# p: pink location: 3-48.0 (proximal to hb and dsx). phenotype: Eye color varies from pink to dull ruby with pur- plish tone depending on allele. Larval Malpighian tubules colorless. Color autonomous in pp optic disk allowed to undergo metamorphosis in a wild-type host (Beadle and Ephrussi, 1936, Genetics 21: 230). alleles: Mutant alleles of p are listed in the following table, their phenotype in regard to eye color included if described in the literature. allele origin discoverer ref ( eye cytology color | ___________________________________________________________________________ p1 spont Morgan, 10g 3, 4, 1 11, 15 *p3 spont Bridges, 16d21 5 *p4 spont Richards, 17a7 5 2 *p5 spont Bridges 5 *p21a spont L.V. Morgan 5 *p25g spont Bridges 5 *p53h spont Thoday 14 2 *p56 spont Williams 16 2 *p100.290 X ray Alexander 15 3 In(3)85B3-4;85D12-15 *p100.48 X ray Alexander 15 3 In(3)80-81;85A6-B1 *p100.88 X ray Alexander 15 3 In(3)80-81;94D11-E1 p419 X ray 9 In(3R)84D4-6;86A3 p712 X ray 9 T(2;3)25D;84D4-6;85B6 pp / spont Bridges, 13a24 1, 2, 4, 2 6, 8, 12 *pp56 spont Williams 16 4 *psnb Dobzhansky 13 1 pXT14 Porter 7 T(Y;3)85A pXT15 X ray 10 pXT27 X ray 10 pXT104 X ray 10, 12 pXT117 X ray 10 In(3LR)62E;85A-B pXT126 X ray 10 T(2;3)44F;85A ( 1 = Alexander, 1975, Genetics 81: 493-500; 2 = Beadle, 1937, Genetics 22: 587-611; 3 = Brehme and Demerec, 1942, Growth 6: 651-56; 4 = Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 44; 5 = CP552; 6 = Duncan and Kaufman, 1975, Genetics 80: 733-52; 7 = Jones and Rawls, 1988, Genetics 120: 733-42; 8 = Judd, 1955, DIS 29: 126; 9 = Kemphues, Raff, and Kaufman, 1983, Genetics 105: 345-56; 10 = Lehmann and Nusslein-Volhard, 1987, Dev. Biol. 119: 402-17; 11 = Nolte, 1959, Heredity 13: 233-41; 12 = Tautz, Lehmann, Schnurch, Schuh, Seifert, Kienlin, Jones, and Jackle, 1987, Nature, (London) 327: 383-89; 13 = Silva, 1989, DIS 67: 72; 14 = Thoday, 1954, DIS 28: 78; 15 = Ward and Alexander, 1957, Genetics 42: 42-54; 16 = Williams, 1956, DIS 30: 80. | 1 = Dull ruby with purplish tone; 40% normal red and 33% normal brown pigment; 2 = Lighter and more orange than p; 9% normal red and 15% normal brown pigment (Beadle, 1937); 3 = Pink; 4 = Light ruby with orange tone. / Females heterozygous for pp and a white allele (w, wh, wbf) have brownish eyes (Judd, 1955). cytology: Located in 85A6 on the basis of its association with Df(3R)p25 = Df(3R)85A5-7;85A11 and by in situ hybridization (Jones and Rawls, 1988). molecular biology: The 85A region including p has been cloned by chromosome walking and a restriction map of the region con- structed (Jones and Rawls, 1988). # pGr: see Pu # P: Pale location: 2- or 3- (rearrangement). origin: Spontaneous. discoverer: Bridges, 17j16. references: Bridges, and Morgan, 1923, Carnegie Inst. Washing- ton Publ. No. 327: 184 (fig.). phenotype: Heterozygote a specific dilutor of the we series of white alleles; tends to darken eye color of wa series. Homoz- ygous lethal. RK2A. cytology: Associated with Tp(2;3)P = Tp(2;3)58E3-F2;60D14- E2;96B5-C1 (Morgan, Bridges, and Schultz, 1934, Year Book - Carnegie Inst. Washington 33: 278). # P1: see Fbp1 # P6: see Fbp2 # P37 (J. C. Hall) location: 1-. origin: Induced by ethyl methanesulfonate. discoverer: Deland and Pak. references: Heisenberg and Gotz, 1975, J. Comp. Physiol. 98: 217-41. phenotype: Fast phototaxis not completely absent at high light levels. Optomotor response half as strong as in wild type. In flight, response to movement from front to back is dis- turbed. Poor fixation. # P43 (J. C. Hall) location: 1-. origin: Induced by ethyl methanesulfonate. discoverer: Deland and Pak. references: Heisenberg and Gotz, 1975, J. Comp. Physiol. 98: 217-41. Hall, 1982, Quart. Rev. Biophys. 15: 223-479. phenotype: Holes in optic lobes and brain; lamina abnormal, but with general structure preserved (Pak, Heisenberg and Hengstenberg). Defective phototaxis and optomotor responses. No fixation. No light-on or light-off transient spikes. # P48 (J. C. Hall) location: 1-. origin: Induced by ethyl methanesulfonate. discoverer: Deland and Pak. references: Heisenberg and Gotz, 1975, J. Comp. Physiol. 98: 217-41. phenotype: Variable. Rotatory optomotor response almost as big as in wild type, but absent when striped pattern used. # pa: patulous location: 2-101.0. origin: Spontaneous. references: Edmondson and Meyer, 1949, DIS 23: 61. phenotype: Wings spread wide apart. Excellent viability; fair fertility. RK1. cytology: Placed in 58F2-60E2 on the basis of its being covered by Dp(2;3)P from Tp(2;3)P = Tp(2;3)58E3-F2;60D14-E2;96B5-C1. # pa: see pt #*pads: pads location: 2-55. origin: Spontaneous. discoverer: Bridges, 17e9. references: Morgan, Bridges, and Sturtevant, 1925, Bibliog. Genet. 2: 212 (fig.), 232. Stern, 1934, DIS 1: 36. phenotype: Wings malformed, often remain in condition of those of newly emerged flies. RK2. #*pads2 origin: Spontaneous. discoverer: Mohr, 20b15. references: 1929, Z. Indukt. Abstamm. Vererbungsl. 50: 126. phenotype: Like pads. RK2. # pads-b: see pu # paired: see prd # Paired box: see Pox # pal: paternal loss location: 2-35.7 (between Sp and J). origin: Induced by ethyl methanesulfonate. discoverer: Sandler. synonym: mei-W5. references: Sandler, 1971, DIS 47: 68. Baker, 1972, DIS 49: 55. 