# ph: polyhomeotic (P. Santamaria) location: 1-0.5 (based on 28 y-z recombinants). synonym: Possibly *rsc: reduplicated sex comb (CP 627; Dura et al., 1985). references: Brock and Freeman, 1984, Genetics 107: s14. Dura, Brock, and Santamaria, 1985, Mol. Gen. Genet. 198: 213-20. Perrimon, Engstrom, and Mahowald, 1985, Genetics 111: 23-41. Dura, Randsholt, Deatrick, Erk, Santamaria, Freeman, Freeman, Weddell, and Brock, 1987, Cell 51: 829-39. Dura, Deatrick, Randsholt, Brock, and Santamaria, 1988, Roux's Arch. Dev. Biol. 197: 239-46. Dura and Ingham, 1988, Development 103: 733-41. Smouse, Goodman, Mahowald, and Perrimon, 1988, Genes Dev. 2: 830-42. Santamaria, Deatrick, and Randsholt, 1989, Roux's Arch. Dev. Biol. 198: 65-77. phenotype: A member of the Polycomb group of genes; seems to be the only one that is strongly required both maternally and zygotically for normal embryonic development. Two mutagenic events are necessary to produce null mutations, suggesting that the locus is complex, and in fact molecular determina- tions indicate that the locus comprises a direct repeat. Single-event mutations are viable as males and homozygous females; such mutations produce transformations similar to those of known dominant gain-of-function mutants in the ANTC and BXC, i.e., transformation of wings to halteres, second and third legs to first legs, and anterior abdominal segments to more posterior segments (mutants may also show loss of the humerus). Two-event lethal mutations die in mid embryogenesis and completely lack ventral and abdominal epidermal deriva- tives; they show transformations of most of the segments toward the eighth abdominal segment (Dura et al., 1988). There is an alteration in the pattern of axon pathways in the CNS. The axons fail to form commissures or connectives but instead form large bundles in the middle of each hemi-ganglion (Smouse et al., 1988). Trans heterozygotes between viable and lethal alleles or between viable alleles and a deficiency for ph die in late embryogenesis and exhibit posteriorly directed transformations; i.e. viable alleles are haplo insufficient. Dura et al. (1987) postulate that mutations can occur in either or both of the repeated sequences such that -+/-+ = +- /+- = -+/+- = viable mutant constitutions (--/++ not stated to be mutant); -+/-- = +-/-- = late embryonic lethals; and --/-- = mid-embryonic-stage lethals. The ph+ product is required autonomously in imaginal cells. A total lack of ph+ function prevents viability of the cuticu- lar derivatives of these cells, but amorphic ph clones induced in late third instar survive. ph has a strong maternal effect on segmental identity and epidermal development that cannot be rescued by a single paternally supplied dose of ph+ in the zygote (Dura et al., 1988). The expression of ph is inversely related to dosage of the ANTC and the BXC; the gene interacts with Pc, Pcl, and esc (Dura et al., 1985). At the shortened germ band stage (but not at the blastoderm stage), ph seems to be involved in the regulation, not only of the homeotic genes Scr and Ubx, but also in the regulation of the segmentation genes ftz, eve, and en (Dura and Ingham, 1988). alleles: Almost 50 mutant alleles of polyhomeotic have been isolated, 41 of them being viable as adults and the rest (ph500 - ph505) lethal. allele origin discoverer ref ( comments _______________________________________________________________________ ph1 EMS Gans and 1, 3 cytology normal Komitopoulou ph2 HD 1, 3 cytology normal ph3 | HD Karpen 1, 3 Tp(1;1)2E-F;5B-C;19F-20 `; dominant enhancer of Pc only ph4 HD Karpen 1, 3 cytology normal ph5 DEB 3 ph6 EMS 1, 3 ph7 / HD Karpen 1, 3 dominant enhancer of Pc only ph8 / EMS 3 ph9 / HD Karpen 1, 3 dominant enhancer of Pc only ph10 EMS 3 ph10-1 | X ray 3 cytology normal ph11 X ray 3 cytology normal ph101 EMS 3 ph102 EMS 3 ph203 EMS 3 ph204 EMS 3 ph205 EMS 3 ph207 EMS 3 ph208 EMS 3 ph209 EMS 2, 3 extra sex combs in females with tra-2OTF ph212 EMS 3 ph214 EMS 3 ph216 EMS 3 ph217 EMS 3 ph218 EMS 3 ph220 EMS 3 ph222 EMS 3 ph301 EMS 3 ph303 EMS 3 ph305 EMS 3 ph400 X ray 3 cytology normal ph401 X ray 3 cytology normal ph403 X ray 3 cytology normal ph404 X ray 3 cytology normal ph409 / X ray 3 cytology normal ph410 ` X ray 3 In(1)2D;13-14 ph500 - EMS 3 lethal amorph ph501 - EMS 2, 3 lethal hypomorph ph502 - EMS 3 lethal amorph ph503 - EMS 3 lethal amorph ph504 - EMS 3 lethal amorph ph505 - EMS 2, 3 lethal amorph phbr EMS Rutledge 2, 3 lethal as pharate adult phk EMS Perrimon 4 phrsc EMS B.S. Baker 3 phTing EMS C.T. Wu 3 phVA174 EMS Perrimon 3 cytology normal ( 1 = Dura, Brock, and Santamaria, 1985, Mol. Gen. Genet. 198: 213-20; 2 = Dura, Deatrick, Randsholt, Brock, and San- tamaria, 1988, Roux's Arch. Dev. Biol. 197: 239-46; 3 = Dura, Randsholt, Deatrick, Erk, Santamaria, Freeman, Freeman, Weddell, and Brock, 1987, Cell 51: 829-39; 4 = Perrimon, Engstrom, and Mahowald, 1985, Genetics 111: 23-41. | Viable over deficiencies for ph. (Dura et al., 1987). / Chromosome mutant for ph and wapl but not for the interven- ing Pgd; probably carries an inversion with breaks in ph and wapl (Dura et al., 1987); ph3 separable from the associated Tp(1;1)2E-F;5B-C;19F-20 (Dura et al., 1985). ` Carries In(1)2D;13-14. - Lethal derivative of ph209. Extra row of bristles on wing margin; structures like vagi- nal plates in sixth and seventh sternites of female abdomen (Dura et al., 1988). cytology: Placed in 2D3-4; uncovered by Df(1)JA52 = Df(1)2C10- D1;2D3-4 and Df(1)pn38 = Df(1)2D3-4;2E3 (Perrimon et al., 1985; Dura et al., 1987); Df(1)Pgd-kz = Df(1)2D3-4;2F5 is bro- ken within ph sequences; not covered by Dp(1;1)dorY18T = Dp(1;1)1A;2D1-2. molecular biology: The ph gene was localized within a 240 kb chromosome walk, using deficiencies and mutations that result from chromosome rearrangements. Hybridization analyses