Lcp6S population 1, 2 slow ( 1 = Chihara and Kimbrell, 1986, Genetics 114: 393-404; 2 = del Puerto, 1985, Thesis, University of San Francisco; 3 = Fristrom, Hill, and Watt, 1978, Biochemistry 17: 3917- 24. # Lcp7 phenotype: Structural gene for CP7, which is antigenically related to CP5, CP6, and CP8. alleles: One active allele plus a null allele, Lcp7n (Fristrom, Hill, and Watt, Biochemistry 17: 3817-24). # Lcp8 location: 3-11 (not separated from Lcp5 in 563 F1). allele origin ref ( comments ______________________________________ Lcp8+ population 1, 2 Lcp8S population 1 slow ( 1 = Chihara and Kimbrell, 1986, Genetics 114: 393-404; 2 = Fristrom, Hill, and Watt, 1978, Biochemistry 17: 3917- 24. # Lcp10 location: 3-11 (not separated from Lcp5 in 524 F1). synonym: Rho. references: Chihara and Kimbrell, 1986, Genetics 114: 393-404. phenotype: No gene product detectable in wild type, only in the ethyl methanesulfonate-induced allele, Lcp10rho; migrates between CP3 and CP4. Not clear that the mutant product is confined to third-instar larval cuticle. alleles: allele origin comments ___________________________________________ Lcp10+ population naturally repressed Lcp10rho EMS derepressed # ld: loboid location: 3-102 [between ca and bv (Lewis, 1956, DIS 30: 130)]. origin: Spontaneous. discoverer: Curry, 39a. references: 1939, DIS 12: 45. phenotype: Eyes resemble L/+. Malformation of eyes ranges from slight dorsoventral seam across middle of eye to a more extreme effect in which growth of anterior part is completely inhibited in most-extreme cases. Antenna-like outgrowth fre- quent where growth of eyes is suppressed. Tends to overlap wild type. In the presence of a sex-linked modifier, opht [opht; ld designated ldoph by Kobel (1968, Genetica 39: 329- 44)] ld flies show homeotic transformation of eye to wing tis- sue (Ouweneel, 1969, Wilhelm Roux's Arch. Entwicklungsmech. Org. 164: 1-114 and 14-36; 1970, 166: 76-88; 1970, Genetica 41: 1-20). RK3. alleles origin discoverer synonym ref ( comments __________________________________________________________________ ld1 spont Curry, 39a 1 *ld52a spont Edmonson, 52a 2 like ld1 ldeyr spont eyr 3, 4 details below ( 1 = Curry, 1939, DIS 12: 45; 2 = Edmonson, 1952, DIS 26: 60; 3 = Edwards and Gardner, 1963, DIS 37: 47; 4 = Edwards and Gardner, 1966, Genetics 53: 785-98. cytology: Tentative; placed in 99C-F based on its genetic localization. #*ldeyr: loboid-eyes reduced origin: Found among flies grown on food containing copper sul- fate. phenotype: Eyes vary from normal to absence of ommatidia. Shows some degree of dominance; many heterozygotes have some eye abnormality, usually a nick in anterior region of one or both eyes; an abnormal growth of wing tissue may be associated with the nick. ldeyr; ey4 flies have very small heads, usu- ally without ommatidia. Viability greatly reduced. RK2. # lds: lodestar location: 3-47. synonym: early. references: Tearl and Nusslein-Volhard, 1987, DIS 66: 209-26. phenotype: Maternal. In nuclear cycles 9-10, multiple complex anaphase spindles share several centrosomes. Multiple groups of chromosomes are often directed to same pole. Elongated polyploid nuclei develop. Mitotic abnormalities in larval brain cells (Gatti). alleles: Four alleles, lds1-lds4, isolated as 042, 072, 098, and 298. cytology: Placed in 88D13-14 (Ashburner). # lea: leak location: 2-3. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. phenotype: Embryonic lethal. Head involution incomplete. In combination with Pc-like mutants, abdominal transformations occur. alleles: Two, lea1 and lea2, isolated as 25 and IIS. cytology: Placed in 21F2-22B1 based on its inclusion in Df(2L)S2 = Df(2L)21C6-D1;22A6-B1 but not Df(2L)S3 = Df(2L)21D2-3;21F2-22A1. # leg: see run # leg tumor: see lgt #*lem: lemon location: 1-17.5. origin: Spontaneous. discoverer: E. M. Wallace, 12h. references: Morgan and Bridges, 1916, Carnegie Inst. Washington Publ. No. 237: 48 (fig.). phenotype: Body color pale yellow with dark trident and black bristles. Wings and veins pale yellow. Easily distinguished from wild type, viability about 70% wild type, and most flies sterile. RK3. # Les: Lesbian (J.C. Hall) location: Complex genetic etiology. origin: Isolated from a series of related, balancer-containing strains (used to maintain the Fs(2)B mutation). references: Cook, 1975, Nature 254: 241-42. phenotype: Females exhibit male-like courtship, including uni- lateral wing display, directed at other females; courtship bouts relatively short; not all females of the strain show the anomalous behavior; these behaviors have been observed in females of other strains (Cook, 1981, Z. Naturforsch. 36C: 475-83). # lethal ( ): see l( ) # Lethal hybrid rescue: see Lhr # Leucine aminopeptidase A: see Lap-A # Leucine aminopeptidase D: see Lap-D # Levente: see Fs(3)Sz28 # lf: little fly location: 1-68.1. phenotype: Small fly with markedly narrow abdomen, frequently with small tumors. Eclosion delayed; low viability and fer- tility in both sexes, especially females; some alleles lethal. RK3. allele origin ( discoverer synonym ref | comments ____________________________________________________________________________ lf1 N Mustard Fahmy, 1954 1 lf2 CB1506 Fahmy, 1954 1 lf3 EMS Fahmy, 1954 1 lf4 EMS Fahmy, 1954 1 lf5 CB1592 Fahmy, 1954 1 lf6 CB3007 Fahmy, 1954 1 lf7 CB3025 Fahmy, 1954 1 lf8 CB3051 Fahmy, 1954 1 lf9 X ray Fahmy, 1954 1 lf10 X ray Lifschytz l(1)A58 3, 4, 5 probably multilocus lf11 EMS Lifschytz l(1)M122 5 on y+Ymal+ lf12 X ray Lefevre l(1)L40 2 lf13 X ray Lefevre l(1)HC142 2 ( CB1506 = 2-chloroethyl methanesulfonate; CB1592 = ?; CB3007 = DL-p-N,N-di-(2-chloroethyl)aminophenylalanine; CB3025 = L-p-N,N-di-(2-chloroethyl)aminophenylalanine; CB3051 = ?. | 1 = Fahmy, 1959, DIS 33: 87; 2 = Lefevre, 1981, Genetics 99: 461-80; 3 = Lifschytz and Falk, 1968, Mut. Res. 6: 235-44; 4 = Lifschytz and Falk, 1969, Mut. Res. 8: 147-55; 5 = Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84. cytology: Placed in 19E5-6 based on its inclusion within Df(1)T2-14A = Df(1)19E5-6;19E7-8 but not in Df(1)Q539 = Df(1)19E6;19F6-20A1. # lfb: little faint ball location: 3-26. origin: Induced by ethyl methanesulfonate. references: Jurgens, Kluding, Nusslein-Volhard, and Wieschaus, 1983, DIS 59: 157-58. phenotype: Embryonic lethal; embryo resembles faint little ball? Dorsal closure incomplete. alleles: Five. # Lff11: see l(1)ff11 # lfl: Little fly like location: 1- {66}. phenotype: Lethal under crowded conditions, but semilethal (20-30% survival) under optimal conditions. Survivors delayed three days in emergence. Adults small like lf but without the narrow abdomen. lfl2/Df not particularly small; lack thoracic hairs and bristles on head and thorax; also have rough eyes; lfl2 males: survival of 1% expected; phenotype as in above females. FM6/lfl2 females and y+Ymal106/lfl2 males frequently lack ocellar, postvertical and humeral bristles; posterior crossveins may be interrupted and vein L5 usually interrupted; some thoracic hairs absent. FM6/lf1 females normal. alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________________ lfl1 X ray Lifschytz l(1)B56 4, 5, 7 lfl2 X ray Lifschytz l(1)B96 4, 5, 7 lfl3 Lifschytz l(1)J22 6 lfl4 X ray Lefevre l(1)C94 2 lfl5 X ray Lefevre l(1)C231 2 T(1;3)19F1-2;80 lfl6 X ray Lefevre l(1)JA128 2 lfl7 X ray Lefevre l(1)N109 2 lfl8 EMS Lefevre l(1)DF970 3 lfl9 EMS Lefevre l(1)EF446 4 lfl10 EMS Lefevre l(1)VA241 5 lfl11 HMS Kramers l(1)HM46 1 ( 1 = Kramers, Schalet, and Huiser-Hoogteyling, 1983, Mut. Res. 107: 187-201; 2 = Lefevre, 1981, Genetics 99: 461-80; 3 = Lefevre, and Watkins, 1986, Genetics 113: 869-95; 4 = Lifschytz and Falk, 1968, Mut. Res. 6: 235-44; 5 = Lifschytz and Falk, 1969, Mut. Res. 8: 147-55; 6 = Lifschytz and Yakobovitz, 1978, Mol. Gen. Genet. 