1975, Genetics 80: 267-96. Hall, Gelbart, and Kankel, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 265-314. Baker and Hall, 1976, The Genetics and Biology of Drosophila (Ashburner and Novitski, eds.). Academic Press, London, New York, San Francisco, Vol. 1a, pp. 351-434. phenotype: Behaves as a recessive meiotic mutant in males; causes the loss of paternally-derived chromosomes among the progeny of homozygous males. Different chromosomes are lost at different rates. Loss may occur in the zygote and affect the whole body or during early mitotic divisions giving rise to mosaicism. The site responsible for the sensitivity of the X chromosome to pal has been located at or near the X cen- tromere. pal+ function seems to be necessary during meiosis for normal transmission of paternal chromosomes in the early divisions of the fertilized egg. cytology: Located in either 28C-D or 29F-30F since it is uncovered by Dp(2;Y)B231 = Dp(2;Y)27C;31E and is not deleted by deficiencies for 27D-28C, 28D-29F, 30F-31D, and 31C-D in segmental aneuploids (Lindsley, Sandler, Baker, Carpenter, Denell, Hall, Jacobs, Miklos, Davis, Gethmann, Hardy, Hessler, Miller, Nozawa, Parry, and Gould-Somero, 1972, Genetics 71: 157-84). other information: Mosaics with large patches can be generated by early chromosome loss in the progeny of pal males and allows the construction of fate maps of the blastoderm. # Palat: see Fs(3)Sz19 # pale: see ple # Pale: see P # pale ocelli: see po # pale wing: see plw # pallid: see pld # palsied: see pls # pannier: see pnr # par: paralog location: 1-1.4. origin: Recovered after ethyl methanesulfonate treatment of a v24 chromosome; may have been spontaneous in the stock. discoverer: Gans. synonym: fs(1)A1122ts. references: Gans, Audit, and Masson, 1975, Genetics 81: 683- 704. Zalokar, Audit, and Erk, 1975, Dev. Biol. 47: 419-32. Thierry-Mieg, 1982, Genetics 100: 209-37. phenotype: Recessive temperature-sensitive female-sterile mutant. At 29, homozygous females have small ovaries and abnormal egg chambers, the few eggs that are laid dying before hatching; at 23 par females are viable and fecund, but 60% of their progeny die without forming a complete blastoderm and the remainder form a blastoderm lacking in pole cells and develop into sterile adults with cuticular defects; at 16, only 20-30% of the progeny of par females are agametic and few of these show cuticular defects. May act as a dominant enhancer of spl causing a spl phenotype in par spl/FM3 hetero- zygotes. A modifier Su(par) (mapping to right of v on X) decreases in a semidominant way the frequency of agametic flies (from 95-100% to 51-61%) and abdominal defects (from 26-49% to 5-14%) (Thierry-Mieg, 1982). The temperature- sensitive period is restricted to the mother's lifespan and the frequency of progeny defects is independent of the geno- type of the zygote. The mutation interacts zygotically in trans with loci in the neighboring regions 3A2, 3A3, 3C1-2, 3C4, and 3C6-8. When za and/or wa (wild-type eye color) are combined with par, a zygotic semidominant temperature- sensitive interaction takes place resulting in za par hetero- zygotes that are brown-eyed and za par wa heterozygotes that are white-eyed. Interactions between par and N are also reported by Thierry-Mieg, 1982, such as the zygotic dominant suppression of Notch wing in par N+/par+ N- females (the Notch mutants being Df(1)N-8 and Df(1)N-264-105 but not N264-69, a point mutant). An interaction between par and a deficiency for 3A2 results in almost complete sterility in females with a paternal par X and in aging females with a maternal par X. alleles: One temperature-sensitive allele, parX1122 (Gans et al., 1975). cytology: Placed in 3B3 based on its inclusion in both Df(1)64f1 = Df(1)3A9-B1;3B2-3 and Df(1)w258-45 = Df(1)3B2- 3;3C2-3. other information: Probably represents a new complementation group in the z-w region since allelism tests at 23 and 29 show full complementation for all par characteristics by l(1)3Bb [l(1)zw6], l(1)3Bc [l(1)zw12], and l(1)3Bd [l(1)zw7] (Thierry-Mieg, 1982). # para: paralytic (J.C. Hall) location: 1-52.1 (between m and f; Homyk and Pye, 1989). origin: Induced by ethyl methanesulfonate or hybrid dysgenesis. discoverer: R. Williamson. references: Grigliatti, Williamson, and Suzuki, 1970, Genetics 64: s27. Suzuki, 1970, Science 170: 695-706. Suzuki, Grigliatti, and Williamson, 1971, Proc. Nat. Acad. Sci. USA 68: 890-93. Grigliatti, Suzuki, and Williamson, 1972, Dev. Biol. 28: 352-71. Grigliatti, Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-14. Wu and Ganetzky, 1980, Nature (London) 286: 814-16. Falk, Roselli, Curtiss, Halliday, and Klufas, 1984, Mut. Res. 126: 25-34. Ganetzky, 1984, Genetics 108: 897-911. Kyriacou and Hall, 1985, Nature (London) 314: 171-73. Ganetzky, 1986, J. Neurogenet. 3: 19-31. Jackson, Wilson, and Hall, 1986, J. Neurogenet. 3: 1-17. Homyk and Pye, 1989, J. Neurogenet. 5: 37-48. Loughney, Kreber, and Ganetzky, 1989, Cell 58: 1143-54. phenotype: Exposure to 29-30 causes rapid paralysis that is quickly reversed on shift to 22-25. Larvae are paralyzed, too, at somewhat higher temperatures. Flies of some para strains seem sluggish at lower temperatures. When these mutants are still paralyzed (i.e. at high temperatures), they appear to retain many of their "vital functions," their heart still beats (Grigliatti, Suzuki and Williamson, 1972), and they quickly regain normal behavior when shifted to 22 after several hours at 29 (Suzuki et al., 1971); in fact, after a less prolonged exposure (30 min) to high temperature, the still-heated mutant flies regain weak mobility and are even able to right themselves and walk (Suzuki et al, 1971). parats/+ adults become paralyzed at 40 within one min [10 min required to paralyze wild-type (Hall, 1973, DIS 50: 103-04)]. parats1 larvae stop "tracking" at high temperature (Wu, Ganetzky, Jan, Jan and Benzer, 1978, Proc. Nat. Acad. Sci. USA 75: 4047-51). parats1 is nearly unconditionally lethal when uncovered by a deletion or other para-locus aberration, whereas other alleles lead to reduced viability (uncondi- tional) when heterozygous with chromosomal aberrations at the locus (Ganetzky, 1984). Action potentials in larval nerves are reversibly heat-sensitive (Wu and Ganetzky, 1980), and the same can be inferred for at least some adult neurons (indi- cated by brain stimulation and recording of responses in thoracic muscles [Siddiqi and Benzer, 1976, Proc. Nat. Acad. Sci. USA 73: 3253-57; Benshalom and Dagan, 1981, J. Comp. Physiol. 