indi- cate that ph contains a large, highly-conserved direct but not quite contiguous repeat, each element of which contains an opa sequence, and each is transcribed (Freeman, Randsholt, Deatrick, and Brock). One repeat, distal to the distal break- point of Df(1)Pgd-kz = Df(1)2D3-4;2F5, is unbroken and con- tains molecular deletions in mutant alleles, ph2, ph4, ph10a, and ph401. The proximal element is interrupted by an unre- lated sequence and is deleted by Df(1)Pgd-kz; mutant alleles ph3 and ph7 contain inserted sequences in the proximal repeat element; ph409, and ph410 have breakpoints in the element. A restriction site polymorphism is found in the 1.95 kb fragment separating the repeat components (Dura et al., 1987). All of the ph lesions map within a 20 kb region between the distal breakpoint of Df(1)pn38 and the proximal breakpoint of Df(1)JA52. DNA fragments from coordinates 122 to 149 on the molecular map of the 2C1-2 to 2E1-2 region (0 being the distal point of the walk) hybridize to two major embryonic poly(A)+ RNA's of 6.4 and 6.1 kb (Dura et al., 1987). # ph: see ms(3)K81 # phantom: see phm # phase-angle2: see psi2 # phase-angle3: see psi3 # Phb: Photophobe location: 2R. origin: Induced by ethyl methanesulfonate in a sevLY3 strain. references: Ballinger and Benzer, 1988, Proc. Nat. Acad. Sci. USA 85: 3960-64. phenotype: Dominant mutation that reverses the color-choice behavior of sevLY3 mutants - i.e. sevLY3; Phb/+ flies, like wild-type flies, prefer UV over green light, while sevLY3;+/+ flies prefer green over UV. When tested in a T-maze for preference between darkness and green light (550 nm), both wild type and sevLY3 flies show positive phototaxis, while sevLY3;Phb/+ and sevLY3;Phb/Phb flies show negative photo- taxis. Similarly, tests in a countercurrent apparatus for movement toward and movement away from white light indicate marked preference of wild-type flies for light and of sevLY3;Phb/+ flies for darkness. Both the positive phototac- tic response of sevLY3 and the negative phototactic response of sevLY3;Phb/+ flies increase with age, reaching a maximum at 4-6 days. The interaction between Phb and sev is allele specific, as is indicated in the following table: genotype phototaxis _____________________________ sevd2;Phb/+ + sevE1;Phb/+ + sevE4;Phb/+ + sevE5;Phb/+ + sevf3IE;Phb/+ + sevLY3;Phb/+ - sevP3;Phb/+ - sevx3;Phb/+ + Photoreceptor cell R7, missing in all of the sev alleles, was not restored in any mutant combination of Phb and sev. # Phenol oxidase: see Phox # phl: pole hole location: 1-0.5. synonym: l(1)2Fe; l(1)ph. references: Konrad and Mahowald, 1983, Molecular Aspects of Early Development (Malacinski and Klein, eds.). Plenum Press, New York, pp. 167-88. Perrimon, Engstrom, and Mahowald, 1984a, Dev. Biol. 105: 404-14. 1984b, Genetics 108: 559-72. Perrimon and Mahowald, 1986, Symp. Soc. Dev. Biol. 44: 221- 35. Ambrosio, Mahowald, and Perrimon, 1989, Nature (London) 342: 288-91. Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52. phenotype: The wild-type allele of phl seems to be involved in the setting up of positional values in embryos and also in the proliferation of diploid cells in imaginal disks (Ambrosio, Perrimon, and Mahowald, 1988). phl mutants are recessive early-pupal lethals, which display very small imaginal disks. Embryos derived from germ-line clones and lacking phl+ activity show the "torso" or "pole hole" phenotype; structures at the anterior and the posterior end (spiracles, anal tufts, and the entire eighth abdominal segment) fail to develop (Per- rimon et al., 1984; Ambrosia, Mahowald, and Perrimon, 1988). The fate map of the blastoderm is shifted posteriorly and fewer segments with more cells result. A partial rescue of these mutants has been obtained with phl+ sperm (Ambrosio, Engstrom, and Mahowald); all structures posterior to abdominal segment seven are missing (Perrimon and Mahowald, 1986). alleles: allele origin discoverer synonym ref ( ________________________________________________ phl1 X ray Lefevre l(1)C110 2, 3 phl2 | X ray Lefevre l(1)GA79 2, 3 phl3 / X ray Lefevre l(1)JC59 2, 3 phl4 EMS Lefevre l(1)DA503 2, 3 phl5 EMS Lefevre l(1)DC817 2, 3 phl6 EMS Lefevre l(1)DF903 2, 3 phl7 EMS Lefevre l(1)EA75 2-5 phl8 EMS Lefevre l(1)VA88 2, 3 phl9 EMS Lefevre l(1)VE733 2, 3 phl10 EMS Lefevre l(1)VE791 2, 3 phl11 spont Schalet l(1)11-29 4 phl12 HMS ` l(1)HM7 1 ( 1 = Kramers, Schalet, Paradi and Huiser-Hoogteyling, 1983, Mutat. Res. 107: 187-201; 2 = Lefevre, 1981, Genetics 99: 461-80; 3 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 4 = Schalet, 1986, Mutat. Res. 163: 115-44. | Cytology: T(1;3)2F-3A;82C. / Cytology: T(1;3)3A1;92F-93A. ` HMS = hycanthon methanesulfonate. cytology: Located in 2F6 since included in Df(1)JC19 = Df(1)2F6;3C5, Df(1)TEM75 = Df(1)2F5-3A1;3C2-4, and Df(1)X12 = Df(2F5-3C1;3B5-C1, but not in Df(1)62g18 = Df(1)3A1-2;3A4. molecular biology: Three transcripts (3.5, 4.8, and 5.3 kb long) have been reported (Ambrosio, Perrimon, and Mahowald). Gene shows homology to the serine-threonine kinase oncogene v-raf; the Drosophila raf gene has been shown by molecular analysis to be phl (Ambrosio et al., 1989). # phm: phantom location: 1-64 (average of five alleles). origin: Induced by ethyl methanesulfonate. references: Wieschaus, Nusslein-Volhard, and Jurgens, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 296-307. phenotype: Male lethal. Cuticle of lethal embryos not well differentiated and contracted posteriorly. alleles: Five phm ethyl-methanesulfonate-induced alleles. cytology: Located in 17A-18A since uncovered by Df(1)N19 = Df(1)17A1;18A2. # Phosphoenolpyruvate-carboxykinase: see Pepck # Phosphofructokinase: see Pfk # Phosphoglucomutase: see Pgm # Phosphogluconate dehydrogenase: see Pgd # Phosphoglucose isomerase: see Pgi # Phosphoglycerate kinase: see Pgk # Photophobe: see Phb # photorepair: see phr # Phox: Phenol oxidase location: 2-80.6. references: Batterham and McKechnie, 1980, Genetica 54: 121- 26. Batterham, 1981, Genetics 97: s8. Batterham and Chambers, 1981, DIS 56: 18-19. phenotype: Structural gene for a phenol oxidase component other than A1, A2, or A3. [PHOX (E.C. 1.10.3.1)]. It is a tyro- sinase, oxidizing mono- and o-diphenols. Three electro- phoretic variants have been described by Batterham and McKech- nie (1980), but no null alleles. The molecular weight of the native enzyme is 108,000 daltons. PHOX is believed to be a dimer with a subunit molecular weight of 54,000 (Batterham and Chambers, 1981). alleles: PhoxF (fast), PhoxI (intermediate), and PhoxS (slow). PhoxI is the most common allele in Australasia, occurring with a minimum frequency of 0.85 (Batterham, 1981). No alleles affecting activity levels have been demonstrated, although the possible allelism between Phox and the mutant Bc [with the same genetic location as Phox (2-80.6)] has been suggested (Treat-Clemons and Doane, 1984, DIS 60: 17-42; Wright, 1987, Adv. Genet. 24: 127-222). other information: tyr1 and lz3 show no PHOX activity (Wright, 1987). # phr: photorepair location: 2-56.8 (between pr and c). origin: Spontaneous in a standard laboratory stock. references: Boyd and Harris, 1985, Genetics 110: s85. 1987, Genetics 116: 233-39. phenotype: Deficient in photorepair of pyrimidine dimers; par- tially deficient in excision repair. Since phr/phr larvae show little or no photoreactivation after exposure to short wavelength UV light, the phr+ function is thought to play a significant role in UV resistance. # pi: pied location: 2-17. origin: Spontaneous. discoverer: Harnly, 38k31. phenotype: Eyes like S but more extreme, smaller, and rougher; facets jumbled. Wings larger, flimsy, arched, and fringed. Male usually sterile, have abnormal genitalia. Viability erratic, varying from 20 to 80%. RK3. # pic: piccolo location: 3-52.1 (distal to ry and snk). synonym: l(3)87D. references: Schalet, Kernaghan, and Chovnick, 1964, Genetics 50: 1261-68. Hilliker, Clark, and Chovnick, 1980, Genetics 95: 95-110. Hilliker, Clark, Gelbart, and Chovnick, 1981, DIS 56: 65-72. Clark and Chovnick, 1986, Genetics 114: 819-40. phenotype: Lethal or semilethal as homozygotes or heteroallelic heterozygotes. Survivors show the pic visible phenotype, i.e. short and thin or missing thoracic bristles, abnormal tergite morphology (as in bb), and, occasionally, wing defects. alleles: One semilethal and 32 lethal alleles have been identi- fied. Six of the lethals show some interallelic complementa- tion for viability, but not for the visible phenotype. allele origin discoverer synonym ref ( ___________________________________________________________ pic1 | X ray Schalet 1, 4, 5, 6 pic2 / X ray Schalet pic2l 6 pic3 X ray Schalet pic3l 6 pic4 EMS Hilliker, Clark l(3)3-119 5 pic5 EMS Hilliker, Clark l(3)8-107 5 pic6 EMS Hilliker, Clark l(3)8-181 5 pic7 EMS Hilliker, Clark l(3)12-196 5 pic8 EMS Hilliker, Clark l(3)33-1 5 pic9 EMS Hilliker, Clark l(3)A3-3 5 pic10 EMS Hilliker, Clark l(3)A12-3 5 pic11 EMS Hilliker, Clark l(3)A19-1 5 pic12 EMS Hilliker, Clark l(3)A19-2 5 pic13 EMS Hilliker, Clark l(3)A34-3 5 pic14 EMS Hilliker, Clark l(3)A42-1 5 pic15 EMS Hilliker, Clark l(3)A80 5 pic16 EMS Hilliker, Clark l(3)A111 5 pic17 EMS Hilliker, Clark l(3)A112 5 pic18 EMS Hilliker, Clark l(3)B2-4 5 pic19 / ray Hilliker, Clark l(3)C-9-2 5 pic20 / ray Hilliker, Clark l(3)C-17-3 5 pic21 / ray Hilliker, Clark l(3)C-18-1 5 pic22 EMS Hilliker, Clark l(3)D64 5 pic23 EMS Gelbart l(3)G23 2, 3, 5 pic24 / ray Gelbart l(3)G26 5 pic25 EMS Hilliker, Clark l(3)H10 5 pic26 / ray Hilliker, Clark l(3)H19 5 pic27 / ray Hilliker, Clark l(3)H22 5 pic28 EMS Hilliker, Clark l(3)H49 5 pic29 EMS Hilliker, Clark l(3)H51 5 pic30 EMS Hilliker, Clark l(3)H54 5 pic31 EMS Hilliker, Clark l(3)H59 5 pic32 EMS Hilliker, Clark l(3)H72 5 pic33 EMS Hilliker, Clark l(3)m10 5 ( 1 = Clark and Chovnick, 1986, Genetics 114: 819-40; 2 = Gelbart and Chovnick, 1979, Genetics 92: 849-59; 3 = Gelbart, McCarron, and Chovnick, 1976, Genetics 84: 211-32; 4 = Hilliker, Clark, and Chovnick, 1980, Genet- ics 95: 95-110; 5 = Hilliker, Clark, Gelbart, and Chovnick, 1981, DIS 56: 65-72; 6 = Schalet, Kernaghan, and Chovnick, 1964, Genetics 50: 1261-68. | Semilethal. / May show interallelic complementation for viability, but survivors are pic in phenotype (Hilliker et al., 1980, 1981; Clark and Chovnick, 1986). cytology: Located in 87D11-14 since included in Df(3R)l26d = Df(3R)87D11-13;87E3-5, Df(3R)ry75 = Df(3R)87D1-2;87D14-E1, and Df(3R)ry614 = Df(3R)87D2-4;87D11-14, but not in Df(3R)ry36 (Hilliker et al., 1981; Clark and Chovnick, 1986). molecular biology: Clark and Chovnick (1986) place pic at -152 kb on the molecular map of Bender, Spierer, and Hogness (1983, J. Mol. Biol. 168: 17-33); 0 coordinate is the 87E1-2 break- point of In(3R)Cbxrv1. # pied: see pi #*pig: pigmy location: 1-29. origin: X ray induced. discoverer: Muller, 26l8. synonym: pg (preoccupied). references: 1935, DIS 3: 30. phenotype: Fly small and melanotic. Viability about 25% wild type. RK3. # Pig1: Pre-intermolt gene 1 location: 1- (distal to Sgs4). discoverer: Mathers and Meyerowitz. references: Chen, Malone, Beckendorf, and Davis, 1987, Nature (London) 329: 721-26. phenotype: Expressed in larval salivary glands, RNA reaching a peak in second larval instar. cytology: Located in 3C11-12. molecular biology: Transcript is 630 bp long and lies between coordinates -46.4 and -47, 840 bp distal to Sgs4 (Rogers and Beckendorf). Encodes a poly(A)+ RNA of about 750 bp (an unique genomic sequence; dnc or Sgs4 transcribed on the oppo- site strand). # Pigmentless: see Ps # pigmy: see pig # pil: see plo #*pil3: pilosus on third chromosome location: 3- (near or identical with tra). discoverer: Goldschmidt. references: 1953, J. Exp. Zool. 122: 53-96 (fig.). phenotype: Produces setae on sixth sternite of male or transformed female. Semidominant. Enhanced by pil-X. RK3. # Pilis: see Fs(3)Sz2O # pillow: see plo # pilosus on third chromosome: see pil3 # pilosus on X: see pilX #*pilX: pilosus on X location: 1- (left of w). discoverer: Goldschmidt. references: 1953, J. Exp. Zool. 122: 53-96 (fig.). phenotype: Produces setae of varying numbers and sizes on the sixth sternite of normal male and of X/X; tra/tra female. Effect enhanced by presence of pil3 and also by Y chromosome of tra stock. RK3. # pim: pimples locations: 2-30. origin: Induced by ethyl methanesulfonate. references: Nusslein-Volhard, Wieschaus, and Kluding, 1983, DIS 59: 158-60. 