161: 275-84; 7 = 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 19F1-3 based on its inclusion in Df(1)DCB35b = Df(1)19F1-2;20E-F but not in Df(1)17-257 = Df(1)19F3;20A1-2. #*Lg: Large location: 1-27. origin: Induced by P32. references: Bateman, 1950, DIS 24: 55. phenotype: Heterozygote large, late eclosing, with visibly smaller hairs; viability excellent. Tendency toward shorten- ing of L4 and L5, missing postvertical bristles, and islands of vein tissue on either side of L2. Homozygous lethal. RK2. #*lgh: long haired location: 1-20.7. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1959, DIS 33: 87. phenotype: Small fly; size reduction most noticeable in head and thorax. Wings short and slightly altered in shape. Ante- rior thorax frequently dented in the mid-dorsal line. Hairs deranged; bristles long and scraggly. Abdomen nearly always abnormally pigmented, ranging from no melanization of tergites 5-7 to small, irregular, under-pigmented patches on these ter- gites. Male viability about 25% wild type. Males sterile. RK3. # lgl: see l(2)gl # lglG: see ovoDrv22 #*lgt: leg tumor location: 2- (not located). origin: Spontaneous. discoverer: Spencer, 36c20. references: 1937, DIS 7: 14. phenotype: Black tumor growth inside thorax ventrally at bases of posterior legs. Sterile in both sexes; poor viability. RK3. # lh: late hatching location: 1-57. origin: Spontaneous. discoverer: Bridges, 31d6. phenotype: Slow-developing semigiant. RK3. # LHP: see Lsp2 # Lhr: Lethal hybrid rescue location: 2-95 (in Drosophila simulans). origin: Spontaneous. references: Watanabe, 1979, Jpn. J. Genet. 54: 325-31. Takamura and Watanabe, 1980, Jpn. J. Genet. 55: 405-08. phenotype: When Drosophila simulans carries Lhr, classes of hybrids between D. simulans and D. melanogaster that do not ordinarily survive are recovered. Crosses of D. melanogaster females by D. simulans males, which ordinarily produce only daughters, produce sons and daughters in a 1:1 ratio. Crosses of D. simulans females to D. melanogaster males, which ordi- narily produce only sons, produce 86% sons and 14% daughters. Crosses of C(1)RM - bearing D. melanogaster females to D. simulans males, which normally produce only sons, yield a few daughters when the D. simulans males carry Lhr. # light: see lt # lightoid: see ltd # limited: see lm # lin: lines (C. Nusslein-Volhard) location: 2-59. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. phenotype: Embryonic lethal; small anterior portion of each segment deleted; A8, spiracles, and anal plates absent. Head abnormal. alleles: Three alleles, lin1-lin3, isolated as 5E, IIF, and IIV. cytology: Tentatively placed in 44F-46D. # little faint ball: see lfb # little fly: see lf # little fly like: see lfl # lix: little isoxanthopterin location: 1-23. origin: Spontaneous. discoverer: Hessler, 1959. references: 1960, DIS 34: 50. Hubby, 1962, Genetics 47: 109-14. phenotype: Most likely the structured gene for dihydropterin oxidase. Flies indistinguishable from wild type; dissected testis sheath dark yellow-orange, but this character is not dependable for classification; causes striking changes in com- pounds that fluoresce in ultraviolet light on paper chromato- grams of testes. Isoxanthopterin content of testis sheath greatly reduced. No detectable dihydropterin oxidase activity (Ordono, Silva, and Ferre, 1988, DIS 67: 63). A blue fluorescent compound not otherwise detected in D. melanogaster (the lix substance) is present. Drosopterins present in the testis sheath, and quantities of sepiapteridine, biopterin, "Compound A," and a "riboflavinlike" compound are elevated. The colored pteridine gives testis sheath its darker color. Pteridine accmulation in testis sheath alone is affected. RK3. cytology: Placed in 7D10-F2 based on its inclusion in Df(1)RA2 = Df(1)7D10;8A4-5 but not Df(1)KA14 = Df(1)7F1-2;8A6 (Silva, Escriche, Ordono, and Ferre). # liz: see fs(1)A1621 # ll: lanceolate location: 2-106.7. origin: Spontaneous. discoverer: Bridges, 23d3. synonym: lance-b. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 227. Bridges, 1937, Cytologia (Tokyo, Fujii Jub., Vol. 2: 745-55. phenotype: Wings narrowed at tips and slightly divergent. Eyes slightly smaller than normal and bulging; head narrow. Wad- dington finds wing effect detectable in middle pupal stage. RK3. cytology: Placed in region between 59E2 and 60B10 on the basis of its being to the right of In(2R)bwVDel = In(2R)41B2- C1;59E2-4 and to the left of Df(2R)Px = Df(2R)60B8-10;60D1-2. ll2: lanceolate-2 Edith M. Wallace, unpublished. # ll2 origin: Spontaneous. discoverer: Bridges, 23d25. phenotype: Wings pointed and narrow. Eyes small and bulging. Head narrow. Wing shape first seen in early contraction stage of wing development (23-hr pupa at 25) (Waddington, 1939, Proc. Nat. Acad. Sci. USA 25: 303). More extreme and more useful than ll. RK2. # llb: see l(3)89Ea # lm: limited location: 2-50. origin: Spontaneous. discoverer: Bridges, 29l25. phenotype: Sternites small, rounded, or irregular; bristles sparse. Females sterile. RK3. cytology: Not included in Df(2L)64j = Df(2L)34E5-F1;35C3-D1 (E. H. Grell). #*lme: lame location: 1-47.8. origin: Induced by 2-chloroethyl methanesulfonate (CB. 1506). discoverer: Fahmy, 1956. references: 1959, DIS 33: 87. phenotype: Legs weak, frequently deformed, and generally shor- tened as a result of reduction in length of tarsal segments. Wings atypically shaped and abnormally held. Flies so crip- pled they cannot move; they die soon after eclosion. RK3. # lme: see l(2)me # Lms: see kl- # Lobe: see L # loboid: see ld # lobula-plateless: see lop # lon: longevity location: 1-21.7. origin: Induced by ethyl methanesulfonate. references: King, Bahns, Horrowitz, and Larramendi, 1978, Int. J. Insect Morphol. Embryol. 