# po: pale ocelli location: 2-65.2. origin: Spontaneous. discoverer: Bridges, 38d1. phenotype: Ocelli virtually colorless; some pigment bordering inner margins. Eye color slightly brighter than wild type. RK2. #*po2 origin: Spontaneous. discoverer: Bridges, 20j13. synonym: do: dilute ocelli. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 224. phenotype: Ocelli pale. RK3. # Po: Pyridoxal oxidase location: 3-57.1 (0.08 unit to left of Aldox). synonym: lpo. references: Collins and Glassman, 1969, Genetics 61: 833-39. Dickinson and Weisbrod, 1976, Biochem. Genet. 14: 709-21. phenotype: The structural gene for the enzyme, pyridoxal oxi- dase [PO (EC 1.2.3.8)]; molecular weight approximately 225,000 daltons. Enzymatic characterization by Hanley (1980, Mol. Gen. Genet. 180: 455-62). Substrate specificities explored by Cypher, Tedesco, Courtright, and Kumaran (1982, Biochem. Genet. 20: 315-32). As PO is a molybdenum-containing protein (Warner and Finnerty, 1981, Mol. Gen. Genet. 184: 92-96), its activity is absent from cin, mal, and lxd flies, but cross reacting material is present in the latter two (but not the former) genotypes (Warner, Watts, and Finnerty, 1980, Mol. Gen. Genet. 180: 449-53). Enzyme activity present in all major organs except cardia, crop, imaginal discs, ovarian fol- licle cells, paragonia, pericardial cells, and wreath cells (Cypher et al., 1982). Developmental profile shows dramatic increase in activity beginning in late pupa and continuing into adult life (Dickinson and Weisbrod, 1976). The nearly amorphic allele, Polpo, exhibits 2% normal activity; little if any cross reacting material is detectable in Polpo. alleles: In addition to Polpo, electrophoretic variants PoS (common) and PoF (rare) have been recorded (Dickinson and Weisbrod, 1976). In(3R)LVM reported to carry a hypomorphic allele, PoLVM. cytology: Placed in 89A1-3 based on its inclusion in Df(3R)Po3 = Df(3R)89A1-2;89A11-13 but not Df(3R)c3G2 = Df(3R)89A2- 3;89A4-5 (Hughes, Nelson, Yanuk and Szauter). other information: Name changed from lpo to Po in order to con- form to terminology for other structural genes for enzymes. # pod: podgy location: 2-55. references: Ashburner, 1991, DIS 69. # pod foot: see pdf #*podG: podoptera of Goldschmidt location: Multifactorial. origin: Spontaneous. discoverer: Goldschmidt, 1943. references: 1945, Science 101: 389-90. 1945, J. Morphol. 77: 71-103 (fig.). Goldschmidt, Hannah, and Piternick, 1951, Univ. Calif. Publ. Zool. 55: 67-294. phenotype: Wing transformation into legs varies from almost wild type to three-jointed, leg-like appendages. Penetrance of 1-2% was increased to 2-4% by selection. Scalloped, blistered, and unexpanded wings and various abnormalities of legs are pleiotropic effects. RK3. other information: Podoptera may be similar to tetraltera effects. # podgy: see pod #*podH: podoptera of Hannah location: Multifactorial (principal factor on chromosome 2). origin: Spontaneous. discoverer: Hannah, 1943. references: Goldschmidt, Hannah, and Piternick, 1951, Univ. Calif. Publ. Zool. 55: 67-294. phenotype: Wings transformed into leg-like appendages. Legs characteristically changed and parts often duplicated. Aver- age penetrance of 2.5% increases to 5% in selected lines. Somatic elimination of X chromosome produces more than 2% gynandromorphs. RK3. other information: Claimed to have a maternally inherited com- ponent. #*podK: podoptera of Kellen-Piternick location: Multifactorial. origin: Spontaneous. discoverer: Kellen-Piternick, 1944. references: Goldschmidt, Hannah, and Piternick, 1951, Univ. Calif. Publ. Zool. 55: 67-294. phenotype: Like podG. Wings sometimes replaced by palpus-like structure. Average penetrance 30% in X/X/Y females and X/Y males. Females without Y or YL do not show podoptera pheno- type. Rough eyes, notched wings, and absence of postverticals occur. RK3. #*podM: podoptera in M(3)w-124 location: Multifactorial. origin: Spontaneous. discoverer: Kellen-Piternick, 1944. references: Goldschmidt, Hannah, and Piternick, 1951, Univ. Calif. Publ. Zool. 55: 67-294. phenotype: Wings transformed into leg-like structures. Penetrance of 15% in selected stocks is increased by presence of YL. RK3. # podoptera: see podG, podH, podK, podM # poi: see svrpoi # pointed: see pnt # Pointed wing: see Pw # Pointedoid: see BxJ # pol: see spapol # pole hole: see phl # poliert: see spapol # polo: polo location: 3-46. references: Sunkel and Glover, 1988, Jour. Cell Sci. 89: 25- 38. phenotype: Maternal-effect mitotic mutation and male meiotic mutation. The wild type allele functions in the early embryo and in the imaginal and neuroblast cells of the larva. About 7% of polo1 homozygotes (offspring of polo1/+ females mated to polo1/+ or polo1/polo1 males) survive to adulthood, but most of them die as late third instar larvae, their imaginal disks and neuroblast cells failing to proliferate. polo2 homozy- gotes (offspring of polo2/+ females mated to polo2/+ males) never eclose, dying as early third-instar larvae. Some polo1/polo2 heterozygotes (less than 7%) survive, but show very abnormal cuticle formation in the abdominal tergites. Offspring of surviving polo1/polo1 females die very early in development, the embryos showing an abnormal distribution of nuclei that fail to cellularize and then become polyploid before breaking down. Spindles of these embryonic nuclei are highly branched and have broad, barrel-shaped poles. In third instar larvae homozygous for polo1, many of the neuroblast cells show mitotic abnormalities. In anaphase, the chromosomes are often in a circular arrangement and may or may not be polyploid or aneuploid; these chromosomes, however, are never fragmented and seem to undergo normal condensation. In ana- phase, chromosomes frequently lie in a random orientation at one or both poles. Surviving polo1/polo1 males are fertile, but often show mei- otic abnormalities. Many of the meiotic spindles are irregu- lar in shape and structure amd a high frequency of nondisjunc- tion occurs, mostly in the second meiotic division. alleles: alleles origin discoverer comments ___________________________________________________________ polo1 EMS Nusslein-Volhard recessive semilethal; a few survivors polo2 HD Karess recessive lethal cytology: Located in 76B2-77C (from Ashburner). # polychaetoid: see pyd # polychaetous: see pys # Polycomb: see Pc # polycombeotic: see E(z) # Polycomblike: see Pcl # Polygenic Locus: see PL # polyhomeotic: see ph # polymorph: see ade2 # polyphene: see pyp # polyphene 61: see pph # polyphenic: see pph # polyubiquitin: see Ubi-p # ponte thermosensible: see pts #*pop: popeye location: 1-0.4. origin: Induced by p-N,N-di-(2-chloroethyl)amino-phenylbutyric acid (CB. 1348). discoverer: Fahmy, 1952. references: 1958, DIS 32: 73. phenotype: Eyes small, round, bulging, and rough. Often some central ommatidia protrude. Small body. Wings short, broad, and frequently blistered. Male sterile; viability less than 10% wild type. RK3. # porc: porcupine location: 1-59. origin: Hybrid dysgenesis. references: Perrimon, Engstrom, and Mahowald, 1989, Genetics 121: 333-52. phenotype: Homo- and hemizygous lethal that affects segmenta- tion pattern. porc/Y embryos from porc/porc germline clones show a segment polarity phenotype; porc/+ progeny from the germline clones become normal females. cytology: Located in 16E-17B from meiotic position. #*port: port location: 3- (not located). discoverer: Morgan, 14c. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 125. phenotype: Eye color slightly diluted. RK3. #*port-b: port-b location: 3- (not located). discoverer: Bridges, 19i11. references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 214. phenotype: Eye color maroon. RK3. # Positive spike II group: see nonA # posterior cell blister: see pcb # posterior crossvein: see pcv # Posterior sex combs: see Psc # postverticalless: see pvt # Pox: Paired box Two tissue-specific Drosophila paired box genes, Pox-m and Pox-n, both lacking homeodomains, are described in subsequent sections. No mutants have been discovered. references: Bopp, Jamet, Baumgartner, Burri, and Noll, 1989, EMBO J. 8: 3447-57. molecular biology: Genomic libraries of Drosophila melanogaster were screened with paired box probes from the prd gene and the two gsb genes (Frigerio, Burri, Bopp, Baumgartner, and Noll, 1986, Cell 47: 735-46; Baumgartner, Bopp, Burri, and Noll, 1987, Genes Dev. 1: 1247-67). The genes Pox-m and Pox-n were isolated and analyzed; they were found to share DNA and puta- tive amino acid sequences with the paired box regions of prd and the two gsb genes. Pox-m and Pox-n, however, have no homeodomains. Both genes are believed to be controlled by prd, which has both paired- and homeodomains (Bopp et al., 1989). The proteins of both Pox-m and Pox-n are located in the cell nucleus and may belong to the same regulatory cascade as the other paired domain genes. # Pox-m: Paired box-meso location: 3-{48}. phenotype: Pox-m shows tissue-specific, segmentally-repeated expression in the somatic mesoderm, starting at germ band extension. Transcripts are observed posterior to the paraseg- mental grooves (restricted to the mesodermal layer). The pro- tein has been observed by immunostaining in the somatopleura that gives rise to the somatic musculature, but is not found in the splanchnopleura and the mesectodermal cells (Jamet). Groups of cells in the clypeolabrum, the cephalic mesoderm, and the primordia of the telson and the proctodeum also express Pox-m. cytology: Located in 84F11-12 by in situ hybridization to the salivaries. The distal breakpoint of Df(3R)dsx5 is located at 84F11-12 in the intron of the Pox-m gene. # Pox-n: Paired box-neuro location: 2-{48}. phenotype: Pox-n shows tissue-specific, segmentally-repeated expression in the central and peripheral nervous system at about 5 hr after fertilization. Transcripts are apparently expressed in neural precursors of the peripheral and the cen- tral nervous system. Cells expressing this gene seem to be clonally related. cytology: Located in 52C9-52D3 by in situ hybridization to polytene chromosomes. It is uncovered by Df(2R)WMG = Df(2R)52C4;52E3 (Gelbart) and is located between the distal breakpoint of Df(2R)XTE-18 at 52C9-D1 and the prox- imal breakpoint of Df(2R)KL-9 at 52D3. molecular biology: The Pox-n gene has an intron with the paired domain preceding the region encoding the helix-turn-helix motif (Bopp et al., 1989). # Pp1: Protein phosphatase 1 location: 3- and 1- (see molecular biology). references: Dombradi, Axton, Glover, and Cohen, 1989, Eur. J. Biochem. 183: 603-10. phenotype: Encodes a protein phosphatase 1 catalytic subunit that shows a high degree of similarity to rabbit protein phos- phatase 1( in its enzymatic and physiochemical characteristics and has a predicted protein sequence that is 92% identical to that of rabbit PP-1(. cytology: The major site of Pp1 has been placed at 87B6-12 by in situ hybridization to the polytene chromosomes. In addi- tion, three secondary sites have been demonstrated at 96A2-5, 9C1-2, and 13C1-2. molecular biology: A 1.2-kb cDNA clone carrying the full coding sequence of Drosophila Pp1 was isolated from a Drosophila head library using a 0.76-kb rabbit PP-1( cDNA as a probe. The nucleotide and predicted amino acid sequences of this Droso- phila Pp1 were determined. A polypeptide of 302 amino acids with a molecular mass of 34.5 kd is encoded. The sequence of the 1.2-kb cDNA contains an open reading frame of 906 nucleo- tides flanked by 5' and 3' noncoding sequences. Abundant transcripts of 1.6 kb and 2.5 kb were detected in embryos, larvae, pupae, and adults. Another cDNA clone of 0.6 kb was isolated from the Drosophila head library with the same probe, and was found to hybridize to 9C1-2, indicating that there are at least two transcriptionally active Pp1 genes in Drosophila melanogaster. #*pph: polyphenic location: 1-60.8 (originally located at 61.0 but genetic loca- tion arbitrarily interchanged with that of sby for consistency with cytological observations). origin: Induced by D-1:6-dimethanesulfonyl mannitol (CB. 2511). discoverer: Fahmy, 1959. synonym: pph-61: polyphene 61. references: 1964, DIS 39: 58. phenotype: Body small. Eyes brighter than normal. Wing size and shape slightly altered. Scutellar bristles occasionally kinked. Both sexes viable; fertility of homozygous female low. RK3. cytology: Not included in deficiency for 18A4 through 18B8 pro- duced by combining left end of In(1)y4 = In(1)1A8-B1;18A3-4 and right end of In(1)sc9 = In(1)1B2-3;18B8-9 (Norton and Valencia, 1965, DIS 40: 40). # pph-61: see pph # pr: purple location: 2-54.5. references: Bridges, 1919, J. Exp. Zool. 28: 264-305. Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 169. Mainz, 1938, Z. Indukt. Abstamm. Vererbungsl. 75: 256-76. Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85. Wilson and Jacobson, 1977, Biochem. Genet. 15: 321-32. Yim, Grell, and Jacobson, 1977, Science 198: 1168-70. Tobler, Yim, Grell, and Jacobson, 1979, Biochem. Genet. 17: 197-206. Dorsett and Jacobson, 1982, Biochemistry 21: 1238-43. Wiederrect and Brown, 1984a, J. Biol. Chem. 259: 14121-27. Wiederrect, Paton, and Brown, 1984b, J. Biol. Chem. 259: 2195-2200. Searles and Voelker, 1986, Proc. Nat. Acad. Sci. USA 83: 404-08. phenotype: Eye color ruby at hatching, darkening to purplish ruby with age [Sturtevant and Beadle, 1939, An Introduction to Genetics, W.B. Saunders Co., Philadelphia and London, p. 64 (plate I)]; orange in combination with st, reddish brown in combination with bw (Mainz, 1938). pr eye color autonomous in larval optic disks transplanted into wild-type hosts (Beadle and Ephrussi, 1936, Genetics 21: 230). Larval Malpighian tubules wild-type in color (Beadle, 1937, Genetics 22: 587- 611). Mutants deficient in pteridines (Hadorn and Mitchell, 1951, Proc. Nat. Acad. Sci. USA 37: 650-65; Wilson and Jacob- son, 1977; Yim et al., 1977); sepiapterin and the drosopterins are markedly reduced relative to wild type in pr1 and prbw (Wilson and Jacobson, 1977; Dorsett and Brown, 1982), the effect being greater in prbw than in pr1. The enzyme sepiapterin synthase A, which is involved in early steps lead- ing to the synthesis of the drosopterins (Wiederrect et al., 1984a, 1984b), is most active in wild-type Drosophila in late pupae and young adults when sepiapterin accumulation begins and the eyes become pigmented (Krivi and Brown, 1979, Biochem. Genet. 