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. phenotype: Homozygous lethal in embryo. Cuticle poorly dif- ferentiated with necrotic patches. Head abnormal. cytology: Located in 31B-32A (Nusslein-Volhard et al., 1984); uncovered by Df(2L)J27 = Df(2L)31B-D;31F-32A. alleles: Only one allele was reported by Nusslein-Volhard et al. (1984). # Pin: Pin location: 2-107.3 (to the right of sp). phenotype: Thoracic bristles, especially dorso-centrals and scutellars, shortened and thick at base, sharply tapered at tip. This bristle phenotype is stronger in homozygotes than heterozygotes in the homozygous-viable allele Pin1. alleles: Five Pin alleles have been described. Phenotypes of the homozygous lethal alleles follow the table. allele origin discoverer ref ( _________________________________________ Pin1 spont Ives, 39a9 4 Pin2 spont Grell, 57b 3 PinB EMS Bacher, 66 1 PinTac spont Weiskettel, 57l 5 PinYt spont Grell, 57e 2 ( 1 = Craymer, 1980, DIS 55: 197-200; 2 = Grell, 1957, DIS 31: 81; 3 = Grell, 1960, DIS 34: 50; 4 = Ives, 1940, DIS 13: 50; 5 = Kadel, 1958, DIS 32: 80. cytology: Located between 60C5 and 60D2 since Pin2 is lethal over Df(2R)Px = Df(2R)60B8-10;60D1-2 or Df(2R)Px2 = Df(2R)60C5-6;60D9-10. # Pin2 phenotype: Thoracic bristles of Pin2/+ flies very short at nor- mal room temperature, but wild type at 17. Homozygotes almost lethal, the few survivors having virtually no thoracic bris- tles. Pin2/Pin mutants have smaller bristles than Pin2/+ and lower viability. Pin2/PinYt is lethal, as are Df(2R)Px/Pin2, Df(2R)Px2/Pin2, and Df(2R)Px4/Pin2. Pin2/+ flies carrying bw+Y have longer bristles than Pin2/+ but shorter than wild type. # PinB: Pin-Bacher phenotype: Thoracic bristles of PinB/+ flies are pale yellow, thin and twisted (like PinYt/+ flies but more extreme). PinB/Pin1 has only vestiges of chaetae on the thorax; also has soft, watery-appearing cuticle. Homozygotes lethal. # PinTac: Pin-Tack phenotype: Thoracic bristles of PinTac/+ flies very small at 22, but almost wild type at 18. Older females hold wings in abnormal position. Homozygous lethal. # PinYt: Pin-Yellow-tip phenotype: Thoracic bristles of PinYt/+ flies are pale yellow, thin, and slightly twisted distally; cuticle appears soft. Homozygous lethal and lethal over Pin1 and Pin2; survives in combination with Df(2R)Px and resembles PinYt/+. # pink: see p # pink wing: see pw # pink-wing: see ltpk # pink wing c: see pwc # pinkish: see pkh # pinkoid: see ltpk # pip: pipe location: 3-47. origin: Induced by ethyl methanesulfonate. references: Anderson and Nusslein-Volhard, 1984, Nature (Lon- don) 311: 223-27. Anderson, Bokla, and Nusslein-Volhard, 1985, Cell 42: 791-98. Carroll, Winslow, Trombly, and Scott, 1987, Development 99: 327-32. phenotype: Maternal-effect lethal; homozygous females are sterile. As in the mutant dl, lethal embryos produced by pip females lack ventral and lateral elements; all cells differen- tiate like the dorsal-most cells of normal embryos (Anderson and Nusslein-Volhard, 1984). Dorsalization is also observed in the pattern of ftz stripes in pip embryos (Carroll et al., 1987). Embryos are not rescued by injection of wild-type cytoplasm; injection of cytoplasm from ventralized embryos of Tl5/+ females, however, partially restores the pip+ embryonic pattern, resulting in differentiation of filzkorper in 25-40% of the treated pip embryos (Anderson et al., 1985). alleles: The alleles pip1 and pip2 recovered as pip286 and pip664. # pk: prickle location: 2-55.3. discoverer: Ives, 38k. references: 1947, DIS 21: 68-69. Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Lit- tlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91. Gubb and Garcia-Bellido, 1982, J. Embryol. Exp. Morphol. 68: 37-57. phenotype: Polarity pattern of wing, haltere, and notum altered in mutants. Chaetae of triple row on anterior wing slanted anteriorly instead of posteriorly. Trichomes near L2 vein arranged in counterclockwise whorl on right wing blade, in clockwise whorl on left blade; trichomes in anterior wing occasionally duplicated (Gubb and Garcia-Bellido, 1982). On the notum, the posterior acrostichals are irregularly erect and whorled. Occasionally, extra dorsocentral and scutellar bristles appear at temperatures above 23. Mutant flies slightly larger than wild type. Gubb and Garcia-Bellido (1982) describe somatic clones of homozygous pk cells. alleles: All alleles viable and pk over Df(2R)pk78k, indicating no lethal alleles at locus (Gubb and Garcia-Bellido, 1982). allele origin discoverer ref ( __________________________________________ pk1 spont Ives 2 pk78a | X ray Gubb 1 pk78b X ray Gubb 1 pk78d / X ray Gubb 1 pk78f X ray Gubb 1 pk78g X ray Gubb 1 pk78l X ray Gubb 1 pk78m | X ray Gubb 1 ( 1 = Gubb and Garcia-Bellido, 1982, J. Embryol. Exp. Morphol. 