7: 359-75. phenotype: Homozygotes and hemizygotes exhibit delay in eclo- sion of four days; become paralyzed at nine to ten days of age and die on day eleven or twelve. cytology: Distal to the breakpoint of T(1;Y)B138, which is in 7F6-8. # long haired: see lgh # lop: lobula-plateless (J.C. Hall) location: 2-ca. 70. origin: Induced by ethyl methanesulfonate. synonym: N684. discoverers: Heisenberg and Fischbach. references: Fischbach and Heisenberg, 1984, J. Exp. Biol. 112: 65-93. Bulthoff and Buchner, 1985, J. Comp. Physiol. 156: 25-34. Helfrich, 1986. J. Neurogenet. 3: 321-43. phenotype: Lobula plate (third-order optic ganglion) missing most of its usual neuropile (Fischbach and Heisenberg, 1984), including an absence of most "small-field" visual neurons; but the giant fibers of this lobe remain; certain of these (i.e. "VS"-cells) enter the neuropile of a more peripheral lobe (the medulla), as opposed to their orthodox (more central) targets; optomotor roll and pitch responses to movements in the visual field are weak or absent. Visually mediated stimulus-specific labelling (in 2-deoxyglucose experiments) does not occur in lobula plate, though it is normal in the mutant's lamina (first order optic lobe) and medulla (Bulthoff and Buchner, 1985). Circadian rhythms of locomotor activity are quite robust and have normal ca. 24 hours free-running periodicities (Helfrich, 1986). alleles: One mutant allele, lop1 (=lopN684). # lot (J.C. Hall) location: 1-unlocalized. synonym: lot-235. origin: Induced by ethyl methanesulfonate. references: Falk and Atidia, 1975, Nature 254: 325-26. phenotype: Like Lot but non-allelic and recessive. # Lot (J.C. Hall) location: 1-55.5 (to left of f between 55.5 - 56.0). origin: Induced by ethyl methanesulfonate. synonym: Lot-94. references: Falk and Atidia, 1975, Nature 254: 325-26. Atidia and Baker, 1974, DIS 51: 72. Falk, 1979, J. Insect Physiol. 25: 87-91. phenotype: Adults consume solutions of sodium chloride 10X more concentrated than will wild type; largely due to fact that Lot/Lot > Lot/+ > +/+ in liquid consumption; named Lot (Genesis 19 v 26) based on a perceived reduction in aversion to salt. Subsequently found that the amount of NaCl that had to be added to 0.1 M sucrose to switch preference from 0.1 M to 0.01 M sucrose same as wild type (Falk, 1979, J. Insect Physiol. 25: 87-91). alleles: Lot1, semidominant; Lotr (= Lot114), completely reces- sive. # low aldehyde oxidase: see Aldox # low xanthine dehydrogenase: see lxd # lozenge: see lz # lozenge-like: see rstl # lozengelike: see lzl # lpo: see Po # lrb: see l(3)89Ee # Lsp1: Larval serum protein 1 Genes encoding three related polypeptides that combine in random hexamers to form LSP1, a heterogenous larval serum pro- tein of 450,000 to 480,000 daltons (Wolfe, Akam, and Roberts, 1977, Eur. J. Biochem. 79: 47-53). LSP1 synthesized in fat body; appears early in third instar attaining peak levels at the white prepupal stage; level begins to decline at mid-pupal stage reaching base line about four days into adult lift (Roberts, Wolfe, and Akam, 1977, J. Insect Physiol. 23: 871- 78). Highly homologous to one another and all three share amino-acid homology with LSP2. Antigenically related as well but antisera to LSP1 polypeptides do not crossreact with LSP2 (Brock and Roberts, 1980, Eur. J. Biochem. 106: 129-35). Lsp1(: Larval serum protein-1 ( chain (D.B. Roberts) location: 1-39.5 (27/47 of the distance from v to g). discoverer: Evans-Roberts, 1977. references: Roberts, Wolfe, and Akam, 1977, J. Insect Physiol. 23: 871-78. Roberts and Evans-Roberts, 1979, Genetics 93: 663-79. Smith, McClelland, White, Addison, and Glover, 1981, Cell 23: 441-49. McClelland, Smith and Glover, 1981, J. Mol. Biol. 153: 257- 72. Roberts and Evans-Roberts, 1979, Nature 280: 691-92. Ghosh, Chatterje, Bunick, Manning and Lucchesi, 1989, EMBO J. 8: 1191-96. phenotype: Codes for the ( polypeptide of LSP1; molecular weight 83,000 (Brock and Roberts, 1980, Eur. J. Biochem. 106: 129-35). alleles: Electrophoretic variants isolated from natural popula- tions: Lsp1(F, Lsp1(S1, and Lsp1(S2. cytology: Localized to 11A7-9 by in situ hybridization (Smith et al.). Included in Df(1)HF368 = Df(1)11A2;11B9 but not Df(1)v65b = Df(1)9F13-10A1;11A7-8 (Roberts and Evans-Roberts). molecular biology: The Lsp1( gene has been cloned; the cloned DNA cross hybridizes to the Lsp1| and / genes; encodes a 2.85 kb polyadenylated mRNA (Smith et al.); clone DNA partially characterized and shows that the gene has a short intervening sequence of about 50 bp 400 nucleoties from the 5' end (McClelland et al.). 1.5 kb at 5' end of gene sufficient for normal control of tissue and stage specificity (Yedvobnick and Levine, 1982, Nature 297: 239-41). Transformants carrying the bacterial Cat gene linked to 377 base pairs of upstream sequence from Lsp1( express CAT with the same developmental and tissue specificity as the endogenous Lsp1( gene (Delaney, Sunkel, Genova-Seminova, Davies, and Glover, 1987, EMBO J. 6: 3849-54). other information: Although X-linked Lsp1( is not dosage com- pensated (Roberts and Evans-Roberts); however when relocated by transformation to an autosomal site or to an ectopic site on the X, the gene does show dosage compensation (Ghosh et al., 1989). Lsp1| (D.B. Roberts) location: 2-1.9 (4/28 of the distance from al to dp). references: Roberts, Wolfe, and Akam, 1977, J. Insect Physiol. 23: 871-78. Roberts and Evans-Roberts, 1979, Genetics 93: 663-79. Smith, McClelland, White, Addison, and Glover, 1981, Cell 23: 441-49. McClelland, Smith, and Glover, 1981, J. Mol. Biol. 153: 257- 72. Brock and Roberts, 1981, Chromosoma 83: 159-68. phenotype: Codes for the polypeptide of LSP1|; a phosphorylated polypeptide of molecular weight 80,000 (Brock and Roberts, 1980, Eur. J. Biochem. 106: 124-35). alleles: Naturally occurring electrophoretic variants: Lsp1|+ (the predominant allele), Lsp1|F and Lsp1|n, a null allele. cytology: Located to 21D3-5 by in situ hybridization (Smith et al.). molecular biology: The Lsp1| gene has been cloned; the cloned DNA cross hybridizes to the Lsp1( and / genes; encodes a 2.85 kb polyadenylated mRNA (Smith et al.); cloned DNA par- tially characterized; shows a short intervening sequence of about 50 bp 400 nucleotides from the 5' end of the gene (McClelland et al.). Transformants carrying the bacterial Cat gene linked to 471, but not 66, base pairs of upstream sequence from Lsp| express CAT with the same developmental and tissue specificity as the endogenous Lsp| gene (Delaney, Sunkel, Genova-Seminova, Davies, and Glover, 1987, EMBO J. 6: 3849-54). other information: Dp(2;2;2;2;2)S probably carries five copies of the Lsp1| gene (Brock and Roberts). Lsp1/ (D.B. Roberts) location: 3-1.4 (2/15 of the distance from Dp(1;3)scJ4 to ve). references: Roberts, Wolfe, and Akam, 1977, J. Insect Physiol. 