144: 409-17]). Other "excitable phenomena," such as the electroretinogram responses and synaptic transmission, appear to be normal in parats adults at high temperature (Suzuki et al., 1971; Siddiqi and Benzer, 1976); also parats1 does not block action potentials in the cervical giant fiber at high temperature (Nelson and Baird, 1985, Neurosci. Abstr. 11: 313) in contrast to results of recording from larval motor neurons (Wu and Ganetzky, 1980); other studies of the giant fiber pathway (involving adult mosaics bilaterally split, externally, for parats1 and para+) indicate that at least certain elements of the pathway (if not the giant fiber itself) fail to fire action potentials at elevated temperature (Benshalom and Dagan, 1981), and recordings from mosaics of this type also suggest "functional coupling" between left and homologous right sides of this giant fiber pathway (Benshalom and Dagan, 1985, J. Comp. Physiol. 156: 13-23). parats1 causes first larval instar death when in combination with napts (Wu and Ganetzky, 1980; Ganetzky, 1984); similar lethal- ity occurs when para+ dosage is decreased in a napts back- ground (Ganetzky, 1984). Other para alleles, in combination with napts, lead to reduced viability, with parats115 having the strongest effect, followed by paraST76 and paraST109 (Ganetzky, 1984). In combination with the tipE mutation, para mutations again cause decreased viability, but the allele- specific interactions are different from those of the series just noted [i.e. with respect to napts (Ganetzky, 1986)]. Surviving para; tipE double mutants are weak, and show accen- tuated heat-sensitivity (in regard to mobility and nerve con- duction); para alleles are dominant for behavioral defects in a homozygous tipE background (Ganetzky, 1985). In adults dou- bly mutant for parats1 and napts, sensory cells (developing from imaginal discs in mosaics) appear to have no nerve con- duction (Burg and Wu, 1984, Neurosci. Abstr. 10: 513). In mosaics involving para mutations only one allele (paraST109) causes all legs to be either paralyzed or normal in different individual gynandromorphs (Siddiqi and Benzer), in contrast to independent paralysis of legs in mosaics constructed with respect to parats1 [Grigliatti et al., 1972; Siddiqi and Benzer, 1978, Genetic Mosaics and Cell Differentiation (Gehr- ing, ed.). Springer-Verlag, Berlin, pp: 259-305]. These results (and others, Benshalom and Dagan, 1985, for example), reveal poor correlation of the externally mutant genotype (in mosaics) and behavioral or physiological malfunctions [con- sistent with internal (no doubt neural) "foci" for para's action]. In other studies, parats1 mosaics with mutant heads (scored externally) usually are immobile at high temperature, but maintain normal posture (Suzuki et al., 1971; Grigliatti et al., 1972). Exposure of parats1 males to high temperature causes arrest of the oscillator underlying rhythmic component of courtship song (Kyriacou and Hall, 1985). At permissive temperatures, parats1 neurons (unlike those influenced by napts) seem normal, except that there is slightly increased resistance of cultured parats1 larval neurons to killing effects of veratridine, shift to high temperature causing that resistance to increase (Suzuki and Wu, 1984, J. Neurogenet. 1: 225-38). Other pharmacological studies (tetrodotoxin sen- sitivity of action potentials or binding assays involving that toxin) have revealed no para-induced abnormalities (Ganetzky and Wu, 1980; Kauvar, 1982, Molec. Gen. Genet. 187: 172-73). It was reported (based on injection of parats1 adults with picrotoxin and the ensuing inhibition of paralysis at high temperatures) that the mutation is involved in a generalized augmentation of inhibition mediated by gamma-amino-butyric acid [Williamson, Kaplan and Dagan, 1974, Nature (London) 252: 224-26] but further physiological data (involving administration of picrotoxin) dispute this hypothesis. parats1 is reported to cause an anomalous inflection point in Arrhenius plots, with respect to activity of the mitochondrial enzyme succinate cytochrome c reductase, at a temperature close to that which induces paralysis (S|ndergaard, 1976, Hereditas 82: 51-56). alleles: Mutant alleles of para are included in the following table. alleles discoverer ref ( comments molecular biology ___________________________________________________________________________ paracs 2 ts (cold) parahd1 11 ts; no P at 14C-D; 2.5 kb insert at no wild-type 45-45.6 kb revertants parahd2 10, 11 lethal; P at 14C-D; 0.9 kb insert at HD->wild-type 2.0-2.6 kb revertants parahd5 11 lethal; HD->wild- 1.0 kb insert at type revertants 1-2.6 kb parahd8 11 P at 14C-D; HD-> 2.6 kb insert at partial reversion 42.3-43 kb (2nd with loss of insert insert at -3.3 to -2.8 kb retained in revertants) parahd9 11 ts; no P at 14C-D; 3.5 kb insert at no wild-type 14.3-16.8 kb revertants paraID30 11 lethal; In(1)14C6;14D1 break at 0-1 kb paralk1 T(1;2)14C7-D1;41A paralk2 11 lethal; In(1)14C6;14D1 break at 20.5-23 kb paralk4 In(1)13E9-14;14C7-8 paralk5 Kreber 3 paraST42 12 paraST76 4, 12 paraST109 4, 12 paraTP3 Siddiqi paraTP8 Siddiqi paraTP10 Siddiqi paraTP11 Siddiqi parats1 | 1, 4-7, ts 9, 11, 13-15 parats2 | 4, 5 ts parats3 8 ts parats4 4 ts parats115 ts insertion and deletion? break at 8-9 kb ( 1 = Benshalom and Dagan, 1985, J. Comp. Physiol. 