68: 37-57; 2 = Ives, 1947, DIS 21: 68-69. | Homozygotes indistinguishable from pk1/pk1. / Homozygotes show slight alteration in polarity pattern of posterior wing (below L5 vein); otherwise same as pk1/pk1. cytology: Located between 43A1 and 43A3; included in Df(2R)pk78k = Df(2R)42E3;43C3, but not in Df(2R)ST1 = Df(2R)43B3-5;43E18 (Ashburner et al., 1981). # Pk: Protein kinase Genes in Drosophila melanogaster encoding products related (by sequence comparison) to the serine-threonine protein kinases of mammals have been isolated from Drosophila clones obtained with mammalian probes. These genes are listed in the following table: gene location synonym cytology comments ___________________________________________________________ Pka-C1 2-{34} DC0 30C cAMP-dependant Pka-C2 3-{102} DC1 100A cAMP-dependant Pka-C3 3-{42} DC2 72A cAMP-dependant Pka-R1 3-{47} RI 77F cAMP-dependant Pkc1 2-{78} dPKC53E(br) 53E Ca++-dependant Pkc2 2-{78) dPKC53E(ey) 53E4-7 Ca++-dependant Pkc3 2-{99} dPKC98F 98F Ca++-dependant Pkg1 2-{0.2} DG1 21D cGMP-dependant Pkg2 2-{9} DG2 24A cGMP-dependant Pk?1 2-{52} 1C 36A ? Pk?2 3-{64.6} 1J 91C ? Pk?3 2-{59} 3-2 45C ? Pk?4 1-{60} 3-10 17E ? Pk?5 3-{42} 5-23 72A ? Pk?6 3-{18} 7-10 64F ? Pk?7 2-{78} 8-6 53C ? The three protein kinase gene families that have been charac- terized in Drosophila, Pka, Pkc, and Pkg, are described in the following sections. # Pka: Protein kinase-cAMP Drosophila c-AMP-dependent protein kinase has been purified from the bodies of adult flies; the enzyme is made up of cata- lytic and regulatory subunits (Foster, Guttman, Hall, and Rosen, 1984, J. Biol. Chem. 259: 13049-55). The catalytic subunit has a molecular weight of 40,000 and the regulatory subunit a molecular weight of 52,000 or 58,000 (based on elec- trophoretic mobilities in sodium dodecyl sulfate- polyacrylamide gels). This enzyme was found in all developmen- tal stages of Drosophila melanogaster. Another c-AMP- dependent protein kinase occurs in larvae and during the first half of pupation, but not in embryos and adults. Genes encod- ing the protein found throughout the lifetime of Drosophila have been identified by molecular methods (Foster et al., 1988; Kalderon and Rubin, 1988). These genes are very similar in their amino acid sequences to their mammalian counterparts. A description of the genes follows. # Pka-C1 references: Foster, Higgins, and Jackson, 1988, J. Biol. Chem. 263: 1676-81. Kalderon and Rubin, 1988, Genes Dev. 2: 1539-56. phenotype: Encodes one of the isoforms of the catalytic subunit form of Pka. molecular biology: Pka-C1 has been cloned using mammalian probes and its nucleotide and putative amino acid sequences determined (Foster et al., 1988; Kalderon and Rubin, 1988). This gene shows 82% overall sequence identity to the c-AMP- dependent protein kinase catalytic gene in mouse. Pka-C1 is the source of at least four different transcripts (Kalderon and Rubin, 1988). The coding portion of the gene contains no introns and encodes a protein of 352 amino acids. An insertion of two amino acids not found in bovine and mouse enzymes has been located near the N terminus of the protein; 273 of the remaining 350 amino acids are identical to those of the bovine and mouse enzymes (Foster et al., 1988). other information: 11 additional Drosophila melanogaster DNA clones whose sequences are similar to that of Pka-C1 within the kinase domain have been identified by nucleic acid hybrid- ization. cDNAs have been obtained for ten of the genes involved (Kalderon and Rubin, 1988). The putative protein products of two genes (Pka-C2 and Pka-C3) show 45% and 49% amino acid identity to the corresponding mouse protein kinase. # Pka-R1 references: Kalderon and Rubin, 1988, Genes Dev. 2: 1539-56. phenotype: Encodes the type I regulatory subunit form of Pka. molecular biology: A cAMP-dependent protein kinase regulatory subunit gene has been cloned using mammalian probes and its nucleotide and putative amino acid sequences determined (Kal- deron and Rubin, 1988). Pka-RI is the source of at least three distinct transcripts that originate from different pro- moters that are spliced to a common coding region. The gene encodes at least three putative RI polypeptide products; it shows 71% amino acid identity to the mammalian RI subunit. Only the RNA class that encodes a full-length RI protein can be detected at all stages of development. other information: There are two separate genes transcribed in opposite orientation to Pka-RI within the first and largest intron; the function of these genes is unknown. # Pkc: Protein kinase-c The protein kinase C (PKC) enzyme in Drosophila is encoded by a gene family made up of three genes which are expressed pri- marily in adult flies. The deduced amino acid sequences of these genes are quite similar to each other and those of the mammalian PKC family (Schaeffer et al., 1989). # Pkc1: Protein kinase-c1 references: Rosenthal, Rhee, Yadegari, Paro, Ullrich, and Goeddel, 1987, EMBO J. 6: 433-41. Schaeffer, Smith, Mardon, Quinn, and Zuker, 1989, Cell 57: 403-12. phenotype: Structural gene for protein kinase C (PKC) that is expressed primarily in the brain of adult flies. molecular biology: Pkc1 has been isolated from Oregon-R DNA clones identified by using bovine PKC cDNA probes and its nucleotide sequence and predicted amino acid sequence obtained (Rosenthal et al., 1987). A single open reading frame from the combined sequences of two overlapping cDNAs encodes a 657-amino acid, 75-kd protein with extensive similarity to bovine, rat, and human protein kinase C. This Drosophila melanogaster PKC, like the mammalian forms, carries an amino- terminal cysteine-rich repeat region. The carboxy- terminal region of the Pkc1 protein shows about 88% identity to the corresponding region of the mammalian PKC proteins. Pkc1 contains 13 coding exons of 32-623 pb and at least one untranslated 5' exon. Introns range in size from 54 to more than 8000 bp. The coding regions of Pkc1 in Oregon-R and Canton-S strains differ by 15 silent changes and one change at amino acid 428 (from isoleucine to methionine); in addition, there are three insertion-deletion