23: 871-78. Roberts and Evans-Roberts, 1979, Genetics 93: 663-79. Smith, McClelland, White, Addison, and Glover, 1981, Cell 23: 441-49. McClelland, Smith, and Glover, 1981, J. Mol. Biol. 153: 257- 72. phenotype: Codes for the / chain of LSP1; a phosphorylated polypeptide of molecular weight 77,000 (Brock and Roberts, 1980, Eur. J. Biochem. 106: 129-35). alleles: In addition to Lsp/+, four null alleles recorded: Lsp/01, Lsp/02, Lsp/03, and Lsp/04. Lsp2F said to be homozy- gous lethal (Brock and Roberts, 1980, Eur. J. Biochem. 106: 129-35). cytology: Localized to 61A1 by in situ hybridization (Smith et al.); 61A1-3 (Brock); uncovered by the deficiency generated by T(Y;3)S50 (Roberts and Evans-Roberts). molecular biology: The Lsp1/ gene has been cloned; cloned DNA cross hybridizes to the Lsp1( and | genes; encodes a 2.85 kb polyadenylated mRNA (Smith et al.); cloned DNA partially characterized; shows short intervening sequence of about 50 bp 400 nucleotides from the 5' end of the gene (McClelland et al.). # Lsp2: Larval serum protein-2 (D.B. Roberts) location: 3-37 (3/17 of the distance from vin to gv). discoverer: Akam, 1977. synonym: Pt-1, LHP. references: Hubby, 1963, Genetics 48: 871. Roberts, Wolfe, and Akam, 1977, J. Insect Physiol. 23: 871- 78. Akam, 1977, D. Phil. Thesis, Oxford University. Akam, Roberts, Richards, and Ashburner, 1978, Cell 13: 215- 25. Akam, Roberts, and Wolfe, 1978, Biochem. Genet. 16: 101-19; Lepesant, Levine, Garen, Lepesant-Kejzlarova, Rat, and Somme- Martin, 1982, J. Mol. Appl. Genet. 1: 371-83. Paco-Larson, Nakanishi, Levine, and Garen, 1986, Dev. Genet. 7: 197-203. Paco-Larson, Nakanishi, Levine, and Garen, 1986, Dev. Genet. 7: 197-203. phenotype: Codes for LSP2, a glycosylated polypeptide of 80,000 molecular weight (Brock and Roberts, 1980, Eur. J. Biochem. 106: 129-35) and one of the major serum proteins of third- instar larvae; a homohexamer of molecular weight 450,000 with subunit molecular weight of 78-83 X 103 daltons. LSP2 appears during the third larval instar and levels increase until mid- way through the pupal stage; then levels decline reaching base line early in adult life. Transcription detectable only in third-instar fat body, ecdysone dependent; in presence of temperature-sensitive ecd, Lsp2 transcription off at re- strictive temperature; resumes following ecdysterone adminis- tration or shift to permissive temperature; juvenile hormone blocks ecdysterone stimulation. alleles: Naturally occurring alleles, Lsp2F and Lsp25. cytology: Localized to 68E3-4 by deficiency mapping (Akam et al. 1978); 68E by in situ hybridization (Lepesant et al.). molecular biology: The Lsp2 gene has been cloned (Lepesant et al.). # lt: light location: 2-55.0. references: Bridges, 1931, Eos 7: 229-48. de Zulueta, 1931, Eos 7: 249-53. phenotype: Eye color yellowish pink-lighter at high tempera- ture, darker at low. Ocelli colorless; Drosopterins drasti- cally reduced; no maternal effect on eye pigmentation (Nickla, 1972, Can. J. Genet. Cytol. 14: 105-11). When combined with st, eye color only slightly lighter than with lt alone; with bw it is clear yellow, pinkish in old flies (Schultz and Dobzhansky, 1934, Genetics 19: 344-64; Mainx, 1938, Z. Indukt. Abstamm. Vererbungsl. 75: 256-76). Eye color auto- nomous in mutant optic discs transplanted into wild-type hosts (Beadle and Ephrussi, 1936, Genetics 21: 230). Larval Mal- phighian tubes colorless in lt offspring of lt mothers; some color in tubes if mother is lt/+. The quantity of yellow pig- ment, composed primarily of riboflavin, in Malpighian tubes exhibits parallel maternal effects in larvae, pupae, and adults (Nickla, 1972, Can. J. Genet. Cytol. 14: 391-96); the amount of such pigment increases with maternal age for both lt/+ and lt/lt parental females (Nickla, 1973, Can. J. Genet. Cytol. 15: 437-42). lt stw homozygotes completely inviable (Purdom); however, lt stw3 homozygotes have good viability. car lt double mutants are also invariably lethal; the time of death varying from the third larval instar to late pupa, depending on the number of normal alleles of either gene car- ried by the mother (Nickla, 1977, Nature 268: 638-339). Lethal focus of the lethal interaction as measured in car/+; lt/lt, car/0; lt/lt gynandromorphs is in ventral nervous tis- sue (Nickla, Lilly, and Brown, 1980, Experientia 36: 402-03); larval brain histologically abnormal (McCarthy and Nickla, 1980, Experientia 36: 1361-62). alleles: allele origin discoverer synonym ref ( comments ____________________________________________________________________________ lt1 spont Bridges, 24d8 2, 3, 4 *lt2 spont Bridges, 30b14 2, 3 weak allele lt3 spont Beadle, 36e23 3 in In(2L+2R)Cy, al2Cy cn2L4sp2 intermediate allele lt4 UV Meyer, 50d 3, 9 homozygotes short lived, sterile *lt5 UV Meyer, 51d 3, 8 lethal allele lt6 EMS Hilliker 5 lt7 EMS Hilliker 5 lt8 EMS Hilliker 5 lt9 EMS Hilliker 5 lt10 EMS Hilliker 5 lt11 EMS Hilliker l(2)EMS40-12 5 lethal lt12 EMS Hilliker l(2)EMS40-17 5 lethal lt13 EMS Hilliker l(2)EMS56-03 5 lethal lt14 P Wakimoto lthd51 no P insert lt15 P Wakimoto lthd52 P insert lt16 EMS ltH lt17 X ray ltX54 lt18 X ray ltX69 lt19 spont ltVO17 lt20 P lthd1 P insert lt21 P lthd2 P insert *lt56c spont Meyer 3, 7 with Alu56c, strong allele ltm100 X ray Spieler, 60a25 1 homozygous lethal *ltpk spont Lancefield, pinkoid 2, 3, 6 intermediate allele, 18c18 pink wing reduced viability ( 1 = Baker and Rein, 1962, Genetics 47: 1399-1407; 2 = Bridges, 1931, Eos 7: 229-48; 3 = CP 627; 4 = de Zulueta, 1931, Eos 7: 249-53; 5 = Hilliker, 1976, Genetics 83: 765-82; 6 = Lancefield, 1918, Bio. Bull. 35: 207-10; 7 = Meyer, 1956, DIS 30: 77; 8 = Meyer and Edmondson, 1951, DIS 25: 73; 9 = Meyer, Edmondson, Byers, and Erickson, 1950, DIS 24: 60. cytology: Located in 40F; proximal to the secondary construc- tion on 2L (Hilliker and Holm, 1975, Genetics 81: 705-21). Placed in h35 of 2L heterochromatin (Pimpinelli). molecular biology: Region cloned by transposon tagging; lesions of some mutations characterized (Wakimoto). # ltm: light mottled A series of X-ray induced light-variegated chromosome rear- rangements (Hessler, 1958, Genetics 43: 395-403). Some have a mixture of light and wild-type ommatidia and are classified as pale; others have a mixture of wild-type and occasional darker ommatidia and are classified as dark. allele ( phenotype cytology ______________________________________________ ltm1 pale T(2,3)40B-F;63E-F ltm2 dark In(2L)22F-23A;40B-F ltm3 dark In(2LR)40B-F;60D ltm4 dark T(2;3)40B-F;67E ltm5 pale T(2;3)40B-F;98C ltm6 pale T(2;3)26E-F;40B-F;96E ltm7 pale T(2;3)40B-F;100F ltm8 dark T(2;3)40B-F;92B ltm9 dark In(2LR)40B-F;56E ltm10 dark T(2;3)40B-F;64E ltm11 dark