156: 13- 23; 2 = Falk and DeBoer, 1980, Mol. Gen. Genet. 180: 419- 24; 3 = Ganetzky, 1984, Genetics 108: 897-911; 4 = Ganetzky, 1986, J. Neurogenet. 3: 19-31; 5 = Grigli- atti, Hall, Rosenbluth, and Suzuki, 1973, Mol. Gen. Genet. 120: 107-114; 6 = Grigliatti, Suzuki, and Williamson, 1972, Dev. Biol. 28: 352-71; 7 = Grigliatti, Williamson, and Suzuki, Genetics 64: s27; 8 = Homyk and Pye, 1989, J. Neu- rogenet. 5: 37-48; 9 = Kyriacou and Hall, 1985, Nature (London) 314: 171-73; 10 = Loughney and Ganetzky, 1985, Neu- rosci. Abstr. II: 782; 11 = Loughney, Kreber, and Ganetzky, 1989, Cell 58: 1143-54; 12 = Siddiqi and Benzer, 1976, Proc. Nat. Acad. Sci. USA 73: 3253-57; 13 = Suzuki, Grigli- atti, and Williamson, 1971, Proc. Nat. Acad. Sci. USA 68: 890-93; 14 = Williamson, Grigliatti, and Suzuki, 1970, Can. J. Genet. Cytol. 12: 400-401; 15 = Williamson, Kaplan, and Dagan, 1974, Nature (London) 252: 224-26. | Marked reduction in number of embryonic neurons in cell cul- ture expressing sodium currents in these alleles (O'Dowd, Germeraad, and Aldrich, 1987, Soc. Neurosci. Abstr. 13: 91; 1989, Neuron 2: 1301-11). cytology: Located at 14C7-8 by in situ hybridization; included in Df(1)80-Df(1)82 (Falk et al., 1984) and covered by Dp(1;4)r+ = Dp(1;4)14A1-2; 16A1-2; 102F2-3. molecular biology: Genomic DNA from the para region was cloned from a library of parahd2 using P element DNA as a probe (Loughney and Ganetzky, 1985, Neurosci. Abstr. II: 782). The P element in this mutant was found to reside in a 4.5 kb EcoRI fragment; the 14C6-D1 breakpoint of In(1)D30 (which behaves as para-) is also within this 4.5 kb fragment. Another para- inversion breakpoint, 14C7-8 [in In(1)paralk4], has been localized to a site approximately 20 kb distal to the 4.5 kb fragment. Seven other alleles were distributed over a region of 45 kb. The locus includes a minimum of 26 exons. The com- plete nucleotide sequence of five para cDNAs was obtained. There are 5461 nucleotides in one open reading frame (Loughney et al., 1989). Sequence analysis of the cDNAs indicates that para encodes a protein with extensive amino acid identity to membrane spanning domains in the rat, implicating the sodium channels (Loughney and Ganetzky, 1988; Loughney et al., 1989) in Drosophila neu- rons. The para transcript appears to produce several subtypes of the sodium channel by alternative splicing. # paralog: see par # paralytic: see para # parched: see pch # parted: see ptd # parted: see ab2 # pas: see shakB # pat: see ptc #*pat: patchytergum location: 1-32.4. origin: Induced by triethylenemelamine (CB. 1246). discoverer: Fahmy, 1952. references: 1958, DIS 32: 73. phenotype: Wings divergent. Pigmentation of anterior border of fifth tergite patchy. Ocelli light. Male sterile; viability about 10% wild type. RK3. other information: One allele induced by CB. 3007. # patch: see ptc #*patch: patched location: 2- (not located). origin: Spontaneous. discoverer: Bridges, 13k25. references: Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 241. phenotype: Abdominal sclerites fewer or sharply cut into tri- angular segments obliquely fitted together. Overlaps wild type. RK3. # patched: see tuf # *patched: see patch # patchytergum: see pat # paternal loss: see pal # patulous: see pa # pawn: see pwn # pb: see ANTC # pbl: pebble location: 3-26. 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. Mutant embryos have rudimentary head skeleton, denticle bands and filzkorper; pos- terior end is on dorsal side. Mitosis defective resulting in fewer and much larger cells in embryo. alleles: Five ethyl-methanesulfonate-induced cold-sensitive alleles. allele synonym ________________ pbl1 pbl5B pbl2 pbl5D pbl3 pbl7O pbl4 pbl8J pbl5 pbl11D cytology: Located in 66A-C based on segmental aneuploidy of Y- autosome translocations. # pbx: see BXC # pby: pebbly (F. Waddle) location: 1-31 (approximate). origin: Spontaneous. discoverer: Waddle, 1985. phenotype: Eyes rough, tend to be smaller and more nearly oval in shape; facets irregular. RK1. # Pc: Polycomb location: 3-47.1, between ri and eg (Puro and Nygren, 1975). discoverer: P.H. Lewis. references: 1947, DIS 21: 69. E.B. Lewis, 1956, DIS 30: 76. Hannah-Alava, 1958, Genetics 43: 870-905. Puro and Nygren, 1975, Hereditas 81: 237-48. Denell, 1978, Genetics 90: 277-89. E.B. Lewis, 1978, Nature (London) 276: 565-70. Jimenez and Campos-Ortega, 1981, Wilhelm Roux's Arch. Dev. Biol. 190: 370-73. Struhl, 1981, Nature (London) 293: 36-41. Botas, Moscoso del Prado, and Garcia-Bellido, 1982, EMBO J. 1: 307-10. Denell, 1982, Dev. Genet. (Amsterdam) 3: 103-13. Duncan, 1982, Genetics 102: 47-70. Duncan and Lewis, 1982, Symp. Soc. Dev. Biol., 40th, pp. 533- 54. Sato, Russell, and Denell, 1983, Genetics 105: 357-70. Paro, Lauer, and Hogness, 1984, Genetics 107: s81. Kennison and Russell, 1987, Genetics 116: 75-86. Zink and Paro, 1989, Nature (London) 337: 468-70. phenotype: Pc+ may be considered a negative regulator of the bithorax complex (BXC) and the Antennapedia complex (ANTC), with a decreasing gradient of activity from anterior to poste- rior. When homozygous or hemizygous, Pc mutants are late embryonic lethals. Embryos with at least one dose of the BXC show incomplete head development and caudad transformations, the thoracic