changes in the 5' untranslated region. Transcripts of about 4.3, 4, and 2 kb (equally abundant) are found in the head of adult flies, but were not found in 0-3 hr embryos (Rosenthal et al., 1987). Transcription occurs in most neurons of the adult head, including photoreceptor cells (Schaeffer et al, 1989). other information: Molecular data indicate that Pkc1 lies approximately 20 kb from Pkc2, another PKC gene with 53E cyto- logical location (Schaeffer et al., 1989). # Pkc2: Protein kinase-c2: references: Schaeffer, Smith, Mardon, Quinn, and Zuker, 1989, Cell 57: 403-12. phenotype: Structural gene for protein kinase C (PKC); expressed primarily in photoreceptors of adult flies. molecular biology: Pkc2 has been isolated from Oregon-R DNA clones identified by using bovine PKC cDNA probes and its nucleotide sequence and predicted amino-acid sequence obtained (Schaeffer et al., 1989). There is a single open reading frame which encodes a 700 amino-acid protein that is similar to other PKCs. The protein encoded by Pkc2 , like the mammalian forms of the enzyme, carries an amino-terminal cysteine-rich repeat region. The carboxy-terminal region of the Pkc2 protein (ATP binding site and catalytic domain) shows a high degree of identity to the corresponding region of mammalian PKC pro- teins. Transcripts are expressed in head (not body) tissue of adult flies. A 2.5 kb transcript accumulates in late pupal stages during the terminal differentiation of photoreceptor cells; it is found in both compound eyes and ocelli of wild type individuals (Schaeffer et al., 1989). # Pkc3: Protein kinase-c3 references: Schaeffer, Smith, Mardon, Quinn, and Zuker, 1989, Cell 57: 403-12. phenotype: Structural gene for protein kinase C (PKC); expressed primarily in adult flies. molecular biology: Pkc3 has been isolated from Oregon-R DNA clones identified by using bovine PKC cDNA probes and its nucleotide sequence and predicted amino-acid sequence obtained (Schaeffer et al., 1989). There is a single open reading frame which encodes a 634 amino-acid protein that shows 61% identity to the mammalian PKC (Ono, Fujii, Ogita, Kikkawa, Igarashi, and Nishizuka, 1988, J. Biol. Chem. 263: 6927-32); the Pkc3 protein, however, diverges markedly from that of Pkc1, Pkc2, and the classical mammalian PKC genes in its amino-terminal region. Pkc3 encodes a major 5.5 kb transcript that is found throughout development, although in reduced amounts in embryos; two other transcripts (4.3 and 4.5 kb) show increased embryonic expression. Adult transcription occurs in the cell bodies of the brain (Schaeffer et al., 1989). # Pkg: Protein kinase-cGMP Genes in Drosophila melanogaster encoding products related (by sequence comparison) to cGMP-dependent protein kinases of mam- mals have been isolated by using a Drosophila cAMP-dependent protein kinase catalytic subunit gene as a probe. # Pkg1 references: Kalderon and Rubin, 1989, J. Biol. Chem. 264: 10738-48. phenotype: Encodes a product with putative cGMP-dependent bind- ing and kinase domains that is 14% larger than the correspond- ing mammalian enzyme. It is believed to bind cGMP and to undergo changes enabling its catalytic site to interact with appropriate substrates. This gene is unusually polymorphic in various Drosophila stocks. The role of the gene and its enzyme in the organism as a whole is unknown at present. molecular biology: Pkg1 cloned and three cDNAs isolated with the genomic DNA as a probe; DNA and putative protein sequences determined (Kalderon and Rubin, 1989). A fragment that is part of the cGMP-dependent protein kinase gene (or a close homolog) was also cloned and sequenced (Foster, Higgins, and Jackson 1988, J. Biol. Chem. 263: 1676-81). There are four introns (one in the coding region, another in the regulatory domain, and two in the catalytic domain); the first intron is about 2 kb long. One major transcript of 2.8 kb was found in all developmental stages examined; this transcript is found mainly in the head in adult flies. The protein product differs from the bovine lung sequence at the amino terminus; it shows 61% identity to the mammalian enzyme in the putative cGMP binding domain and 70% identity in the kinase domain; both domains are arranged in consecutive order on the same polypeptide as in the mammalian cGMP-dependent protein kinase. # Pkg2 references: Kalderon and Rubin, 1989, J. Biol. Chem. 264: 10738-48. phenotype: Encodes products with putative cGMP-dependent pro- tein kinase activities (indicated by sequencing data obtained for all but two of the predicted proteins). The role of the gene and its enzymes in the organism as a whole is unknown at present. molecular biology: Multiple cDNA clones were isolated and the sequence of representative cDNAs and the corresponding genomic DNAs determined (Kalderon and Rubin, 1989). There are three major RNA species of different sizes (4.6, 4.4, and 3.6 kb). The protein product shows 64% identity to the bovine lung cGMP-dependent protein kinase; one of the Drosophila products contains an additional 384 amino acids at the extreme amino terminus. All three of the major Pkg2 transcripts can be detected throughout development. There are seven introns, three of which are located within two nucleotides of the corresponding introns in Pkg1; the positions of these introns do not correspond to the boundaries of the domains in the encoded proteins. #*pkh: pinkish location: 2-100. discoverer: Bridges, 14g27. references: 1919, J. Exptl. Zool. 28: 365. Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 247 (fig.). phenotype: Specific dilutor of we. RK3. # pl: pleated location: 1-47.9. origin: X ray induced. discoverer: Moore, 31c15. references: 1935, DIS 3: 27. phenotype: Wings folded lengthwise in pleats. Overlaps wild type at 25, more extreme at 19. RK3. cytology: Placed in salivary chromosome region 13B2-F17 on the basis of its being included in Dp(1;f)A12 = Dp(1;f)1B-C;13B1-5 but not in the proximal part of the X derived from T(1;4)A4 = T(1;4)13F6-14A1;102F (inferred from Patterson, 1938, Am. Nat. 72: 193-206, also frontispiece of Texas Univ. Publ. 4032). # pl: see pld #*Pl: Pearl location: 2-6. origin: Spontaneous. discoverer: Rosin, 1948. references: 1951, DIS 25: 75. 1952, Rev. Suisse Zool. 59: 261-68. Nef, 1958, Z. Indukt. Abstamm. Vererbungsl. 89: 272-319 (fig.). phenotype: Heterozygote has pearl-like nodes in wings. Wing margins often snipped; venation disturbed. Bristle pattern defective. Eyes small and rough. At 28, at least one of these characters always present; at 18, phenotype virtually normal. Viability good; fertility of male slightly reduced. Fraction of cells die in all imaginal disks. In wing disks, dead cells surrounded by epithelial cells and produce pearl- like structures in adult wing. Homozygote dies as pupa (Tschanz). RK2. # PL: Polygenic Locus A genetic locus consisting of one or more closely linked genes at which allelic substitutions contribute to variance in a specified quantitative character such as the number of ster- noplural bristles (Thompson and Thoday, 1974, Heredity 33: 430-37). The symbol PL is followed parenthetically by the chromosome involved and then by a symbol for the locus. A table of polygenic loci from the data of Thoday and his col- leagues follows: locus location synonym ref ( ________________________________________ PL(1)spS1 | 1-2.4 3, 6 PL(1)spS2 1-51.5 3, 6 PL(2)L4a / 2-72.5 5 PL(2)spG1 2-27.5 1, 6 PL(2)spG2 2-47.5 1, 6 PL(2)spS3 2-41.1 II 3, 6 PL(3)spT1 3-30.2 3a 4, 6 PL(3)spT2 3-32.6 3b 4, 6 PL(3)spW1 3-49 a 6, 7 PL(3)spW2 3-51 b 6, 7 PL(3)wS 3-13 IIIw 2, 6 ( 1 = Gibson and Thoday, 1962, Heredity 17: 1-26; 2 = Spick- ett, 1963, Nature (London) 199: 870-73; 3 = Spickett and Thoday, 1966, Genet. Res. 7: 96-121; 4 = Thoday, Gibson, and Spickett, 1964, Genet. Res. 5: 1-19; 5 = Thompson, 1976, Genetics 81: 387-402; 6 = Thompson and Thoday, 1974, Heredity 33: 430-37; 7 = Wolstenholme and Thoday, 1963, Heredity 18: 413-31. | "sp" = sternopleural bristles. / "L4a" = L4 wing vein. # platinum: see pt #*pld: pallid location: 1-0. origin: Found in progeny of flies treated with Janus green. discoverer: Muller, 28e20. synonym: pl. references: 1935, DIS 3: 30. phenotype: Body and wings pale. Viability about 10% wild type. RK3. other infomation: Possibly an allele of svr. # ple: pale location: 3-18.8. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. Budnick and White, 1987, J. Neurogenet. 4: 309-14. Neckameyer and Quinn, 1989, Neuron 2: 1167-75. phenotype: Homozygous lethal in embryo. Mutant embryos have unpigmented cuticle and head skeleton. Catecholamine levels reduced or absent (Budnick and White, 1987). alleles: allele synonym comments ________________________________________ *ple1 *ple7F ple2 ple70 *ple3 *ple11F temperature-sensitive ple4 ple14A cytology: Located in 65A-E based on segmental aneuploidy pro- duced by Y-3 translocations. other information: ple may encode tyrosine hydrolase since ple and Th both map to 65B. The ability of Th DNA to rescue ple mutants has not been tested. # pleated: see pl # Plexate: see Px # plexus: see px # pll: pelle location: 3-92. origin: Induced by ethyl methanesulfonate. references: Anderson and Nusslein-Volhard, 1984, Nature (Lon- don) 311: 223-27. Muller-Holtkamp, Knipple, Seifert, and Jackle, 1985, Dev. Biol. 110: 238-46. Carroll, Winslow, Twombly, and Scott, 1987, Development 99: 327-32. phenotype: Maternal-effect lethal; homozygous females sterile. As in the mutant dl, lethal embryos produced by pll females lack ventral and lateral elements (Anderson and Nusslein- Volhard, 1984). Extreme pll embryos consist of a long, hollow tube with dorsal cuticular structures (Muller-Holtkamp et al., 1985). Dorsalization is also observed in the pattern of ftz stripes in pll embryos (Carroll et al., 1987). Injection of wild-type cytoplasm into pll embryos partially restores the normal embryonic pattern of development (Muller-Holtkamp et al., 1985). cytology: Located in 97F. alleles: allele synonym __________________ pll1 pll019 pll2 pll078 pll3 pll74 pll4 pll122 pll5 pll312 pll6 pll316 pll7 pll385 pll8 pll628 pll9 pll864 pll10 pllrm8 # plo: pillow location: 2- [52]. origin: Induced by ethyl methanesulfonate. synonym: pil. references: Steward and Nusslein-Volhard, 1986, Genetics 113: 665-78. phenotype: Semilethal over Df(2L)H20. Alleles, as trans- heterozygotes, show a visible recessive phenotype of small- lobed eyes. alleles: plo1, plo2, plo3. cytology: Placed in 36A8-C1 since included in Df(2L)H20 = Df(2L)36A8-9;36E1-2, but not in Df(2L)H68 = Df(2L)36B2- C1;37A1-B1. # pls: palsied location: 1-14.5 (approximate). origin: Induced by ethyl methanesulfonate. references: Singh and Siddiqi, 1981, Mol. Gen. Genet. 181: 400-02. phenotype: Adults paralyzed by high temperature; shake legs just before paralysis. # Plum: see bwV1 #*plw: pale wing location: 1-37.2. origin: Spontaneous. discoverer: Fahmy, 1952. references: 1959, DIS 33: 88. phenotype: Body, wings, and bristles pale silvery yellow. Eclosion delayed; viability low. RK3. # Pm: see bwV1 # Pm2: see bwV32g # PmD1: see bwA # PmK: see PuK # pn: prune location: 1-0.8. references: Beadle and Ephrussi, 1936, Genetics 21: 230. Demerec, Kaufman, Fano, Sutton, and Sansome, 1942, Year Book- Carnegie Inst. Wash. 41: 191. Nolte, 1959, Heredity 13: 233-41. Lifschytz and Falk, 1969, Genet. Res. 14: 53-61. Orevi and Falk, 1975, Mutat. Res. 33: 193-200. Ilyina, Sorokin, Belyaeva, and Zhimulev, 1980, DIS 55: 205. Teng, Bender, Engele, Tsubota, and Venkatesh, 1991, Genetics 128: 373-80. phenotype: Eye color of newly emerged flies transparent brown- ish red, becoming brownish purple with age. The eyes of pn males have about 25% as much drosopterin (red pigment) as the eyes of wild-type males (Gearhart and MacIntyre, 1970, Anal. Biochem. 