T(2;3)40B-F;96F ltm12 dark In(2LR)40B-F;60D ltm13 dark T(2;3)40B-F;64F ltm14 dark T(2;3)40B-F;95F ltm15 pale T(2;3)40B-F;95F ltm16 pale T(1;2)11A;12F;22D;40B-F ltm17 pale T(2;3)40B-F;95C-D ltm18 dark T(2;3)40B-F;98A ltm19 dark T(2;3)40B-F;94B ltm20 pale In(2L)32C;40B-F ltm21 dark T(2;3)40B-F;93D ltm22 dark In(2LR)40B-F;59D ltm23 pale T(2;3)40B-F;62F ltm24 pale T(2;3)40B-F;59F;75C ltm25 pale In(2LR)40B-F;57C-D ltm26 pale In(2L)27C;40B-F ltm27 pale T(2;3)40B-F;88E-F ltm28 pale T(2;3)40B-F;97E ltm29 pale T(2;3)40B-F;99F ltm30 dark T(2;3)40B-F;99C ltm31 pale T(1;2)8F;28D;40B-F ltm32 pale T(2;3)40B-F;97A ltm33 pale In(2LR)40B-F;58E ltm34 pale T(2;3)40B-F;61B ltm35 pale T(2;3)40B-F;64C ltm100 | T(2;3)40B-F;97F ( All alleles except ltm29 and ltm100 lost (CP627). | Also see data on previous lt table. # ltv: light variegated origin: X ray induced as part of the construction of SM5. references: Mislove and Lewis, 1955, DIS 29: 75. # ltd: lightoid location: 2-{59}. origin: Spontaneous. discoverer: Nichols-Skoog, 36d6. phenotype: Eye color clear, light, translucent yellowish pink. Resembles lt but is lighter, darkens with age. Ocelli color- less; larval Malpighian tubes colorless. Deficient in ommo- chrome synthesis. Lack detectable levels of 3OH kynurenine despite normal levels of kynurenine hydroxylase activity; administration of 3 hydroxykynurenine without effect (Phil- lips, Simmons, and Dowman, 1970, Biochem. Genet. 4: 481-87; Sullivan, Kitos, and Sullivan, 1973, Genetics 75: 651-61). Exhibits reduced levels of phenoazinone synthetase, an enzyme involved in the condensation of 3OH kynurenine molecules to xanthommatin, as do other mutants deficient in ommochrome syn- thesis (Phillips, Forrest, and Kulkarni, 1973, Genetics 73: 45-56). Uptake of kynurenine, which is produced in the fat body, by the Malpighian tubes, where it is converted to 3-hydrokynurenine, is defective; similar defect seen in eye discs (Sullivan and Sullivan, 1975, Biochem. Genet. 13: 603- 13). Sullivan and Sullivan postulate that ltd is a transport mutant that prevents the substrate kynurenine from reaching the sites of its conversion to ommochrome. Phenotypic interaction with other eye-color mutants examined by Rudy and Carvalier (1971, J. Hered. 62: 131-34) and by Silva and Mensua, 1985, DIS 61: 156); produces nearly white eyes when combined with either rb or g. cytology: Placed in 44E-46E based on inclusion in Dp(2;3)eve1.18 = Dp(2;3)44B;46D-E; chrom3 (Hooper) but not in Dp(2;3)P32 = Dp(2;3)41A;42D-E;44C-D;89D7-E1 (Lewis) or Df(2R)44CE = Df(2R)44C;44E1-4 (Hooper). # ltd37b origin: Spontaneous. discoverer: Poulson, 37b. references: Poulson and King. 1948, DIS 22: 55. phenotype: Eye color of newly hatched adult bright red like v, darkens to a color like pr in old flies. Ocelli colorless; larval Malpighian tubes colorless. Viability excellent. RK1. # luc: luckenhaft (T. Schupbach and E. Wieschaus) location: 2-65. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect female sterile: Embryos from homoz- ygous females form cellular blastoderms with local defects; embryos form cuticle with big holes, variable head defects and segment fusions. alleles: lucOG = luc1, lucQA, lucRN # Lvp: Larval visceral protein Three genes that are clustered in an 8 kb segment of DNA and lie 11 kb from the second-chromosome Lcp gene cluster (Snyder and Davidson, 1983, J. Mol. Biol. 166: 101-18). The order of the genes is LvpH--1.7kb--LvpD--1.1kb--LvpL, with LvpH being closest to the Lcp cluster. LvpH and LvpL are transcribed off of the same strand as Lcp1 and Lcp2, and LcpD off of the same strand as Lcp3 and Lcp4. Three genes are completely sequenced and are 50-60% homologous in DNA sequence; they encode polypeptides of approximately 500 amino acids, which contain apparent signal peptide sequences but lack hydrophobic regions indicating that they are secreted rather than being membrane proteins; each has a sequence of 12 amino acids similar to known calcium binding domains of other proteins. The genes are coordinately transcribed in abundance in young larvae and adults, but not in late larvae when Lcp genes are transcribed; whereas Lcp genes are transcribed in the larval cuticle, Lvp transcripts are found in the larval viscera. The time and place of Lvp transcription suggests a possible digestive func- tion of the gene products. genetic cytological locus location location comments ___________________________________________________________ LvpD 2-59.4 44D 353 bp intron at 1322-1323 LvpH 2-59.4 44D LvpL 2-59.4 44D 62 bp intron at 145-146 # lxd: low xanthine dehydrogenase location: 3-34.5. references: Keller and Glassman, 1964, Genetics 49: 663-68. 1964, DIS 39: 61. Schott, Baldwin, and Finnerty, 1986, Biochem. Genet. 24: 509- 27. phenotype: Homozygotes exhibit little or no activity of four molybdenum hydroxylases, i.e., 25% normal levels of xanthine dehydrogenase (XDH) activity (Keller and Glassman), 12% normal aldehyde oxidase (AO) activity (Courtright, 1967, Genetics 57: 25-39), no pyridoxal oxidase (PO) (Keller and Glassman) and 5-10% normal levels of sulfite oxidase (SO) (Bogaart and Bernini, 1981, Biochem. Genet. 19: 929-46) (2% according to Schott, Baldwin and Finnerty). Residual activity of AO and XDH thermolabile (Schott, Baldwin and Finnerty). These reduced activities not accompanied by comparable reductions in the levels of crossreacting material (CRM) indicating that the structural genes for the enzymes are still being expressed (Glassman, Shinoda, Duke, and Collins, 1968, Ann. N.Y. Acad. Sci. 151: 263-73; Browder, Wilkes, and Tucker, 1982, Biochem. Genet. 20: 111-24 and 125-32; Warner, Watts, and Finnerty, 1980, Mol. Gen. Genet. 180: 449-53). lxd+ postulated to be involved in production of an enzyme cofactor (Glassman et al., 1968); dietary molybdenum shown to increase specific activity of AO and XDH in flies homozygous for some, but not all, lxd alleles (Duke, Rushing, and Glassman, 1975, Biochem. Genet. 13: 53-64). lxd homozygotes shown to have only 10% normal molybdenum cofactor activity (Schott, Baldwin, and Finnerty). Tungsten, a known antagonist of molybdemum cofactor, shown to mimic lxd in wild type (Warner and Finnerty, 1981, Mol. Gen. Genet. 184: 92-96) and to exacerbate the effects of lxd (Bentley, Williamson, and Oliver, 1981, Can. J. Genet. Cytol. 23: 597-609). The maternal effects of cin and mal are suppressed in cin lxd and mal lxd offspring of cin/+ and mal/+ mothers respectively; dietary molybdenum counteracts the suppression; lxd also suppresses complementation between vari- ous pairs of partially complementing mal alleles (Courtright, 1975, Mol. Gen. Genet. 