17: 371-90). When pr+ has been translocated into the Y chromosome [Tp(2;Y)prC5], the Tp(2;Y)prC5, cn/prC4cn flies show a variegated eye color (Yim et al., 1977; Tobler et al., 1979) and the mutant late larvae and early pupae show a reduc- tion in sepiapterin synthase A activity as compared to both wild-type and pr1 (Tobler et al., 1979). The suppressors su(s)2 and su(pr)e3 restore the pyrimidine level of pr1 and prbw to that of wild-type or nearly wild-type (Wilson and Jacobson, 1977; Yim et al., 1977). alleles: pr mutants and rearrangements (other than deficien- cies) are described in the following table: allele origin discoverer ref ( eye color cytology ___________________________________________________________________________ pr1 | Bridges, 12b20 1-4, 6, 14 reddish-purple *pr2 L.V. Morgan 8 redder than pr1 pr40 11 In(2L)21D-E; 38B *pr42d spont Nolte, 42d 10 redder than pr1 pr80d spont Najera, 80d 9b pr81d spont Najera, 81d 9, 9a pr112 X ray Wright 13 pr156 X ray 13 prbw | spont Bridges, 38d20 14 brownish-pink prC4 / EMS Yim 12, 14 prC4/pr1: lighter than pr1/pr1 prC5 EMS Yim 12, 14 pr variegated Tp(2;Y)prC5 prlM60 / spont Meyer, 60g 7 prlM60/pr1: small purple deficiency? *prM60 X ray Meyer, 60g 7 prM60/pr1: dark brown *prs ` X ray Ives, 38k 5 weak pr prv X ray 13 pr variegated T(Y;2)TW124 ( 1 = Beadle, 1937, Genetics 22: 587-611; 2 = Beadle and Ephrussi, 1936, Genetics 21: 230; 3 = Bridges, 1919, J. Exp. Zool. 28: 264-305; 4 = Bridges and Morgan, 1919, Car- negie Inst. Washington Publ. No. 278: 169; 5 = Ives, 1937, DIS 13: 50; 6 = Mainx, 1938, Z. Indukt. Abstamm. Verer- bungsl. 75: 256-76; 7 = Meyer, 1963, DIS 37: 51; 8 = Mor- gan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 233; 9 = Najera, 1984, DIS 60: 241; 9a = Najera, 1985, DIS 61: 215; 9b = Najera, 1986, DIS 63: 167; 10 = Nolte, 1957, DIS 31: 84; 11 = Reuter and Wolfe, 1981, Mol. Gen. Genet. 182: 516-19; 12 = Tobler, Yim, Grell, and Jacobson, 1979, Biochem. Genet. 17: 197-206; 13 = Wright, Hodgetts, and Sherald, 1976, Genetics 84: 267-85; 14 = Yim, Grell, and Jacobson, 1977, Science 198: 1168-70. | pr1 and prbw suppressed by su(s)2 and su(pr)e3 (see "pheno- type"). / Homozygous lethal. ` prs/prs females sterile, males fertile; viability of males and females good. prs/+ and prs/pr1 females fertile. cytology: Placed in 38B5-C2 based on its inclusion in the region of overlap of Df(2L)pr2b = Df(2L)38B5-C1;38D2-E1 and Df(2L)pr-A20 = Df(2L)38A3-4;38B6-C1. molecular biology: The transposable element 412 is inserted in cytological interval 38B4-6 in pr1 and prbw, as indicated by hybridization of cloned 412 to salivary squashes (Searles and Voelker, 1986). Pr: Prickly From Muller, 1930, J. Genet. 22: 299-334. # Pr: Prickly location: 3-90.0. references: Muller, 1930, J. Genet. 22: 299-334 (fig.). 1935, DIS 3: 30. Knust, Tietze, and Campos-Ortega, 1987, EMBO J. 6: 4113-23. phenotype: Bristles very short; tips thin and twisted. Post- dorsocentrals and scutellars usually missing; dark granule present beneath normal bristle location. Homozygote has low viability. PrK complements some dominant traits of E(spl) and is in turn enhanced by it, showing severe defects and loss of bristles. alleles: allele origin ref ( molecular biology | _____________________________________________ Pr1 X ray 1, 2 -4.5 to 0 PrK 2 -4.5 to 0 PrL / spont 1, 2 -4.8 to -3.8 ( 1 = CP627; 2 = Knust, Tietze, and Campos-Ortega, 1987, EMBO J. 6: 4113-23. | The positions of DNA polymorphisms; relation to mutations unclear. DNA coordinates (kb) of the walk in region 96F8-13 where E(spl) has been mapped ("+" values to the right, "-" values to the left). / Partial revertant of Pr1. Bristles of PrL/+ about one-third normal length (longer than bristles of Pr1/+). PrL homozy- gote viable with small vestiges of bristles. PrL/H resem- bles Pr1/+. cytology: Located in 96F8-13 from molecular data; also located in 96F10-97C1. #*pra: prawny abdomen location: 1-15.2. origin: Induced by DL-p-N,N-di-(2-chloroethyl)amino- phenylalanine (CB. 3007). discoverer: Fahmy, 1954. references: 1959, DIS 33: 88. phenotype: Thorax narrow. Abdomen slender, often flexed between fourth and fifth segments. Wings short, rather broad, and often held atypically. Eclosion delayed. Viability about 15% wild type. RK3. # prat: pratfall (T. Schupbach) location: 2-98. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal effect lethal; embryos from homozygous mothers do not hatch. In cuticle preparations they show irreg- ular segmentation and variable segment fusions. alleles: pratPD = prat1. cytology: Placed in 57B4-14 or in 57D8-58B (Schupbach and Wieschaus, 1989). # prawny abdomen: see *pra # prd: paired location: 2-45. references: Nusslein-Volhard and Wieschaus, 1980, Nature (Lon- don) 287: 795-801. Nusslein-Volhard, Kluding, and Jurgens, 1985, Cold Spring Har- bor Symp. Quant. Biol. 50: 145-54. Frigerio, Burri, Bopp, Baumgartner, and Noll, 1986, Cell 47: 735-46. Kilchherr, Baumgartner, Bopp, Frei, and Noll, 1986, Nature (London) 321: 493-99. phenotype: The wild-type allele of prd is required for normal segmentation in embryos and larvae. Mutant alleles and defi- ciencies show no maternal effects and are embryonic lethals with half the normal number of segmental units. In strong mutants, the anterior part of segments T1, T3, A2, A4, A6, and A8 and the posterior part of T2, A1, A3, A5, and A7 (i.e., odd-numbered parasegments) are deleted (Nusslein-Volhard et al., 1985). Weak mutants such as prd2 show small and less regular segmental deletions. Structures missing in prd mutants include: derivatives of the mandibular segments, labial sense organs, anterior prothorax, posterior mesothorax, anterior metathorax, and alternating posterior and anterior abdominal segments, including the telson and the posterior lateral sense organs (Nusslein-Volhard et al., 1985). No head fold visible at gastrulation. Experiments with a temperature-sensitive mutant indicate that the TSP occurs dur- ing the cellular blastoderm stage (Nusslein-Volhard et al., 1985; Kilchherr et al., 1986). alleles: prd mutants and rearrangements (except for deficien- cies) are described in the following table. allele origin synonym ref ( comments _______________________________________________________________ prd1 EMS 4 prd2 EMS 4 prd3 X ray prd2.27 3, 5 Tp(2;3)31B;33D-E;97C-D prd4 X ray prd2.45.17 1, 2, 7 strong allele prd5 X ray prd5.12 3, 5 Tp(2;Y)33A;35B prd6 EMS prd6L 7 strong allele prd7 X ray prd32.12 7 strong allele prd8 | EMS prdFR1 6, 7 strong allele prd9 EMS prdIIB 7 weak allele prd10 EMS prdIIN 7 temperature sensitive prd11 EMS prdIIW 7 weak allele prd12 X ray prdX3 7 strong allele ( 1 = Frigerio, Burri, Bopp, Baumgartner, and Noll, 1986, Cell 47: 735-46; 2 = Kilchherr, Baumgartner, Bopp, Frei, and Noll, 1986, Nature (London) 321: 493-99; 3 = Nusslein- Volhard, Kluding, and Jurgens, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 145-54; 4 = Nusslein-Volhard and Wieschaus, 1980, Nature (London) 287: 795-801; 5 = Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82; 6 = Sander, Lohs- Schardin, and Baumann, 1980, Nature (London) 287: 841-43. 7 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. | Larva moves in egg case, but fails to hatch. 