and first seven abdominal segments being par- tially transformed into the eighth abdominal segment (Lewis, 1978; Denell, 1982; Haynie, 1983, Dev. Biol. 100: 399-411; Denell and Frederick, 1983, Dev. Biol. 97: 34-47). This homeotic effect in homozygotes is enhanced by increasing the dosage of the BXC. Transformations involve brain and ventral nerve cord as well as epidermis (Jimenez and Campos-Ortega, 1981). Pc+ alleles in the mother weaken the homeotic effect (Denell, 1982; Lawrence, Johnson, and Struhl, 1983, Cell 35: 27-34). Pc2/Pc2 or Pc3/Pc3 clones induced in leg and eye-antennal tissue during larval development also show simi- lar posteriorly-directed transformations (Struhl, 1981; Duncan and Lewis, 1982). Pc/+ flies carrying at least one dose of the BXC show caudad transformations, i.e. partial conversion of wings into hal- teres and of anterior abdominal segments into more posterior ones. Some Pc heterozygotes show phenotypes characteristic of ANTC mutants, i.e. partial conversion of antennae into legs and of second and third legs into first legs (with sex combs in males) (Hannah-Alava, 1958; Duncan, 1982). The frequency of wing transformations varies directly with the BXC dosage, but does not seem to be changed by variation in ANTC dosage (Duncan and Lewis, 1982; Botas et al., 1982). The number of abdominal transformations, however, varies inversely with the doses of the BXC while it increases as the doses of the ANTC are increased (Duncan, 1982; Duncan and Lewis, 1982). Other changes observed in Pc/+ flies include a transforma- tion of ventral to dorsal wing (Tiong; Sato et al., 1983), elevated, divergent, or crinkled wings, terminal gaps in the L4 wing vein, bent humeral or notopleural bristles, and defec- tive sternopleural bristles, all abnormalities being less extreme in males than in females (sometimes absent in males). When doubly heterozygous with AntpYu and AntpB, Pc enhances Antp. The expression of all Pc mutant heterozygotes (includ- ing deficiencies for the locus) is enhanced by the second chromosome dominant, E(Pc) (Sato et al., 1983, 1984). Pc3/Pc3/Dp(1;3;4)7 flies (carrying a Pc+ duplication) show stronger leg and wing transformations than E(Pc)/+;Pc3/+ flies (Duncan and Lewis, 1982; Sato et al., 1983). alleles: In addition to the alleles described in the following table, six more alleles with a Pc phenotype were induced by EMS in males carrying three doses of the BXC (Botas et al., 1982). Mapping data and noncomplemention with Df(3L)Pc con- firmed the allelism. All of the alleles listed in the table show partial transformations of second and third legs into first legs in Pc/+ heterozygotes, and, in the case of PcT3, in homozygotes (Sato et al., 1983). allele origin discoverer synonym ref ( ______________________________________________________________ Pc1 X ray P.H. Lewis 2-7, 10, 12, 13, 15, 17 Pc2 X ray Puro 3, 6, 13, 14, 18 Pc3 | EMS E.B. Lewis 3-5, 10, 11, 16, 17 Pc4 / ray Russell PcR1 1, 8, 17 Pc5 / EMS Tiong PcT3 17 Pc6 EMS Nusslein-Volhard Pc9M Pc7 EMS Nusslein-Volhard PcE213 Pc8 EMS Nusslein-Volhard PcET12 Pc9 EMS Nusslein-Volhard PcET23 Pc10 X ray Nusslein-Volhard PcXH1 Pc11 X ray Nusslein-Volhard PcXL5 Pc12 X ray Nusslein-Volhard PcXM1 Pc13 X ray Nusslein-Volhard PcXM75 Pc14 X ray Nusslein-Volhard PcXM80 Pc15 X ray Nusslein-Volhard PcXT109 Pc16 `- EMS Kennison PcK1 9, 18 Pc17 - EMS Kennison PcK2 9 *Pc18 EMS Hayes *PcH1 Pc19 EMS Russell PcR2 Pc20 Williams PcW1 Pc21 EMS Tiong PcT1 Pc22 EMS Tiong PcT2 Pc23 EMS Kennison PcK2 Pc24 / ray Tiong PcT4 Pc25 / ray Tiong PcT5 Pc26 / ray Tiong PcT8 ( 1 = Carroll, Laymon, McCutcheon, Riley, and Scott, 1986, Cell 47: 113-22; 2 = Denell, 1973, Genetics 75: 279-97; 3 = Denell, 1978, Genetics 90: 277-89; 4 = Denell, 1982, Dev. Genet. (Amsterdam) 3: 103-13; 5 = Denell and Freder- ick, 1983, Dev. Biol. 97: 34-47; 6 = Hannah-Alava, 1969, DIS 44: 75; 7 = Haynie, 1983, Dev. Biol. 100: 399-411; 8 = Kennison and Russell, 1987, Genetics 116: 75-86; 9 = Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40; 10 = Lewis, E.B., 1978, Nature (London) 276: 565-70; 11 = Lewis, E.B., 1980, DIS 55: 207-08; 12 = Lewis, P.H., 1947, DIS 21: 69; 13 = Puro and Nygren, 1975, Hereditas 81: 237-48; 14 = Puro, Nygren, and Nuutila, 1973, DIS 50: 108; 15 = Sato and Denell, 1985, Dev. Biol. 110: 53-64; 16 = Sato, Hayes, and Denell, 1984, Dev. Genet. (Amsterdam) 4: 185-98; 17 = Sato, Russell, and Denell, 1983, Genetics 105: 357-70; 18 = Struhl, 1981, Nature (Lon- don) 293: 36-41. | Sex combs of males are larger and resemble those of Scx. / Homozygous viable? ` Two kb deletion. - Enhances extra sex combs phenotype of Pc4. Cytology: In(3L)76C;78B + In(3L)78C-D;78E5-6. cytology: Located in 78D7-8 by molecular methods and in 78E by deficiency mapping (Duncan and Lewis, 1982); uncovered by Df(3L)Pc = Df(3L)78D12;79A4-C1 of Jurgens (Haynie, 1983, Dev. Biol. 100: 399-411). molecular biology: Pc region cloned from salivaries (Paro, Lauer, and Hogness) by microexcision. Breakpoints of rear- rangements associated with mutant alleles located on the molecular map (Paro et al., 1984). Three transcripts found by Paro, Zink, Messmer, Franke, and Roddewig (Crete, 1988), a 2.5 kb transcript found throughout development, a 2.0 kb maternal and zygotic transcript, and a 1.0 kb transcript abundant in third instar larvae. The polycomb protein binds to 60 sites on the salivary chromosomes, including those of the ANTC, BXC, and Pc-group genes (Zink and Paro, 1989). other information: Later embryonic stages of homozygous Pc embryos show a decline in the transcript levels of Antp and Ubx and a depression in Antp protein expression in the nervous system (Wedeen, Harding, and Levine, 1986, Cell 44: 739-48; Carroll, Laymon, McCutcheon, Riley, and Scott, 1986, Cell 47: 113-22). # PC13: see tPC13 # PC79: see soc # PC80: see eas # pcb: posterior cell blister (F. Waddle). location: 1-1.2. origin: Spontaneous. discoverer: Waddle, 1985. phenotype: Blistering in one or both wings, usually in second posterior cell, but may be elsewhere. Wings tend to be warped upward around affected area. RK1. # pch: parched location: 1-0.0. synonym: dmd; doomed. references: Benzer, 1971, J. Am. Med. Assoc. 