37: 21-25); the concentrations of xanthopterin and sepiapterin (brown pigments) are increased to about 110% of wild-type (Nolte, 1959). Control of drosopterin synthesis seems to be related to the activity of the enzyme GTP cyclohy- drolase (Evans and Howell, 1979, Biochem. Genet. 16: 13-26). The pn eye color is autonomous in larval optic disks tran- splanted into wild-type hosts (Beadle and Ephrussi, 1936). Larval Malpighian tube color is normal (Brehme and Demerec, 1942, Growth 6: 351-56). Standard pn mutants are homo- and hemizygous viable in a wild-type background, but show a lethal interaction with the third chromosome dominant awkK (Lifschytz and Falk, 1969; Orevi, 1973, DIS 50: 77). Some temperature-sensitive pn mutants (pnts-e), however, are insensitive to the killing action of awkK; one temperature-sensitive mutant (pnts-ek) is insensitive to awkK at permissive temperatures (18, 22), but sensitive to awkK at restrictive temperatures (25, 29) (Orevi, 1973, DIS 50: 80; Orevi and Falk, 1975). The TSP for the eye color phenotype occurs during the late pupal stage, while the TSP for the pn component of the pn-awkK interaction begins at the late pupal stage and lasts until eclosion (Orevi and Falk, 1975). Homo- and hemizygous pn deficiencies and other chromosomal rear- rangements have been induced by Ilyina et al. (1980), as indi- cated in the allele table. alleles: Eye color like pn1 except when otherwise indicated. Alleles interact lethally with awkK except for those affected by temperature (Orevi and Falk, 1975). allele origin discoverer ref ( comments cytology | ______________________________________________________________________________________________________________________________________ pn1 spont Bridges 3, 4, 15, 16, 22 brownish-red eye pn1a X ray 9, 20 homozygous lethal Tp(1;2)2D6-E1;20A2-3;20D;43F-44A1 pn2 / X ray Demerec 2, 6, 16, 19, 22 light brownish-red eye pn2a X ray 9, 20 homozygous lethal T(1;4)2D5-6;101F pn3 Wagenberg, Burdick 22 pn3a X ray 9, 20 homozygous lethal Tp(1;2;3)2E1-2;12E1-2;20A;41A;80C-D pn5 X ray Glass 7, 8 pn12 X ray 9 homozygous lethal T(1;3)2E1-2;98A1-2 pn20 X ray 20 T(1;2)2E1-2;40C1-2 pn25 X ray 9, 20 homozygous lethal Tp(1;3)2E1-2;20A1-2;70A5-6 pn26 X ray 9, 20 homozygous lethal Tp(1;3)2E1-2;20A1-2;70C1-2 *pn26-20 X ray Sobels 21 pn27-9 ` mustard gas Sobels 21, 22 *pn27-22 mustard gas Sobels 21 pn36 X ray 9, 20 homozygous lethal Tp(3;1)2E1-2;61A;62C1-2 + In(1)1A;2E1-2 pn40 X ray 9, 20 homozygous lethal T(1;2)2E1-2;41A pn45 X ray 9, 20 homozygous lethal In(1)2D1-2;20A *pn51b P32 King 11 pn51h X ray W.K. Baker, 51h8 1 pn55 spont Kivett 5 pn59j spont Narayanan, Weir 12, 13, 15 light brown eye pn62 X ray Petty pn63d X ray Mittler 14 eye like pn2 pn68b ` 22 pn69 NNG Kaufman 10 eye like pn2 pnAA1 DES Lifschytz 12, 13 pnFG spont Falk 13 pnFS1 EMS Orevi 18 pnMS2 EMS Lifschytz 13 pntr - EMS Orevi 18 pnts-e EMS Orevi 17, 18 awdK insensitive pnts-ek n EMS Orevi 17, 18 awdK insensitive at 18, 22 ( 1 = Baker, 1956, DIS 30: 69; 2 = Beadle, 1937, Genetics 22: 587-611; 3 = Beadle and Ephrussi, 1936, Genetics 21: 203; 4 = Brehme and Demerec, 1942, Growth 6: 351-56; 5 = Clancy, 1959, DIS 34: 48; 6 = Evans and Howell, 1979, Biochem. Genet. 16: 13-26; 7 = Glass, 1934, DIS 2: 7; 8 = Glass, 1935, DIS 3: 14; 9 = Ilyina, Sorokin, Belyaeva, and Zhimulev, 1980, DIS 55: 205; 10 = Kaufman, 1970, DIS 45: 34; 11 = King, 1952, DIS 26: 65; 12 = Lifschytz and Falk, 1968, DIS 43: 131; 13 = Lifschytz and Falk, 1969, Genetics 62: 343-52; 14 = Mittler, 1967, DIS 42: 38; 15 = Narayanan and Weir, 1964, Genetics 50: 387-92; 16 = Nolte, 1959, Heredity 13: 233-41; 17 = Orevi, 1973, DIS 50: 80; 18 = Orevi and Falk, 1975, Mutat. Res. 33: 193-200; 19 = Schwinck, 1973, DIS 50: 122; 20 = Slobo- dyanyuk and Serov, 1983, Mol. Gen. Genet. 191: 372-77; 21 = Sobels, 1958, DIS 32: 84-85; 22 = Wagenberg and Bur- dick, 1969, DIS 44: 107. | For new orders, see rearrangement listing in the chromosome section. / Synonym: se-like 62. ` pn27-9/pn68b flies are wild type in eye color and insensi- tive to awdK (Wagenberg and Burdick, 1969). - 40 temperature non-sensitive mutants indistinguishable from standard pn alleles (Orevi and Falk, 1975). Nine pnts-e alleles, all insensitive to awdK at all tempera- tures. Eye color light brown at 25 and 29, wild type at 18 and 22 (Orevi and Falk, 1975). n One allele, pnts-ek, sensitive to awdK at 25 and 29, but insensitive at 18 and 22. Eye color light brown at 25 and 29, wild type at 18 and 22 (Orevi and Falk, 1975). cytology: Located in 2E2-3 since included in Df(1)pn7a = Df(1)2E1-2;3A4 and Df(1)pn38 = Df(1)2D3-4;2E3 (Ilyina et al., 1980). Previously located at 2D5-6 by Demerec and Sutton (Demerec et al., 1942) and by J.I. Valencia. # pnr: pannier location: 3-58. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. phenotype: Homozygous lethal. Dorsal anterior of embryo open. alleles: Two alleles, pnr1 and pnr2, recovered as pnr7G and pnr9L. cytology: Placed in 89B9-10 since uncovered by Df(3R)sbd45 = Df(3R)89B4;89B10 but not by Df(3R)sbd105 = Df(3R)88F9- 89A1;89B9-10 (Hughes, Nelson, Yanuk, and Szauter). # pnt: pointed location: 3-79. origin: Induced by ethyl methanesulfonate. references: Jurgens, Wieschaus, Nusslein-Volhard, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 283-95. Mayer and Nusslein-Volhard, 1988, Genes Dev. 2: 1496-1511. phenotype: Homozygous lethal. Zygotic expression in embryo. Head skeleton of embryo pointed; median part of all denticle bands deleted. CNS broad and less dense than wild type. Sen- sory organs (maxillary, antennal, and Keilin's organs) spread. alleles: Two alleles, pnt1 and pnt2, recovered as pnt8B and pnt9J. cytology: Located in 94E; covered by YP3D of T(Y;3)B27 = T(Y;3)94E but not T(Y;3)R13 = T(Y;3)94E.