142: 231-38). Dietary tungsten pro- duces brown eye color in lxd flies, which normally have red eyes; used to select new lxd alleles (Bentley, Williamson, and Oliver); allopurinol used in the same way (Schott, Baldwin, and Finnerty). alleles: All alleles non complementing. allele origin ref ( _____________________________ lxd1 spont 3 lxd2a EMS 1 lxd3a EMS 1 lxd3b X ray 4 lxd4 X ray 4 lxd5 EMS 4 lxd7 X ray 4 lxd10 EMS 4 *lxd11 EMS 4 lxd12 EMS 4 lxd13 EMS 4 *lxd14 EMS 4 lxd16 EMS 4 lxdc spont 2 lxdcb spont 4 lxdck X ray 4 lxdd spont 2 ( 1 = Bentley, Williamson, and Oliver, 1981, Can. J. Genet. Cytol. 23: 597-609; 2 = Dukel, Rushing, and Glassman, 1975, Biochem Genet. 13: 53-64; 3 = Keller and Glassman, 1964, Genetics 49: 663-68; 4 = Schott, Baldwin, and Finnerty, 1986, Biochem. Genet. 24: 509-27. cytology: Localized to 68A4-9 based on its inclusion in Df(3L)lxd9 = Df(3L)68A3-4;68B4-C1 but not Df(3L)vin4 = Df(3L)68A8-9;78F3-6 (Schott, Baldwin, and Finnerty). Ly: Lyra From Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. No. 552: 118. # Ly: Lyra location: 3-40.5. origin: X ray induced. discoverer: Dubinin, 1929. references: Coyne, 1935, DIS 4: 59. Morgan, Bridges, and Schultz, 1937, Year Book - Carnegie Inst. Washington 36: 301. phenotype: Lateral margins of wings excised, giving narrowed shape; angle between veins L2 and L5 reduced. Bristles shor- tened and stubby; postscutellars frequently missing. Eyes somewhat deformed with tufted vibrissae. Abdomen dark and narrow with rear edge of tergites raised. Homozygous lethal. Ly/Df(3L)M69E is lethal. Modification of wings first visible as marginal scalloping of prepupal wing buds; wing fold nar- rower (Waddington, 1939, Proc. Nat. Acad. Sci. USA 25: 304; 1940, J. Genet. 41: 75-139). RK1A. alleles: Ly2 like Ly1 but with rougher eyes; spontaneous (Wad- dle, 1977, DIS 52: 3). Associated with same deficiency as Ly1 (Zhimulev and Feldman, 1982, DIS 58: 152). cytology: Placed in 70A3-5 on the basis of its association with Df(3L)Ly = Df(3L)70A2-3;70A5-6 (Bridges). # lys: lysine location: 2-22.9. origin: Spontaneous. discoverer: E. H. Grell, 1957. references: 1960, DIS 34: 50. 1961, Genetics 46: 925-33. phenotype: Larvae, pupae, and adults contain a higher concen- tration of lysine than wild type. Accumulation of lysine is postulated to result from block in its degradation. Flies homozygous for lys occasionally have faintly reddish fat cells, especially in thorax. This effect enhanced by starva- tion, by combining lys with rc, rc2, or cho. RK3. # lz: lozenge location: 1-27.7. references: Gottschowski, 1936, Zool. Anz. Suppl. 9: 586-91. Anderson, 1945, Genetics 30: 280-96. Oliver, 1947, Univ. Texas Publ. 4720: 167-84. Clayton, 1952, Univ. Texas Publ. 5204: 227-51. Clayton, 1954, Univ. Texas Publ. 5422: 189-209. Anders, 1955, Z. Indukt. Abstamm. Vererbungsl. 87: 113-86 (fig.). Chovnick and Lefkowitz, 1956, Genetics 41: 79-92 (fig.). Chovnick, Lefkowitz, and Fox, 1956, Genetics 41: 589-604. Clayton, 1957, Genetics 42: 28-41 (fig.). Clayton, 1958, Genetics 43: 261-73 (fig.). Clayton, 1959, Genetics 44: 1041-52 (fig.). phenotype: Many alleles with a wide range of phenotypes. Homozygous males have eyes size variably reduced and often ovoid in shape. Surface with fused facets producing a roughened glistening appearance (= glossy), or smooth with pigment either uniformly distributed or concentrated at peri- phery of the eye (= spectacle). Eye pigment variably reduced, and Malpighian tubes slightly lighter than normal (Brehme and Demerec, 1942, Growth 6: 351-56). Tarsal claws reduced to different extents by different alleles. Spermathecae and parovaria (= accessory glands) often missing in homozygotes with abnormal parovaria seen in some heterozygous females (Anderson, 1945). Females often sterile, but sterility appears to be primarily an ovarian defect, since some geno- types which lack parovaria and spermathecae are female fer- tile. Some alleles lack the class of hemocytes called crystal cells, or at least lack the crystalline inclusions of those cells; the inclusions can be shown to comprise prophenoloxi- dase, and flies lacking crystal cells are deficient in phenol oxidase activity and suppress the phenotype of Bc. Five of fifteen alleles tested (lz36f17, lz46, lzD, lzrfg, and lzs) suppress Bc and lack crystal cells and phenol oxidase activity (Rizki and Rizki, 1981, Genetics 97: s90); postulated that lz+ crucial to differentiation of crystal cells, and is not a structural gene for any of the five phenol oxidase moieties. Peeples, Geisler, Whitcraft, and Oliver report defective phenol oxidase activity in lzg (1969, Biochem. Genet. 3: 563-69) lz64j, lz66c, lzs, and lzy4, but not in lz50e, or lzK (1969, Genetics 62: 161-70); Warner, Grell, and Jacobson (1974, Biochem. Genet. 11: 359-65) found no phenol oxidase activity in lzrfg, but normal levels in lz1 and lzg. alleles: allele origin discoverer ref ( comments | ___________________________________________________________________________ lz1 gypsy Bridges, 16b12 8, 14, 26, 27, 36 g/tsp / *lz2 spont Bridges, 19g16 7 lz3 spont Bridges, 22b14 8, 14, 27, 35 g/tspf / lz3n spont Green 8, 14 s/tsp lz4 spont Bridges, 23b6 7 *lz5 spont Bridges, 23k15 7 *lz16i spont Bridges 7 *lz23b spont Morgan 7 *lz23c spont Wallace 7 *lz29a spont Bridges 7 *lz33e Ives, 33e18 7 lz34 spont Beadle, 34k22 2, 8, 14, 35 g/tspf / *lz35 spont Gottschewski, 1935 8, 12 ?/f / lz36 spont Spencer, 36c 8, 14, 35 s/spf *lz36cD Dempster, 36c 8 g/F lz36f17 39 lz37 spont Curry, 37h12 8, 14, 35, 44 g/tsp / *lz41e spont Neel, 41e17 7 *lz41h spont Neel, 41h22 7 lz46 X ray Green 8, 13, 35 g/spf *lz48c X ray 8, 14 s/tspf lz48f mustard Lindsley, 48f 8, 14 s/tspf / *lz48l X ray 8, 14 s/tspf *lz49g spont 8, 14 s/tspf *lz49h X ray W.K. Baker, 49h 8, 14 s/TSPF / lz49KB 35 lz50 33 lz50d X ray Ritterhoff, 50d 8, 10 s/tspf lz50e 32P King 8, 14, 16, 36 s/TSPF / lz50k 35 lz50l Green, 50130 22 *lz51d spont Mossige, 51dt0 8, 28 s/f *lz52c neutrons King, 52c28 8, 19 s/t / *lz55d X ray Clark, 55d 6, 8 s/f lz55l spont Masterson, 55l 5, 8 s/tspf lz57j X ray Mayo, 57j 8, 23 s/tspf lz58d spont Schreckengost, 58d 5, 8 s/tspf *lz59 X ray Polivanov, 1959 8, 37 s/t / lz60f 35 lz61f spont Moynehan, 61f 4, 8, 20, 40 s/f / lz62k X ray Mickey, 62k11 8, 25 s/tspf lz63 X ray Halfer, 1963 s/F / lz63f spont Burdick, 63f17 41 s/tspf_ / lz63i spont Polivanov, 63i 35, 38 lz64j 35, 36 lz66c X ray McCombs 35, 36 lz71a EMS Snyder 42, 43 s/tspf / lz71b EMS Snyder 42 g/Tpf enhanced by su(f) lz75v Golubovsky 11 lz144 16 Tp(1;1)8E;NO lz491 16 Tp(1;1)8E;NO *lz268-29 X ray Hoover T(1;3)8D8-9;81F lz526 35 lzA 33 unstable allele lzBS X ray 8, 14, 32 g/tspf *lzc1 Cu(SO)4 Hadorn, 45b27 1, 8, 15 s/tspf / lzcs EMS Wright 46 cold sensitive lethal lzD spont Novitski, 47i 8, 20, 30, 35 s/tspf / lzEF3 35 *lzf spont Muller 8, 29 F_ lzg X ray Oliver, 31a7 8, 14, 32, 35, 36, 45 g/tspF_ / *lzgl X ray M. Bender, 53k 3, 8 g/ / *lzgM spont 8, 14 g/tspf lzK spont Krivshenko, 55k9 8, 21, 35, 36 g/TSPF / *lzKi spont Kiil,45k14 8, 18 F *lzM58 X ray Meyer, 58k 8, 24 s/tspF_ / lzntg NNG Kaufman 17 lzrfg R.F. Grell 45 lzs X ray Patterson, 1928 8, 14, 34, 35, 36 s/tspf / *lzsB X ray 8, 16, 32, 35 s/spf In(1)8E;20F lzs-ntg NNG Kaufman 17 lzsl 11 lztear spont 44 s/F lztsl 9 lzy4 X ray 8, 14, 32, 35, 36 s/spf / ( 1 = Anders, 1955, Z. Indukt. Abstamm. Vererbungsl. 