218: 1015-22. Flanagan, 1977, Genetics 85: 587-607. Kimura, Shimozawa, and Tanimura, 1985, J. Insect Physiol. 31: 573-80. phenotype: pch2 flies appear normal at eclosion but commence dying immediately; all dead within 12 hr. pch2 progeny recovered about 60% as frequently as expected owing to pre- eclosion mortality in the pupal stage. Approximately 15% of pch2 individuals die before late pupa, 25% in late pupa, and 60% during first 24 hr after eclosion. Adults exhibit uncoor- dinated leg movement and then lose use of legs. In gynandro- morphs, only pch2 tissue shows loss of leg coordination; such mosaics are doomed. pch2 flies killed by light etherization but not by prolonged CO2 narcosis. Fate mapping by method of focusing locates focus of lethal action to thoracic neural ganglia and not to thoracic musculature. Adult pch3 and pch4 flies have higher rates of water loss than wild-type flies, the rapid water loss causing early death in a desiccated environment. In an attempt to compensate for the loss, the mutants drink much more water than wild-type flies. Even dead pch flies lose water more rapidly than their wild-type counterparts, suggesting that a defect in the integument rather than in the digestive or trachea-spiracle systems is the source of the abnormality. pch larvae and pupae are not affected by desiccation. The survival of flies mosaic for pch/+ and pch/0 in a desiccated environment depends on the ratio of wild-type to mutant cuticle. No difference in the chemical composition of the cuticle between pch3 and the wild type detected. The relationship between mutants isolated as parched and doomed remains unclear, considering the reported differences in fate-mapping results (Flanagan vs. Kimura et al.). alleles: Mutations recovered under a number of lethal designations including the adult-lethal mutants called dmd and pch. Complementation tests by Tanimura and Shimozowa show that dmd fails to complement pch3, and Schalet demonstrated that several of the lethal alleles listed below fail to com- plement dmd = pch2. allele origin discoverer synonym ref ( comments ___________________________________________________________________________ pch1 EMS Benzer 1 adult lethal pch2 Sandler dmd 3 adult lethal pch3 EMS Kimura pchKK78 4 adult lethal pch4 EMS Tanimura pchTT362 4 adult lethal pch5 spont Bridges, '28 l(1)7e, l(1)d 2,7,8 pch6 Novitski l(1)149 7 pch7 Novitski l(1)152 7 pch8 Novitski l(1)1403 7 pch9 EMS Lim l(1)EC1 5 pch10 EMS Lim l(1)EC1002 complementing allele | pch11 EMS Lim l(1)EC1009 pch12 EMS Lim l(1)EC191 noncomplementing allele pch13 EMS Lim l(1)EC1111 pch14 EMS Lim l(1)EC1124 pch15 EMS Lim l(1)EC1140 pch16 DNA / Fox l(1)EC1F225 *pch17 X ray Meyer l(1)HM1 *pch18 X ray Meyer l(1)HM2 pch19 X ray Meyer l(1)HM5 *pch20 X ray Lefevre l(1)HC246 5 In(1)1A4;4C9-10 *pch21 X ray Lefevre l(1)HC310 5 pch22 EMS Lefevre l(1)EF463 6 adult lethal; no maternal effect; noncomplementing allele pch23 EMS White complementing allele pch24 X ray White complementing allele pch25 ENU Voelker l(1)A33 noncomplementing allele pch26 MR l(1)32/51B 1 noncomplementing allele pch27 X ray van Zeeland l(1)8913-1E noncomplementing allele pch28 X ray van Zeeland l(1)8919-37E noncomplementing allele pch29 mei9` Schalet l(1)3-2D-82 complementing allele pch30 mei9 Schalet l(1)7-1B-4 complementing allele ( 1 = Benzer, 1971, J. Am. Med. Assoc. 218: 1015-22; 2 = CP 627; 3 = Flanagan, 1977, Genetics 85: 587-607; 4 = Kimura, Shimozawa, and Tanimura, 1985, J. Insect Physiol. 31: 573- 80; 5 = Lefevre, l981, Genetics 99: 461-80; 6 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 7 = Maddern, 1972, DIS 49: 48; 8 = Maddern, 1977, DIS 52:82. | Complementation with pch2 in every instance. / From DNA-injected egg. ` Spontaneous in the paternal X chromosome of a cross between wild-type males and mei9 females, such that the F1 females were pch/mei9. cytology: Provisionally the most distal locus on the X chromo- some. Located in the interval between 1A1 and 1B1 since uncovered by Df(1)260-1 = Df(1)1A1;1B4-6 and covered by Df(1)sc19 = Df(1)1B2;1B4. # Pch: see pyd # Pcl: Polycomblike location: 2-84. discoverer: Duncan. references: Duncan and Lewis, 1982, Symp. Soc. Dev. Biol., 40th, pp. 533-34. Duncan, 1982, Genetics 102: 49-70. Sato, Russell, and Denell, 1983, Genetics 105: 357-70. Jurgens, 1985, Nature (London) 316: 153-55. Kennison and Russell, 1987, Genetics 116: 75-86. phenotype: Pcl+, like Pc+, may be considered a negative regula- tor of the BXC and the ANTC. Strong Pcl mutant alleles (Pcl1, Pcl2) are homozygous lethal, hemizygous lethal, and lethal with each other, the embryos having partial posteriorly- directed transformations of the abdominal segments (segment 1 into segment 2 and segments 2-7 into more posterior segments). These mutants are strong enhancers of Pc3, showing Pc-like transformations in embryos, and are indistinguishable from Pcl deficiencies in complementation behavior. Extreme posteriorly-directed segmental transformations are found in Pcl1/Df(2R)Pcl11B;Pc3/Pc3 