45% of embryos show holes in the larval cuticle and/or lateral fusion of denticle belts (Sander et al., 1980). cytology: Located in 33C1-2 by in situ hybridization; included in Df(2L)prd1.25 = Df(2L)33B6-7;33E2-3 as well as in Df(2L)prd1.7 = Df(2L)33B2-3;34A1-2 (Nusslein-Volhard et al., 1985). molecular biology: prd+ and prd4 have been cloned by micro- dissection of salivaries and chromosome walking and restriction-mapped to the DNA at +170 to +180 kb by Kilchherr et al. (1986) [coordinate 0 at distal end of a 41 kb EcoRI fragment; "+" values to the right, "-" values to the left (Frei, Baumgartner, Edstrom, and Noll, 1985, EMBO J. 4: 979- 87)]. One transcript of 2.5 kb was detected in prd+ embryos; two transcripts of 2.5 and 3.6 kb were detected in embryos from prd4/prd+ parents; a 1.1 kb insertion was found in the mutant DNA (Kilchherr et al., 1986). The 2.5 kb transcript is absent in oocytes, peaks in 2-4 hr embryos, and disappears after gastrulation. The prd+ gene was sequenced by Frigerio et al. (1986) and the amino acid sequence of a putative prd protein (613 amino acids) determined. The longest open reading frame is inter- rupted by a 356 bp intron after the first 22 amino acids. The 1.1 kb insertion in the prd4 DNA has also been sequenced by Frigerio et al.. Two domains shared with the two closely- linked genes at the gsb locus (Bopp, Burri, Baumgartner, Fri- gerio, and Noll, 1986, Cell 47: 1033-40; Baumgartner, Bopp, Burri, and Noll, 1987, Genes and Development 1: 1247-67). During the syncytial blastoderm stage in paired embryos, a transcript pattern of 7 bands, with a periodicity correspond- ing to two primordial segments, appears (Kilchherr et al., 1986). By the time the embryos have reached the cellular blastoderm stage, an additional band appears posterior to band 7, band 1 is narrowed, and bands 2-7 have split, resulting in a 14-banded transcript pattern with single segment periodi- city. prd is first expressed in a pattern similar to that of ftz, h, and eve (pair-rule genes). However, it shares domains with segment-polarity genes such as bcd (Bopp et al., 1986). Expression of en absent with a consequent increase of Ubx expression in odd-numbered parasegments (Martinez-Arias and White, 1988, Development 102: 325-38). # pre: presto (T. Schupbach) location: 2-54. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus, 1989, Genetics 121: 101- 17. phenotype: Maternal-effect lethal; homozygous females lay eggs in which periplasmic clearing occurs, but no signs of cellu- larization are observed. alleles: Two: pre1 and pre2 isolated as PL and ADF respec- tively. cytology: Placed in 36E4-37C1 based on its inclusion in both Df(2L)TW50 = Df(2L)36E4-F1;38A6-7 and Df(2L)TW137 = Df(2L)36C2-4;37B9-C1. # Pre-intermolt gene 1: see Pig1 # presto: see pre # prickle: see pk # Prickly: see Pr # proboscipedia: see pb # prong: see pg # Pros35: Proteasome 35 location: 3-{59}. references: Haass, Pesold-Hurt, Multhaup, Beyreuther, and Kloetzel, 1989, EMBO J. 8: 2373-79. phenotype: Encodes the 35 kd proteasome subunit of Drosophila melanogaster. The proteasome is strongly expressed in the cen- tral nervous system of embryos and the heart muscle and epithelial cells of the stomach and ovary of adults and is localized in the cytoplasm in some cells and/or the nucleus in others. cytology: Pros35 was located by in situ hybridization at the border of 89F/90A. It is a single copy gene. molecular biology: The gene was cloned and its nucleotide sequence and deduced amino acid sequence obtained; the primary translation product is a 31.4 kd protein. This protein is encoded by a mRNA of about 1100 nucleotides which seems to be present in very low abundance. The cDNA is 999 bp long and there is a single open reading frame encoding 279 amino acids. The 35 kd protein subunit carries a consensus sequence for a potential tyrosine phosphorylation site; this subunit may be involved in the regulation of the complete multicatalytic pro- teinase complex. # Protein kinase: see Pk # proximalless: see pxl # prune: see pn # Ps: Pigmentless location: 2-57.5 (inseparable from cn). origin: X ray induced. discoverer: Krivshenko, 56l15. references: 1959, DIS 33: 95. phenotype: Black strips on last abdominal segments of female reduced; expression variable. Male unaffected. Homozygous lethal. RK2. cytology: Salivary chromosomes apparently normal. # Ps2a: see if # Psc: Posterior sex combs location: 2-67. origin: Induced by ethyl methanesulfonate; isolated as embryonic lethal with head defects (Jurgens, 1985). references: Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82. Jurgens, 1985, Nature (London) 316: 153-55. Wu, Jones, Lasko, and Gelbart, 1989, Mol. Gen. Genet. 218: 559-64. phenotype: Psc+ is another gene that may be considered a nega- tive regulator of the BXC or the ANTC. The mutant is homo- and hemizygous lethal, the embryos showing partial transforma- tion of head and thorax into abdomen and of abdominal segments 1-7 into more posterior ones. Psc/Psc embryos that are also homozygous for Asx, Pcl, or Scm show stronger posteriorly- directed transformations; the triple mutant Psc Asx Pcl has a tandem array of posterior abdominal segments including four abdominal denticle bands in the head region (Jurgens, 1985). Psc/+ males may have sex combs on second and third legs. The gene suppresses z1 eye color, which becomes orange-maroon; it is lethal with Su(z)21 and Su(z)25 and semiviable with Su(z)24 (Wu et al., 1989). Psc and Su(z)2 are both members of the Su(z)2 complex. alleles: One allele isolated: PscIIN = Psc1. cytology: Located in 49D3-E5 since included in Df(2R)vg-B = Df(2R)49D3-4;49F15-50A2-3 and Df(2R)vg-D = Df(2)49C1-2;49E4-5; at odds with the above determination is the failure of Df(2R)vg-C = Df(2R)49B2-3;49E7-F1 to uncover Psc (Jurgens, 1985). # psi2: phase-angle2 (J. C. Hall) location: 2-72.0. origin: Induced by ethyl methanesulfonate. references: Jackson, 1983, J. Neurogenet. 1: 3-15. phenotype: Semidominant; emerges prematurely in light-dark cycle. Eclosion and locomotor activity rhythms have abnor- mally long periods (about 25-26 hr instead of normal 24 hr). Mutant males have abnormally long periods of courtship song rhythms (Kyriacou); phenotype recessive. Mutant males also show abnormal conditioning in courtship tests (Jackson, Gai- ley, and Siegel, 1983, J. Comp. Physiol. 151: 545-52). cytology: Located in 49E7-50A2, based on uncoverage of song rhythm defect by Df(2R)vg-B = Df(2R)49D3-4;49F15-50A2 and com- plementation of this defect by Df(2R)vg-C = Df(2R)49B2- 3;49E7-F1 (Kyriacou and Clarkson). other information: May be allelic to quasi-arrhythmic mutant gat, based on similar map positions and lengthened song rhythm periods in psi2/gat males (Jackson and Kyriacou). # psi3 (J. C. Hall) location: 3- (to right of and close to Sb). origin: Induced by ethyl methanesulfonate. references: Jackson, 1983, J. Neurogenet. 1: 3-15. phenotype: Semidominant; emerges prematurely in light-dark cycle. Eclosion rhythm exhibits abnormally long period (about 25 hr), as do males in their rhythmic courtship singing behavior (Kyriacou). Mutant males show abnormal conditioning in courtship tests (Jackson, Gailey, and Siegel, 1983, J. Comp. Physiol. 