87: 113- 86 (fig.); 2 = Beadle, 1935, DIS 4: 9; 3 = Bender, 1955, DIS 29: 69; 4 = Burdick 1963, DIS 37: 47; 5 = Clancy, 1960, DIS 34: 48; 6 = Clark, 1956, DIS 30: 71; 7 = CP552; 8 = CP627; 9 = Cross, 1977, Genetics 86: s13; 10 = Glass, 1951, DIS 25: 77; 11 = Gobulovsky, 1978, DIS 53: 122; 12 = Gottschewski, 1937, DIS 8: 12; 13 = Green and Green, 1949, Proc. Nat. Acad. Sci. USA 35: 586-91; 14 = Green and Green, 1956, Z. Indukt. Abstamm. Vererbungsl. 87: 708-21; 15 = Hadorn and Anders, 1946, DIS 20: 65; 16 = Hannah- Alava, 1971, Mol. Gen. Genet. 113: 191-203; 17 = Kaufman, 1970, DIS 45: 34; 18 = Kiil, 1946, DIS 20: 66; 19 = King, 1951, DIS 26: 65; 20 = Klingele, 1968, DIS 43: 145; 21 = Krivshenko, 1956, DIS 30: 74; 22 = Lefevre and Moore, 1968, Genetics 58: 557-71; 23 = Mayo, 1958, DIS 32: 82; 24 = Meyer, 1959, DIS 33: 97; 25 = Mickey, 1963, DIS 38: 28; 26 = Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. USA 80: 1678-82; 27 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 230; 28 = Mossige, 1951, DIS 25: 69; 29 = Muller, 1946, DIS 20: 67; 30 = Novitski, 1949, DIS 23: 61; 31 = Oliver, 1935, DIS 4: 15; 32 = Oliver, 1947, Texas Univ. Publ. 4720: 167-84; 33 = Osipova, Korochkin, Golubovsky, Khelbodarova, and Kulutchkov, 1981, DIS 56: 104; 34 = Patterson and Muller, 1930, Genetics 15: 495-577; 35 = Peeples, Geisler, Whit- craft, and Oliver, 1969, Biochem. Genet. 3: 563-69; 36 = Peeples, Geisler, Whitcraft, and Oliver, 1969, Genetics 62: 161-70; 37 = Polivanov, 1963, DIS 38: 30-31; 38 = Polivanov, 1970, DIS 45: 37; 39 = Rizki and Rizki, 1981, Genetics 97: s90; 40 = Schwalm, Klingele, and Bender, 1970, DIS 45: 91; 41 = Seiger and Bender, 1963, DIS 38: 31; 42 = Snyder, 1973, DIS 50: 20; 43 = Snyder and Smith, 1976, Biochem. Genet. 14: 611-17; 44 = Thompson and Purnell, 1972, DIS 48: 16; 45 = Warner, Grell, and Jacobson, 1974, Biochem. Genet. 11: 359-65; 46 = Wright, 1973, Mol. Gen. Genet. 122: 101-18. | s/ = spectacle; g/ = glosssy; sf/ = intermediate; t/ = tarsal structures reduced or absent; T/ = tarsal struc- tures present; s = spermathecae absent; S = spermathecae present; p = parovaria absent; P = parovaria present; f = female sterile; F = female fertile. / More detailed phenotype description below. cytology: Placed in 8D8-9 (Lefevre, 1976, Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 31-66). other information: The lz region has been subdivided into four recombinationally separable groups of alleles (Green and Green, 1949, Proc. Nat. Acad. Sci. USA. 35: 586-91; 1956, Z. Indukt. Abstamm. Vererbungsl. 87: 708-21); recombination is observed between but not within groups. Not all alleles have been mapped. The total genetic length of the region is 0.14 cM. Double mutants produced by recombination all have the extreme phenotype of lzs. Mitotic exchange between lz36 and lzy4 reported by Tokunaga (1973, Mol. Gen. Genet. 125: 109- 18). # lz1 origin: Spontaneous; contains gypsy insert (Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. 80: 1678-82). discoverer: Bridges, 16b12. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 230. Green and Green, 1956, Z. Induktive Abstammungs-Vererbungsl. 87: 708-21. phenotype: Eye narrower than wild type and ovoid. Irregular facets in some areas cause rough patches; areas of fused facets appear as smooth patches. Eye color appears normal but, in combination with st, slight reduction in red pigment detectable. Tarsal claws reduced. Developmental study by Wad- dington and Pilkington (1942, DIS 16: 70) shows failure of middle cell layer of optic disk to penetrate between cells of outer layer; surface thus covered with primary pigment cells. Females sterile. Parovaria and spermathecae absent; some lz/+ females have abnormal parovaria (Anderson, 1945, Genetics 30: 280-96). Suppressed by su(f)6 (Schalet, 1970, Genen. Phaenen 14: 16-17), su(Hw)2, e(we)s, and su(pr)e3; enhanced by su(s)3 and su(wa) (Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97). Phenol oxidase activity increased from 17% to 71% normal (Snyder and Smith, 1976, Biochem. Genet. 14: 611-17). RK1. # lz3 phenotype: Eye size sharply reduced; surface smooth. Optic disk of mature larva and prepupa two-thirds normal size (Chen, 1929, J. Morphol. 47: 135-99). Red pigment greatly reduced; color yellowish brown, cream colored in combination with v. Tarsal claws vestigial. Homozygous females lack parovaria and spermathecae and are sterile; lz3/+ females lack parovaria and many have abnormal spermathecae [Anderson, 1945, Genetics 30: 280-96 (fig.)]. Unaffected by su(f)6 (Schalet, Snyder, and Smith, 1976, Biochem. Genet. 14: 611-17). RK1. # lz34 phenotype: Eye phenotype intermediate between lz and lz3. Sur- face of eye has large areas of fused facets with a few normal facets (Clayton, 1957, Genetics 42: 28-41); eye color dark red with small yellowish spots. Larval Malpighian tubes slightly lighter than normal; variable (Brehme and Demerec, 1942, Growth 6: 351-56). Tarsal claws reduced. Spermathecae and parovaria absent from homozygous females, which accumulate stage 14 oocyte and are quite infertile; some lz34/+ females have abnormal parovaria (Anderson, 1945, Genetics 30: 280- 96). Eye effect, but not other aspects of phenotype, enhanced by spae(lz); eye converted from a glossy to a spectacle pheno- type (Beeson and Bender, 1975, J. Exp. Zool. 193: 177-90). In the presence of su(lz34), lz34 flies have virtually normal eyes. Beeson and Bender were unable to confirm previous observations of Bender and Green (1960, Genetics 45: 1563-66) that su(lz34) increases the fecundity of lz34 females. Unaf- fected by su(f)6 (Schalet) or su(Hw)2; however suppressed by su(pr) and enhanced by su(s) and su(wa) (Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97). RK1. #*lz35 phenotype: Eyes reduced and diamond shaped; color opaque brown. Homozygous females sterile. lz35/lz females fertile. RK1. # lz37 phenotype: Eye size reduced. Areas of irregular facets in pos- terior region of eye; eye color normal. Enhanced by su(f)6 (Schalet, 1970, Genen. Phaenen 14: 16-17); also enhanced by su(Hw)2 and su(s) (Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, Genetics 119: 391-97). Phenol oxidase level decreased from 94% to 58% of normal (Snyder and Smith, 1976, Biochem. Genet. 14: 611-17). RK1. # lz48f origin: Induced by mustard gas. discoverer: Lindsley, 48f. references: Green and Green, 1956, Z. Indukt. Abstamm. Verer- bungsl. 