lethal embryos (Duncan, 1982); these embryos are considerably more abnormal than the Pc3 homozy- gotes that are Pcl+. Pcl/Pcl embryos that are also homozygous for Asx, Psc, or Scm show strong posteriorly-directed transformations of the entire body pattern; 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). Pcl1/Pcl1 clones in the second through the sixth abdominal tergites also show caudal transformations; similar clones in the wing often appear to be partially transformed into haltere tissue. Weak Pcl alleles (Pcl3, Pcl4) survive, at least through eclosion, either as homozygotes or as heterozygotes with strong or weak Pcl alleles (Duncan, 1982). Pcl1/Pcl3 and Pcl1/Pcl4 show segmental transformations characteristic of Pc/+ flies, i.e. antenna to leg, second and third leg to first leg, wing to haltere, and posteriorly-directed abdominal transformations (the most frequent abnormality). Increasing the dosage of the BXC in Pcl1/Pcl4 heterozygotes suppresses the posteriorly-directed transformations, but enhances the transformations from leg2 and leg3 to leg1; increasing the dosage of the ANTC enhances both types of transformations (Duncan, 1982). Pcl1/Pcl3 females, which die before or soon after eclosion, show a conversion of parovaria to spermathe- cae. Both strong and weak Pcl alleles are viable as heterozy- gotes (Pcl/+) and may show partial abdominal and leg transfor- mations, the abnormalities increasing in Pcl/+;Pc/+ flies or when Pcl/+ is combined with E(Pc). alleles: allele origin discoverer synonym ref ( comments _______________________________________________________________________ Pcl1 | X ray Duncan 2 homozygous lethal; enhances Pc3 Pcl2 EMS Duncan 2 homozygous lethal; enhances Pc3 Pcl3 EMS Duncan 2 homozygous viable; leg2, leg3 -> leg1 (het) Pcl4 / EMS Duncan 2 homozygous viable; leg2, leg3 -> leg1 (het) Pcl5 ENU Breen PclD5 1 enhances Mcp Pcl6 EMS Struhl PclE33 4 leg2, leg3 -> leg1 (het) Pcl7 EMS Struhl PclE90 4 leg2, leg3 -> leg1 (het) Pcl8 EMS PclE501 Pcl9 ` E.B. Lewis PclP3 3 homozygous lethal Pcl10 / ray Tiong PclT1 5 Pcl11 - / ray Williams PclW4 5, 7, 8 leg2, leg3 -> leg1 (het) Pcl12 / ray Williams PclW6 7, 8 leg2, leg3 -> leg1 (het) Pcl13 X ray PclX21 9 Pcl14 X ray PclXF21 9 Pcl15 X ray PclXM3 9 *Pcl16 X ray PclXT9 9 Pcl17 EMS PclXT56 4 homozygous viable; leg2, leg3 -> leg1 Pcl18 EMS PclK1 6 exhances extra sex combs phenotype of Pc4 ( 1 = Breen and Duncan, 1986, Dev. Biol. 118: 442-56; 2 = Duncan, 1982, Genetics 102: 49-70; 3 = Eberlein, 1984, Genetics 107: s27-28; 4 = Jurgens, 1985, Nature (London) 316: 153-55; 5 = Kennison and Russell, 1987, Genetics 116: 75-86; 6 = Kennison and Tamkun, 1988, Proc. Nat. Acad. Sci. USA 85: 8136-40; 7 = Sato, Hayes, and Denell, 1984, Dev. Genet. (Amsterdam) 4: 185-98; 8 = Sato, Russell, and Denell, 1983, Genetics 105: 357-70; 9 = Tearle and Nusslein-Volhard, 1987, DIS 66: 211-26. | Strong interaction with Pc3. / Homozygotes almost wild type; weakly temperature-sensitive for leg transformations at 29C. ` Partial transformation of legs 2 and 3 to leg 1. Enhances wing to haltere transformation in en1/en28 (Eberlein, 1984). - In(2R)55A;57A. cytology: Located between 55A and 55C1 since Pcl is included in Df(2R)Pcl-W5 = Df(2R)55A-B;55C as well as in Df(2R)Pcl7B = Df(2R)54E8-F1;55B9-C1 and Df(2R)Pcl11B = Df(2R)54F6- 55A1;55C1-3 (Duncan, 1982; Sato et al., 1983). These defi- ciencies act as enhancers of Pc3 and show a strong Pcl pheno- type. # pco: see E(z) # Pcp: Pupal cuticle protein location: 2-20 (based on site of ade3). origin: Sequence analysis of ade3. synonym: Pcpgart; Gart intronic gene. references: Henikoff, Keene, Fechtel, and Fristrom, 1986, Cell 44: 33-42. phenotype: Apparently encodes pupal cuticle protein since in 11 hr prepupae, the Pcp mRNA is found primarily in the abdomen in epidermis involved in cuticle formation. The pupal cuticle protein itself has not been identified. cytology: Placed in 27C. molecular biology: Computer analysis of ade3 sequences located Pcp in an open reading frame of 184 amino acids in a nested arrangement on the noncoding strand within the first ade3 intron (interrupting the GARS domain). The Pcp gene is made up of single copy DNA and contains its own intron between codons 4 and 5. Its cDNA sequence shows strong homology to regions of the genes Lcp1 to Lcp4 (Snyder, Hirsh, and David- son, 1981, Cell 25: 165-77; Snyder, Hunkapiller, Yuen, Sil- vert, Fristrom, and Davidson, 1982, Cell 29: 1027-40). A 0.9 kb transcript was detected primarily, if not exclusively, in prepupal stage (Henikoff et al., 1986). # pcv: posterior crossvein location: 3-. origin: X ray induced. references: Puro, 1982, DIS 58: 205-08. phenotype: Posterior crossvein incomplete. Wings slightly divergent. Not an allele of cv-d since pcv/cv-d is wild type. cytology: Associated with In(3LR)pcv = In(3LR)65B-C;92A. # pcx: pecanex location: 1-0.9. origin: Induced by ethyl methanesulfonate. discoverer: Engstrom (pcx); Romans [mel(1)R1]. synonym: fs(1)pcx; mel(1)R1. references: Romans, 1973, Genetics 74: s233. Romans, Hodgetts, and Nash, 1976, Can. J. Genet. Cytol. 18: 773-81. Mahowald, 1983, Time, Space, and Pattern in Embryonic Develop- ment (Jeffrey, Rand, and Raff, eds.). Alan R. Liss, Inc., New York, pp. 349-63. Perrimon, Engstrom, and Mahowald, 1984, Genetics 108: 559-72. Haenlin, Steller, Pirrotta, and Mohier, 1985, Cell 40: 827- 37. La Bonne and Mahowald, 1985a, Dev. Biol. 110: 264-67. 