151: 545-52). # pt: platinum location: 1-23.1. origin: Deuteron induced. discoverer: Hildreth, 51h. references: Hildreth, 1953, DIS 27: 56. King, Mohler, Riley, Storto, and Nicolazzo, 1986, Dev. Genet. (Amsterdam) 7: 1-20. phenotype: Body color very pale yellow, almost colorless. Bristles colorless and translucent except for dark bases. Male sterile and short lived. Tyrosinase forms in adult (Horowitz and Fling). One allele (pt2) is a zygotic lethal; another (pt4) is female sterile (King et al., 1986); shown to be a maternal-effect lethal rescuable by a normal paternal allele (Mohler and Carrol, 1984, DIS 60: 236-41). alleles: allele origin discoverer synonym ref ( comments ___________________________________________________________________ pt1 deuteron Hildreth pa 1 viable pt2 X ray Lefevre l(1)JC28 2, 3 lethal (zygote) pt3 EMS Lefevre l(1)VA70 3 viable pt4 EMS Mohler fs(1)M47 2 female sterile ( 1 = Hildreth, 1953, DIS 27: 56; 2 = King, Mohler, Riley, Storto, and Nicolazzo, 1986, Dev. Genet. (Amsterdam) 7: 1- 20; 3 = Lefevre and Watkins, 1986, Genetics 113: 869-95. cytology: Located in the 7F region since included in Df(1)7F1- 2;8C6; maps to the left of oc, which is located at 8A1-2. # pt: see ab2 # Pt-1: see Lsp2 # pta: see sldpta # ptc: see tuf # ptd: parted location: 1-52.7. origin: Induced by nitrosoguanidine. references: Kaufman, 1969, DIS 44: 44. phenotype: Wings held at 45 angle from body and slightly elevated. In young flies, the wing tips are usually curved up; in old cultures and old flies, the wings are usually shrivelled. The shrivelled condition (but not the cupping) does not occur at 18. Males viable and fertile, females viable and sterile. # Ptd: see BxJ #*pte: pterygion location: 1-1.4. origin: Induced by 1:4-dimethanesulfonoxybut-2-yne (CB. 2058). discoverer: Fahmy, 1951. references: 1958, DIS 32: 73. phenotype: Wings shortened, usually spread, and slightly droop- ing. Eyes misshapen and somewhat rough. Abdomen dispropor- tionately large. Eclosion slightly delayed and viability about 20% wild type. RK3. other information: Possible allele of dwg. # ptg: pentagon location: 1-23.2. phenotype: Thoracic trident darker than wild-type, especially the pentagonal spot just anterior to the scutellum; more extreme at 19C. Hard to classify in young flies. alleles: Six pentagon alleles are listed in the following table. (ptg2, ptg3, and ptg4 are also given a separate description). allele origin discoverer synonym ref ( ________________________________________________________ ptg1 Bridges, 22l8 ptg2 L.V. Morgan, 24j21 4 ptg3 Kaliss, 35l cro:crown 1, 3 ptg4 spont Curry, 38b8 ptg5 EMS Craymer ptgM1.270 ptg6 EMS Craymer ptgM1.33 ptg7 | EMS Helfand, Carlson ptg3D18 2 ( 1 = Felsenstein, 1937, DIS 7: 21; 2 = Helfand and Carlson, 1989, Proc. Nat. Acad. Sci. USA 86: 2908-12; 3 = Kaliss, 1937, DIS 7: 6,18; 4 = Morgan, L.V., 1935, DIS 3: 14. | Fertility of homozygotes low; response to odor of benzal- dehyde reduced. cytology: Located in salivary region 8A5 by Lefevre (1981, Genetics 99: 461-80). Included in the X chromosome insertion of ct+-ptg+ in Dp(1;2)sn+72d = Dp(1;2)7A8;8A5;32C;58E. # ptg2 phenotype: Pentagonal spot sharper and darker than in ptg1. Scutellum often dark and prongs of tridents may be dark also. # ptg3 phenotype: Trident darker than in ptg1; dark color extends to head, sides, and abdomen. other information: Occasionally reverts to wild type or weak ptg. Allelism with ptg shown by Bridges. # ptg4 phenotype: Darkness of pentagon intermediate between that of ptg1 and ptg2. # ptm: see bwptm # pts: ponte thermosensible location: 3- (near se at 3-26.0). origin: Spontaneous in se/se strain. references: Picard, 1973, Mol. Gen. Genet. 123: 363-68. Anxolabehere, 1980, Genetica 51: 161-65. phenotype: Temperature-sensitive recessive female sterile (Picard, 1973). When homozygous pts females are kept at 30, their eggs fail to hatch or hatch in very small numbers at either 20 or 30; when the females are kept at 20, the eggs hatch at 20 but not at 30. pts/pts females kept at an inter- mediate temperature (25) are fertile, but their eggs take longer to develop than at the permissive temperature (Anxola- behere, 1980). Heterozygous females kept at either 20 or 30 hatch eggs at either temperature; their productivity is greater than that of homozygotes at 20 (Picard, 1973). The temperature-sensitive periods occur at the beginning of oogenesis (for laying) and from 36-60 hr of larval life (for hatching). # pu: pupal location: 2-51. synonym: pads-b. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 232. Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Lit- tlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91. phenotype: Wings unexpanded or incompletely expanded; more extreme at 19. Extreme alleles show erect and crossed postscutellar bristles and a distorted thoracic cage (Ash- burner). Df(2L)A400/Df(2L)el4DA80P, a homozygous pu defi- ciency, is barely viable; escapers are pu. alleles: All alleles are cytologically normal. allele origin discoverer synonym ref ( 25 phenotype ________________________________________________________________ pu1 | spont Duncan, 20d 1, 3 strong pu2 EMS Harrington 1 strong pu3 EMS Harrington 1 strong pu4 EMS Harrington 1 very weak / pu5 | EMS Harrington 1 intermediate ` pu6 EMS Littlewood pu76e 2, 5 strong pu7 EMS puDM7 4 strong ( 1 = Ashburner, Angel, Detwiler, Faithfull, Gubb, Harrington, Littlewood, Tsubota, Velissariou, and Walker, 1981, DIS 56: 186-91; 2 = Ashburner, Faithfull, Littlewood, Richards, Smith, Velissariou, and Woodruff, 1980, DIS 55: 193-95; 3 = Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 232; 4 = O'Donnell, Mandel, Krauss, and Sofer, 1977, Genetics 86: 553-66; 5 = Woodruff and Ashburner, 1979, Genetics 92: 133-49. | pu1/pu5 flies show some wing expansion (Ashburner et al, 1981). / pu4 overlaps wild-type, its wings being almost fully expanded but wavy (Ashburner). ` pu5 shows some wing expansion at 25. cytology: Placed within 35A1-3 since Df(2L)el4DA80P = Df(2L)35A2-4;35A3-4 [from T(Y;2)el4 and T(Y;2)A80] and Df(2L)A400 = Df(2L)35A1-4;35B10 are deficient for pu, but Df(2L)fn2 = Df(2L)35A3;35B2 is not (Ashburner). other information: Not allelic to pads. # Pu: Punch location: 2-97. synonym: upi: unpigmented (Nusslein-Volhard, Wieschaus, and Kluding, 1984, Wilhelm Roux's Arch. Dev. Biol. 193: 267-82). references: Mackay and O'Donnell, 1983, Genetics 105: 35-53. Mackay, Reynolds, and O'Donnell, 1985, Genetics 111: 885-904. Reynolds and O'Donnell, 1987a, Dev. Biol. 123: 430-41. 1987b, Genetics 116: s15. 1988, Genetics 119: 609-17. O'Donnell, Boswell, Reynolds, and Mackay, 1989a, Genetics 121: 273-80. O'Donnell, McLean, and Reynolds, 1989b, Dev. Biol. 10: 273- 86. phenotype: The structural gene for guanosine triphosphate 7,8- 8,9-dehydrolase = GTP cyclohydrolase [GTP CH (EC 3.5.4.16)], which catalyzes the first step in pteridine biosynthesis, the conversion of GTP to dihydroneopterin with the release of formic acid; GTP CH activity proportional to the number of Pu+ alleles. Purification and characterization by Weisberg and O'Donnell (1986, J. Biol. Chem. 261: 1453-58); the active complex has an apparent molecular mass of 575,000 daltons comprised of 39,000-dalton subunits. Developmentally regu- lated with a short-lived activity peak at or shortly before eclosion; 80-90% of activity found in the head; activity not detectable in embryos. Dominant alleles are embryonic lethal as homozygotes and in heterozygotes produce dilute purple eye color; Appear to be antimorphic in that GTP CH activity in heterozygotes reduced to less than the 50% normal levels observed in deficiency heterozygotes, at least in adult tis- sues, and is but 80% normal in genotypes that carry, in addi- tion to the mutant allele, two doses of Pu+. Most are associ- ated with a chromosome rearrangement with one breakpoint in 57 and the other in or near centric heterochromatin. A few recessive alleles are viable and fertile and exhibit reduced GTP CH activity in the head but normal or near-normal levels in prepupae and adult body; however, the majority are embryonic lethals and have reduced activity in prepupae, adult body, and head when heterozygous with viable alleles; rare lethal alleles are defective in neither eye-pigment production nor in postembryonic enzyme activity. Viable alleles comple- ment lethal alleles for viability, at least partially; in com- bination with each other and with lethal alleles they display a wide range of eye pigmentation; some pairs of lethal alleles complement fully or partially for both viability and eye color; prepupal enzyme levels are vari- ably reduced in these combinations in ways that are uncorre- lated with survival; heteroallelic survivors are fertile; heteroallelic survival markedly reduced or absent when reared at 16. Homozygous deficiencies [Df(2R)F36] die as fully formed lar- vae, but prior to hatching; mouth parts and setae completely unpigmented; setae and sensory structures poorly differen- tiated; cuticle thin and fragile; head involution and dif- ferentiation frequently incomplete, beginning at the time of germ-band shortening. Class II mutants display variably simi- lar phenotypes as do class III alleles, but to a less severe extent. 