87: 708-21. phenotype: Unaffected by su(f)6 (Schalet). #*lz49h phenotype: Eye size sharply reduced; surface smooth; red pig- ment distributed over entire eye. Tarsal claws normal. Sper- mathecae and parovaria present and normal in females, which are fertile. Complements all lz alleles tested except lz50e. # lz50e phenotype: Like lz49h. Eyes reduced in size and almond shaped; no indication of facets; covered with indentations, giving a pock-marked appearance. Hairs on eye surface sparse or absent; eye surface glossy with many large black or brown flecks. Tarsal claws normal. Females fertile; spermathecae and parovaria present and normal. lz50e/lz has normal eyes except for a few flecks. Complements most other lz alleles except lz49h, lz52c, and those associated with rearrangements or deficiencies. Unaffected by su(f)6 (Schalet). RK1. #*lz52c origin: Recovered among progeny of male fed H3BO3 and exposed to thermal neutrons. phenotype: Eyes mottled, yellowish brown, darker at rim; facets fused. Males semisterile with missing tarsal claws, although pulvilli and endopodia normal. Third antennal segment slightly reduced. lz52c/lz50e females resemble lz50e. RK1. #*lz59 phenotype: Eyes reduced in size and ovoid; facets fused; sur- face slightly rough and almost or completely hairless; color light brown with darker, slightly reddish rim; almost color- less in combination with v. Tarsal claws practicaly absent as in lzc1. Males sterile, (possibly associated with X-autosome translocation), transmit no motile sperm to females; there- fore, homozygous females not observed. lz59/lz37 females intermediate between the two mutants in eye phenotype, have reduced tarsal claws, and are weakly fertile. RK2. # lz61f phenotype: Facets completely fused; eye color dark, but pigment unevenly distributed and concentrated at margin. Females found to be fertile by Burdicks, but were sterile when studied by Schwalm, Bender, and Klingle (1970, DIS 45: 91) who stu- died the ultrastructure of eggs produced by homozygous females. lz61f/lz females more nearly normal than either mutant; facets disrupted and fused only in posterior third of eye; also fertile. RK1. # lz63 phenotype: Eye shape oval; color brown, darkest at margin; sur- face smooth and glossy. Viability and fertility of both sexes good. RK1. # lz63f phenotype: Eye size moderately reduced; surface smooth; color brownish with darker margin. Tarsal claws and pulvilli strongly reduced. Spermathecae and parovaria absent; female reproductive capability strongly reduced. lz63f complements lz50e but not lz34, lzD, or lz61f (Klingele). Spermathecal number of lz63f/lzK 0-3. RK1. # lz71a phenotype: Phenol oxidase activity severely reduced; further reduced in presence of su(f) (Snyder and Smith), 1976, Biochem. Genet. 14: 611-17. #*lzcl: lozenge-clawless origin: Appeared as a male from an ovary treated in vitro with CuSO4. phenotype: Eyes narrow and small without facets; surface has rough spots; color amber, both pteridines and ommochromes affected, darker at rim. Tarsal claws absent. Third antennal segment reduced; sensilla on antennae abnormal. Phenotype similar in both sexes. Females infertile and lack spermathe- cae and parovaria. Autonomous in transplants. RK1. # lzD: lozenge-Dominant phenotype: Males and homozygous females resemble lzs. Hetero- zygous females sometimes have roughened eyes. Apparent domi- nance shown by H. Bender to be caused by the presence of spae(lz); heterozygous expression additionally enhanced by presence of In(2LR)bwV1. # lzg: lozenge-glossy phenotype: Eyes smaller than wild type; surface glossy from fused facets; a few normal facets also present; color dark blood red, bright red in combination with st or v. Larval Malpighian tubes slightly lighter than normal (Brehme and Dem- erec, 1942, Growth 6: 351-56). Tarsal claws reduced. Sper- mathecae and parovaria absent from homozygous females, which have reduced fertility; lzg/+ females tend to have abnormal parovaria [Anderson, 1945, Genetics 30: 280-96 (fig.)]. RK1. other information: lzg/lzs provided probably the first recorded case of intra-allelic recombination (Oliver, 1940, Proc. Nat. Acad. Sci. USA 26: 452-54; 1940, DIS 13: 73). #*lzgl: lozenge-glued phenotype: Eyes of male reduced and roughened like Gl; color dark; female eyes somewhat less extreme. lzgl/lz intermediate between lzg1 and lz and sterile. Homozygous females fertile. RK1. # lzK: lozenge of Krivshenko synonym: amx55: almondex-55; lzk. phenotype: Eyes narrow and moderately rough; facets irregular; eyes of homozygous females more nearly normal than those of males. Tarsal claws normal. Females fertile; spermathecae and parovaria present. Interactions of lzK with other lz alleles described by Green [1961, Genetics 46: 1169-76 (fig.)]. Unaffected by su(f)6 or su(Hw)2; however suppressed by su(pr) and enhanced by su(s) and su(wa) (Rutledge, Mortin, Schwarz, Thierry-Mieg, and Meselson, 1988, Genetics 119: 391-97). RK1. #*lzM58: lozenge of Meyer phenotype: Eyes small and oval; surface glossy; color brownish. Tarsal claws missing. Homozygous females moderately fertile, although spermathecae absent; lzM58/lzs also fertile. RK1. # lzs: lozenge-spectacled phenotype: Eye size reduced, narrower than normal; no true facets; whole eye has glossy surface; color yellow-brown with darker rim, creamy in combination with v. Tarsal claws vesti- gial. Homozygous females lack spermathecae and parovaria and are sterile. lzs/+ females tend to have abnormal parovaria (Anderson, 1945, Genetics 30: 280-96). RK1. other information: lzs/lzg provided probably the first recorded case of intra-allelic recombination (Oliver, 1940, Proc. Nat. Acad. Sci. USA 26: 452-54; 1940, DIS 13: 73). # lzy4: lozenge in yellow-4 phenotype: Similar to lzs but eye color redder. Homozygous females lack spermathecae and parovaria and are sterile; lzy4/+ females have abnormal parovaria and tend to lack sper- mathecae and parovaria (Anderson, 1945, Genetics 30: 280-96). RK1. # lz-l: see rstl #*lzl: lozengelike location: 1-11. discoverer: Oliver, 29k24. references: 1935, DIS 3: 28. phenotype: Eyes rough. Both sexes fertile. RK3. other information: Possibly an allele of rg (1-11.0). Many spontaneous reversions of ovoD1 result in a phenotype similar to that originally reported for lzl (Busson, Gans, Komito- poulou and Masson, 1983, Genetics 105: 309-25; Oliver, Perri- mon, and Mahowald, 1987, Genes Dev. 1: 913-23; Mevel-Ninio, Mariol, and Gans, 1989, EMBO J. 8: 1549-58). The lzl alleles derived from the ovoD1 chromosome are characterized by rough or glazed eyes. All alleles are semidominant and cold sensi- tive. These mutations are likely to be new alleles of lzl. This cannot be tested as the original lzl allele was lost.