50% of class V mutants die before blastoderm, the remaining 50% dying during late embryogenesis, but with fully pigmented mouth parts and setae and with normal head develop- ment; fusions and deletions of abdominal denticle belts, or the normal number of belts, but all of identically abnormal structure, retaining only the two posterior setal rows; pre- blastoderm nuclear divisions asynchronous, abnormally distri- buted in embryos, and nuclei misshapen (Reynolds and O'Donnell, 1987, Genetics 116: s14). Embryos homozygous for class IV alleles resemble class V mutants, but with additional features characteristic of class II embryos, including unpig- mented setae and mouth parts. In crosses of class V bearing genotypes to Df(2R)F36/+, the Df(2R)F36/Pu embryos resemble class V embryos when the deficiency is maternally inherited and deficiency homozygotes when the Pu allele is maternally inherited. alleles: In the following table, recessive alleles are super- scripted "r" and revertants "rv". Pu deficiences are listed as rearrangements. allele origin discoverer synonym ref ( comments ________________________________________________________________________________________________________________________ Pu1 X ray Oliver, 28k4 5, 7, 8, 10, 12 T(2;3)57B5-C1;79F; viable, dominant Pu2 spont Grell, 57b 4, 5, 6, 12 dominant, noncomplementing, cytologically normal (Class II) | PuE18A EMS Boswell 12 noncomplementing (Class II) PuGr X ray Muller, 29l Gr:Grape 2, 3 dominant, T(2;3)57C;81F PuIN EMS 14 PuIIK EMS 14 PuK X ray Krivshenko, PmK 1, 13 dominant, In(2R)41;57E-F 53k24 PuK5-2 EMS Boswell 12 noncomplementing (Class II), dominant | PuL / ray Lyttle 5 dominant PuPD16 EMS 12 noncomplementing (Class II) Pur1 spont Ives 5, 12 viable, In(2R)57C;57E | Pur331 spont Finnerty 5, 12 viable, eye color intermediate | PurAA1 EMS 5, 6, 12 noncomplementing (Class II) PurAA4 EMS 5, 12 viable PurAA17 EMS 5, 6, 12 noncomplementing (Class II) PurFAMI-2 EMS Boswell 12 noncomplementing (Class II) Purl9 EMS 5, 6, 12 complementing (Class IVc) PurJE5 EMS 12 complementing (Class III) PurK8-2 EMS Boswell 11, 12 noncomplementing (Class V), eye color normal PurP1 EMS 5, 6, 12 partially dominant noncomplementing (Class II) PurP11 EMS 5, 6, 11, 12 complementing (Class IVa) PurP21 EMS 5, 6, 11, 12 noncomplementing (Class II) PurP30 EMS 5, 6, 11, 12 complementing (Class III) PurP42 EMS 5, 6, 11, 12 complementing (Class III) PurP43 EMS 5, 6, 11, 12 complementing (Class IVb) | PurPF7 EMS Boswell 12 noncomplementing (Class II) PurPF12 EMS Boswell 12 noncomplementing (Class II) PurPH30 EMS 12 noncomplementing (Class II) PurPJ15 EMS 12 noncomplementing (Class II) PurS47 EMS 5, 6, 11, 12 complementing (Class IVa) PurSH8 EMS Boswell 12 noncomplementing (Class II) PurTR1 EMS 12 noncomplementing (Class II) PurTR3 EMS 12 noncomplementing (Class II) PurTR5 EMS 12 noncomplementing (Class II) PurTR7 EMS 12 complementing (Class IVc) Purv X ray Oliver, 32l27 9 PurV3 EMS 12 noncomplementing (Class II) PurV9 EMS 5, 6, 12 noncomplementing (Class II) PurV14 EMS 5, 6, 12 noncomplementing (Class II) PurV15 EMS 6, 12 noncomplementing (Class II) PurX17 EMS 5, 12 viable PurW10 EMS 6, 12 noncomplementing (Class II) PurWE67 EMS 11, 12 noncomplementing (Class V) eye color normal PurWE75 EMS 11, 12 complementing (Class V) eye color normal PurWM1 EMS 12 noncomplementing (Class II) PurWM2 EMS 12 viable PurWM3 EMS 12 complementing (Class IVc) PurWM4 EMS 12 noncomplementing (Class II) PurWM5 EMS 12 noncomplementing (Class II) PurWM6 EMS 12 complementing (Class IVa) PurWM7 EMS 12 complementing (Class IVc) PurX25 EMS 6, 12 noncomplementing (Class II) PurZ2 EMS 6, 12 noncomplementing (Class II) PurZ8 EMS 5, 12 viable PurZ19 EMS 6, 11, 12 complementing (Class IVa) PurZ22 EMS 6, 12 noncomplementing (Class II) PuSHC EMS Boswell 5, 12 noncomplementing (Class II), dominant | PuTR6 EMS 12 noncomplementing (Class II) PuW X ray Lewis, 55h dominant, T(2;3)57B-C;80 ( 1 = Krivshenko, 1954, DIS 28: 75; 2 = Glass, 1933, J. Genet. 28: 69-112; 3 = Glass, Am. Nat. 68: 111; 4 = Grell, 1960, DIS 34: 50; 5 = Mackay and O'Donnell, 1983, Genetics 105: 35-53; 6 = Mackay, Reynolds, and O'Donnell, 1985, Genetics 111: 885-904; 7 = Muller, 1930, J. Genet. 22: 326 (fig.); 8 = Oliver, 1932, Z. Indukt. Abstamm. Vererbungsl. 61: 484; 9 = Oliver, 1941, Proc. Int. Congr. Genet. 7th., p. 228; 10 = Oliver, 1935, DIS 3: 14; 11 = Reynolds and O'Donnell, 1987, Dev. Biol. 123: 430-41; 12 = Reynolds and O'Donnell, 1988, Genetics 119: 609-17; 13 = Rowan, 1966, DIS 41: 166-67. 14 = Tearle and Nusslein-Volhard, 1987, DIS 66: 209-69. | More complete description below. cytology: Placed in 57C5-6 based on its inclusion in both Df(2R)F36 = Df(2R)57B16-17;57C6-7 and Df(2R)P112 =Df(2R)57C4;57D8-9; also placed in 57C by in situ hybridization to the salivaries (McLean, Boswell, and O'Donnell, 1990, Genetics 126: 1007-19). molecular biology: Genomic clones of region recovered and mutants shown to cause alterations over a 30 kb segment. The region encodes at least 16 developmentally regulated tran- scripts (O'Donnell et al., 1989b). Northern analysis reveals a 1.7 kb polyadenylated transcript that is abundant in the head and a 9 kb transcript that is transcribed off the same strand, overlaps the 1.7 kb sequence and is expressed at all stages (McLean and O'Donnell, 1987, Genetics 116: s52). The 1.7 kb transcript, which gives rise to a 39 kd polypeptide, is missing from three eye-specific Pu mutants (McLean, Lipsky, and O'Donnell, 1979, Genetics 122: s44). other information: Mutations at this locus comprise a complex of viable and lethal, recessive and dominant, complementing and noncomplementing alleles with different stage and tissue specific defects. A complementation map has been constructed, but recombinational fine structure has not been determined. # Pu2 phenotype: Eye color of Pu2/+ purplish, resembling pr; GTP CH activity reduced to less than 50% normal levels, in prepupae, adult body, and adult head, i.e. lower than observed in defi- ciency heterozygotes. Activity 80% normal in genotypes that carry, in addition to Pu2, two doses of Pu+; Homozygous lethal with death occurring in the embryonic stage; slight transient dilution of eye color in such heterozygotes at eclosion. # PuK5-2 phenotype: Slightly dominant eye-color phenotype. Survives in heterozygous combination with SM1, but behaves as a dominant lethal or displays delayed development in combination with most other second chromosomes tested. # Pur1 phenotype: Homozygous viable recessive allele. GTP CH activity moderately reduced in prepupae and nearly normal in adult bodies of homozygotes; activity appears to be virtually absent in adult heads. Slight transient dilution of eye color in freshly emerged heterozygotes. # Pur331 phenotype: Homozygous viable recessive allele. GTP CH activity in Pur331/Pu+ same as wild type; somewhat reduced in homozy- gotes. # PurP43 phenotype: Homozygous lethal; however, GTP CH activity in heterozygotes nearly normal. In heteroallelic combination with PurZ19 the enzyme produced is unstable at 53; other combina- tions produce relatively heat-stable enzyme. # PuSHC phenotype: Similar to but less severe that that of PuK5-2. Apparent dominant lethal effects more severe when inherited maternally than when inherited paternally. # pub: pubescent location: 1-63. origin: Induced by P32. discoverer: Bateman, 1950. references: 1950, DIS 24: 55. phenotype: Hairs and bristles M-like; black pigment on terminal abdominal segments nearly absent; male sterile. Tendency toward short, fat, gnarled legs; shortened L2; posterior nick- ing of wings. After several generations, only bristle effect and male sterility remained. RK3. #*Pub: Pub location: 1- (rearrangement). discoverer: P. Farnsworth. references: Lefevre, 1954, DIS 28: 75. phenotype: Eye size of heterozygote variably reduced, ranging from something like Bi/+ to wild type. Eyes of homozygote greatly reduced, similar to double Bar. Interacts with B to give small, glazed, almost facetless eyes. RK2A. cytology: Associated with In(1)Pub; breakpoints unknown. # pubescent: see pub # Pudur: see Fs(3)Sz29 # puf: puff location: 2-58. origin: Spontaneous. discoverer: Nichols-Skoog, 35k19. phenotype: Wings puffed or blistered; effect centering in third posterior cell; wings warped and creased longitudinally along vein L3. Penetrance usually 90-100% in female and 20-40% in male. RK3. other information: Possibly an allele of blo (Ashburner). # Pufdi: see Pfd # puff: see puf # pum: pumilio location: 3-48.5. origin: Induced by ethyl methanesulfonate. references: Lehmann and Nusslein-Volhard, 1987, Nature (London) 329: 167-70. Nusslein-Volhard, Frohnfofer, and Lehmann, 1987, Science 238: 1675-81. phenotype: Wild-type allele of pum involved in development of the abdomen (embryos) and of the imaginal disks (larvae or pupae), perhaps having a function in signal transport. Embryos derived from pum/pum females (strong allele) form two instead of eight abdominal segments; head, thorax, and telson are normal. Pole cells are formed by the pum embryos and these cells function normally when transplanted into otherwise sterile embryos. There is no paternal rescue. Partial rescue of the pum abdominal phenotype (at the site of the injection) can be obtained with cytoplasm from the posterior pole of (1) wild-type embryos or (2) pum embryos. When pum is combined with tsl (mutant in which the abdominal region is placed next to the pole plasm), a rescue of abdominal segments may occur. pum opposite a deficiency or another pum allele results in a recessive zygotic visible phenotype; pum adult flies have additional postalar, dorsocentral, and scutellar bristles and reduced viability. alleles: The first pum allele, pum12, was recovered in a screen for maternal-effect mutations (Nusslein-Volhard, Jurgens, Anderson, and Lehmann) and 12 more alleles were located on the basis of failure to complement the maternal phenotype (Leh- mann, Frohnhofer, Anderson, Mayer, and Nusslein-Volhard). All were induced by ethyl methanesulfonate; most are semilethal and have abnormal bristles when homozygous. allele synonym _______________________ pum1 pumET1 pum2 pumET2 pum3 pumET3 pum4 pumET4 pum5 pumET5 pum6 pumET6 pum7 pumET7 pum8 pumET8 pum9 pumET9 pum10 pumET10 pum11 pumET11 pum12 pum21 pum13 pum680 cytology: Placed in region 85C-D since included in Df(3R)p-XT9 = Df(3R)84F14;85C-D but not in Df(3R)p- XT103 = Df(3R)82A;85C1-2. # pun: puny location: 1-41.1. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1950. references: 1958, DIS 32: 73. phenotype: Body small. Wings slightly shorter than normal. Eyes occasionally deformed. Eclosion delayed. Both sexes fertile; viability about 50% wild type. RK3. other information: One allele each induced by CB. 1356 and CB. 3025. # Punch: see Pu # punt: see put # puny: see pun # pupal: see pu # Pupal cuticle protein: see Pcp # Pupilla excentrica: see Pec # pur: purplish ruby location: 3-39.5. origin: Spontaneous in a natural population in Spain. references: Aparisi and Najera, 1987, DIS 66: 12-13. Najera and Aparisi, 1987, DIS 66: 191. 1988, DIS 67: 4-5, 5-6. phenotype: Eye color purplish ruby. Red pigment at 75% wild- type level and brown pigment at 122% normal level. # pur1: purine requiring location: 1-32.35. origin: Induced by ethyl methanesulfonate. references: Falk and Nash, 1974, Genetics 76: 755-66. Johnson, Woloshyn, and Nash, 1979, Mol. Gen. Genet. 174: 287-92. Nash, Woloshyn, Mehl, and Janca, 1981, Can. J. Genet. Cytol. 23: 411-23 (fig.). phenotype: Purine nucleoside auxotroph; lethal on unsupple- mented medium at 29 and poorly viable at 25; rescuable by adenosine or guanosine supplementation. Slight oblique trun- cation of the wing occasionally observed as a small concavity of the wing margin at the distal end of vein L4 in pur1 males and females; pur1/Df(1)ras females display stronger expres- sion; hairs on wing margin regularly disposed, unlike r. alleles: Two alleles, pur11 and pur12; development of pur11 but not pur12 delayed when supplemented with adenosine; guanosine supports normal development of both. cytology: Placed in 9E1-4 on the basis of its inclusion in the region of overlap between Df(1)rasP14 = Df(1)9E1-2;9F3-4 and Dp(1;2)9E1;10A11;56A (Zhimulev, Pokholkova, Bgatov, Semeshin, and Belyaeva, 1981, Chromosoma 82: 25-40). other information: pur1 is but one of four types of mutations belonging to an interrelated complex involved some way in purine metabolism: ras, a nonauxotrophic eye-color mutation; two purine auxotrophs, pur1 and gua1, which complement ras and one another; ras-l, lethal mutations that fail to complement completely the other three types; genetic map order not deter- mined. The complex shares many genetic features with rudimen- tary. # Pur-r: Purine-resistant (A. Chovnick) location: 2-82 (approximate). discoverer: Duck, 1973. origin: Induced by ethyl methanesulfonate. references: Dutton and Chovnick, 1990, Mol. Gen. Genet. 220: 172-76. phenotype: Exhibits elevated resistance to purine [7H-imidazo (4,5-d) pyrimidine] in association with normal levels of xanthine dehydrogenase. Also confers resistance to 2,6- Diaminopurine. Pur-r is associated with elevated activity of adenosine deaminase (ADA); however, gene dosage experiments are inconsistent with the notion that Pur-r represents the structural locus for ADA, and indicate instead that Pur-r encodes a negative regulator of ADA. This view is supported by biochemical studies, which indicate that Pur-r+ encodes a thermolabile component that inhibits ADA activity, presumably analogous to the ADA-binding protein known in mammalian sys- tems (Daddona and Kelley, 1980, Mol. Cell Biochem. 29: 91- 101). # purple: see pr # purpleoid: see pd # Purpleoider: see Pdr # purplish ruby: see pur # put: punt 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 in embryo. Dorsal part of embryo open. cytology: Located in 88C3-E2 based on ability of aneuploid segregants of both Tp(3;1)XM54 = Tp(3;1)20;87C7-D1;88E2-3 and Tp(3;2)kar51 = Tp(3;2)88C2-3;96B11-C1 to cover it. #*pvt: postverticalless location: 1-20.9. origin: Induced by ethyl methanesulfonate. discoverer: Fahmy, 1956. references: 1959, DIS 33: 88. phenotype: Wings either divergent or slightly held up. Thora- cic hairs sparse, and one or both postvertical bristles almost invariably absent. Shape of head and eyes varies from almost normal to anteroposterior flattening of head and deep grooving of eyes. Male viable and fertile; female sterile. RK2. #*pw: pink wing location: 2-14. discoverer: Bridges, 20b17. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 213. 1931, Eos 7: 229-48. phenotype: Eye color like pink. Wings shorter than normal and crumpled. Viability low. RK3. #*Pw: Pointed wing location: 3-94.1. discoverer: Bridges, 21c29. references: Bridges and Morgan, 1923, Carnegie Inst. Wash. Publ. No. 327: 238 (fig.). phenotype: Wings narrowed slightly at tips; extra venation near tips of L3 and L4. Homozygous lethal. RK3. other information: Not an allele of Bd (3-93.8). # pwc: pink wing c location: 2-79. discoverer: Bridges, 31c18. phenotype: Eye color lighter than normal. Wings short and blunt. Overlaps wild type. RK3. Pw: Pointed wing # pwn: pawn location: 2-55.4 [between pk and cn (Ashburner et al., 1981)]. origin: Induced by ethyl methanesulfonate. references: Garcia-Bellido and Dapena, 1973, DIS 50: 179. 1974, Mol. Gen. Genet. 128: 117-30. Lawrence and Morata, 1976, Dev. Biol. 50: 321-37. 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: Homozygous semilethal as zygote (survival 2%); escapers have dark brown eyes and show tanning of cornea cuti- cle (Garcia-Bellido and Dapena, 1973). Cell viable in homozy- gous clones, which have truncated bristles with pale tips and pin-shaped trichomes with basal spurs and thin, transparent hairs (Garcia-Bellido, 1973, 1974; Lawrence and Morata, 1976). Useful as cell marker. cytology: Located in 42E3-43C3; included in Df(2R)pk78k = Df(2R)42E3;43C3 (Ashburner et al., 1981). # px: plexus location: 2-100.5. references: Bridges and Morgan, 1919, Carnegie Inst. Wash. Publ. No. 278: 251. Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 212, 233. Waddington 1940, J. Genet. 41: 75-139. Thompson, 1974, Heredity 33: 389-401. phenotype: Wings have network of extra veins, especially towards tips and margins; L4 vein bent near tip. Semidominant with some Minutes. Suppressed by S (Bedichek, 1936, DIS 4: 24); suppresses expression of ve (Thompson, 1973, DIS 50: 59). Venation effect caused by inadequate contraction of wing during pupal stage, leaving spaces between epithelial layers (Waddington, 1940). Vein patterns of px flies studied in lines selected for increased or decreased expression (Thompson, 1974). px: plexus From "Edith M. Wallace, unpublished." alleles: Phenotype same as px1. allele origin discover ref ( cytology _____________________________________________________________ px1 spont Bridges, 14h20 1, 6 *px2 spont Villee, 40a 7 px52g X ray Iyengar, 52g 2, 4 In(2LR)30A;58F-59B (Lewis) *px54h spont Meyer, 54h 5 *px55k spont Williams, 55k 8 px70 spont Gooskov 3 ( 1 = Bridges and Morgan, 1919, Carnegie Inst. Wash. Publ. No. 278: 251; 2 = Craymer, 1980, DIS 55: 197-200; 3 = Gooskov, 1971, DIS 46: 41; 4 = Iyengar and Meyer, 1956, DIS 30: 73; 5 = Meyer, 1954, DIS 28: 77; 6 = Morgan, Bridges, and Stur- tevant, 1925, Bibliog. Genet. 2: 212, 233; 7 = Villee, 1942, Univ. Calif. Publ. Zool. 49: 125-84; 8 = Williams, 1956, DIS 30: 80. cytology: Placed in 58F on the basis of its inclusion in Df(2R)M-1 = Df(2R)57F11-58A1;58F8-59A1 and Dp(2;3)P from Tp(2;3)P = Tp(2;3)58E3-F2;60D14-E2;96B5-C1 [Bridges, 1937, Cytologia (Tokyo), Fujii Jub. Vol. 2: 745-55]. Also, In(2LR)px52g = In(2LR)30A;58F-59B (Lewis) is mutant for px. Px: Plexate From "Edith M. Wallace, unpublished." # Px: Plexate location: 2-107.2 (approximate). origin: Spontaneous. discoverer: Bridges, 22f6. references: 1937, Cytologia, Fujii Jub. Vol. 2: 745-55. Diaz-Benjumea, Gonzalez-Gaitan, and Garcia-Bellido, 1989, Genome 31: 612-19. phenotype: Wing veins of heterozygote with plexuslike or delta- like thickenings, most often near posterior crossvein, and free fragments of vein, most often in third posterior cell; L4 vein bent near margin. Wings smaller and narrower than wild type and dusky textured. Closely resembles bs. Expression more extreme in female; enhanced by cold (19). Homozygous Df(2R)Px lethal as embryo (Li, 1927, Genetics 12: 1-58); Df(2R)Px2 cell lethal (Ripoll and Garcia-Bellido, 1979, Genet- ics 91: 443-53). Mutants asssociated with deficiencies near tip of 2R. alleles: Eight (Diaz-Benjumea et al, 1989). cytology: A haplo-insufficient locus; placed in 60C6-D1 on basis of the region of overlap between Df(2R)Px2 = Df(2R)60C5-6;60D9-10 and Df(2R)Px = Df(2R)60B8-10;60D1-2. other information: May be part of a pseudoallelic complex with ba and bs. # pxl: proximalless location: 2R (5 units proximal to bw). discoverer: Ransom. phenotype: Temperature-sensitive lethal. Male and female sterile. Lacks proximal region of the retinal photoreceptors. # pyd: polychaetoid location: 3-39. origin: Spontaneous. discoverer: Spencer, 39h31. synonym: Pch; xvt. references: Spencer, 1935, DIS 3: 28. 1937, DIS 7: 15. Neel, 1939, Genetics 24: 81. 1941, Genetics 26: 52-68. 1943, Genetics 28: 49-68. phenotype: Extra bristles present in homozygote at or near almost all normal bristle locations but most frequently in dorsocentral and scutellar regions. Heterozygote in some stocks occasionally shows extra bristles, especially vibris- sae. Character expressed better at low temperatures and in large flies. Combinations with h and Hw generally superaddi- tive for bristle number. RK3. alleles: In addition to pyd1, there are two mutants that resem- ble the original allele, both in chromosome location and bris- tle phenotype; they have been named pydxvt (synonym: xvt) and pyd66. pydxvt appeared in an Australian line selected for an increased number of scutellar bristles (Miller and Fraser, 1968, Aust. J. Biol. Sci. 21: 61-74; Fraser, Erway, and Bren- ton, 1968, Aust. J. Biol. Sci. 21: 75-87; Fraser, 1970, Genetics 65: 305-09). pyd66 appeared in a Spanish line selected for an increased number of dorsocentral bristles; also shows many verticals, orbitals, scutellars, interocel- lars, sternopleurals, and abdominals (Mensua, 1972, DIS 49: 40), the mutant phenotype occurring with a high penetrance. # Pyk: Pyruvate kinase location: 1-[43]. references: Rust and Collier, 1985, J. Hered. 76: 39-44. phenotype: Structural gene for the glycolytic enzyme pyruvate kinase [PYK (EC 2.7.1.40) = ATP: pyruvate phosphotransferase]. Enzyme activity low in larvae and pupae, but it increases in young adults, becoming relatively stable in two-day-old flies. Most of the pyruvate kinase activity of adults is found in the thorax. cytology: Located in the 12A-C region of the X chromosome on the basis of the dosage sensitivity of the region for pyruvate kinase as shown by segmental aneuploids. # pym: see ade2 #*pyp: polyphene location: 1-53.5. origin: Spontaneous. discoverer: Bridges, 37l26. phenotype: Wings spread, yellowish, and have uneven surface. Trace of extra vein in third posterior cell near second crossvein. Eyes rough, pitted, bulging, and smaller than wild type. Trident more darkly pigmented in male. Female sterile. Viability about 70% wild type. RK3. # pyr2: see nuc1 # Pyridoxal oxidase: see Po # Pyruvate kinase: see Pyk # pys: polychaetous location: 2-52. discoverer: Curry, 37k15. phenotype: Extra or double bristles present; most easily seen are scutellars, dorsocentrals, orbitals, and vibrissae. Extra bristles on scutellum curve upward. Overlaps wild type at 19C; classification good at 28-30. RK3.