1985b, Genetics 110: s83. La Bonne, Sunitha, and Mahowald, 1989. phenotype: Maternal-effect-lethal mutation; homozygous mutant females crossed to mutant males produce lethal embryos showing hypertrophy of the central nervous system at the expense of the epidermis, a small patch of dorsal cuticle remaining but no ventral cuticle. This embryonic phenotype (as well as the reduced eye phenotype of viable pcx adults) resembles that of amx. Homozygous pcx lethal embryos can be rescued geneti- cally; some mutant females (but not pcx1 homozygotes) crossed to wild-type males produce viable adult pcx/+ female offspring (Romans et al., 1976; Perrimon et al., 1984); the pcx/Y male offspring are lethal. pcx/+ heterozygous females, which are fertile, crossed to viable pcx/Y males (also fertile) produce viable adult males (pcx/Y and +/Y) and viable adult females (pcx/pcx and pcx/+) (Romans et al., 1976). Homozygous pcx lethal embryos can be partially rescued almost up to hatching by preblastoderm microinjection of wild-type or amx ooplasm (La Bonne and Mahowald, 1985a). Germ line clonal analysis demonstrates the germ-line dependency of the pcx embryonic lethal phenotype (Perrimon et al., 1984). alleles: allele origin discoverer synonym ref ( comments ___________________________________________________________ pcx1 EMS Romans mel(1)R1o 3 pcx2 EMS Romans mel(1)R1r 3 pcx3 EMS Mohler 12-1012 1 pcx4 EMS Mohler 12-1743 1 pcx5 EMS Mohler 12-3014 1 pcx6 EMS Mohler 12-3102 1 pcx7 EMS Mohler 12-3135 1 pcx8 EMS Mohler 12-4169 1 pcx9 EMS Mohler 14-567 1 pcx10 EMS Mohler 14-1153 1 pcx11 EMS pcx1 2 ( 1 = Mohler and Carroll, 1984, DIS 60: 236-41; 2 = Perrimon, Engstrom, and Mahowald, 1984, Genetics 108: 559-72; 3 = Romans, Hodgetts, and Nash, 1976, Can. J. Genet. Cytol. 18: 773-81. cytology: Located in 2E2 since included in Df(1)pn38 = Df(1)2D3-4;3E3 but not Df(1)dor2T = Df(2B6;2E1-2. molecular biology: pcx cloned and transcripts identified (ten- tatively by Haenlin et al., 1985; confirmed by La Bonne et al., 1989). These mRNAs include a rare 9 kb transcript and minor 3.7 and 2.3 kb transcripts; they are detected early (at a low level) in 0-1 hr embryos. The level is highest in 5-10 hr embryos; lower levels persist throughout pupal and adult life (La Bonne et al., 1989). Nucleotide and predicted pro- tein sequences of the 3' portion of the locus have been deter- mined; these sequences suggest that pcx encodes a large transmembrane protein (La Bonne et al.). other information: Named for its phenotypic resemblance to amx. # pd: purpleoid location: 2-106.4. origin: Spontaneous. discoverer: Bridges, 16h31. references: 1937, Cytologia (Tokyo), Fujii Jub., Vol. 2: 745- 55. phenotype: Eye color dark pink or maroon, like pr but less extreme. Semidominant; eye color of heterozygote duller than wild type; color autonomous in larval optic disk transplanted into wild-type host (Beadle and Ephrussi, 1936, Genetics 21: 230). Malpighian tubes wild type (Beadle, 1937, Genetics 22: 587-611). Semilethal with dor (Lucchesi, 1968, Genetics 59: 37-54). RK2. cytology: Placed in region between 59E2 and 60B10 by Bridges (1937) on the basis of its being to the right of In(2R)bwVDel = In(2R)41B2-C1;59E2-4 and to the left of Df(2R)Px = Df(2R)60B8-10;60D1-2. # pdf: pod foot location: 1-57.0. origin: X ray induced. discoverer: Welshons, 57h6. references: 1960, DIS 34: 54. phenotype: Terminal tarsus swollen in one or more legs. Clas- sification, viability, and fertility good. RK2A. cytology: Associated with In(1)pdf = In(1)16B;19F-20A. Tenta- tively placed in 16A and at 57.0 since pdf is covered by BSY but not by Ymal+2. # Pdr: Purpleoider location: 3-46. origin: Spontaneous. discoverer: Bridges, 22f20. phenotype: The combination pd/pd; Pdr/+ gives lighter, yellower eye color than pd alone. pd/+; Pdr/Pdr has eye color like pd/pd. pd/pd; Pdr/Pdr is lethal. Pdr/Pdr is rosier than wild type. Pdr/Pdr and pd/pd; Pdr/+ Malpighian tubes normal (Brehme and Demerec, 1942, Growth 6: 351-56). RK3. #*pe: petit location: 3- (not located). origin: Spontaneous in In(3L)P. discoverer: Mohr, 38k30. references: 1939, DIS 12: 47. phenotype: Body small. Eyes small and rough. Viability good; female fertility low. RK2A. # Pearl: see Pl # peb: pebbled location: 1-7.5+. Mapped by recombination as proximal to rb (Schalet, 1986). discoverer: Dubinin. references: Schalet, 1986, Mutat. Res. 163: 115-44. Oliver, Perrimon, and Mahowald, 1988, Genetics 120: 159-71. Steinmann-Zwicky, 1988, EMBO J. 7: 3889-98. phenotype: Eyes markedly rough at 28-30, slightly rough (like S) at 25, and wild type at 19. RK2 (28-30). alleles: Two spontaneous lethal alleles, peb2 and peb3 isolated as l(1)10-75 and l(1)20-41, (Schalet et al., 1986). cytology: Placed in salivary chromosome region 4C5-7 since included in Df(1)ovo7 = Df(1)4C5-6;4E2-3 and Df(1)rb46 = Df(1)4A3-6;4C6-7 (Oliver et al., 1988). # pebble: see pbl # pebbled: see peb # pebbly: see pby # Pec: Pupilla eccentrica location: 3-65. origin: Spontaneous in a sex-linked lethal stock kept at 26. references: Parkash, 1970, DIS 45: 35. phenotype: Temperature-sensitive change in the appearance of the pupilla of the eye. At 26, this pigment-free circular area is enlarged to a diameter of about 2/5 of the long axis of the eye and is demarcated clearly from the pigmented area; it contains scattered pigment spots. The pigmented part of the eye varies in color from dull red to light brown and the surface of the eye is somewhat rough; ocelli are colorless. As the temperature is lowered, the size of the pupilla is reduced and its boundary becomes blurry until at 16 the eye resembles wild-type. The temperature-sensitive period for development of the Pec phenotype seems to be the first day of pupal life. # pecanex: see pcx # pelle: see pll # pentagon: see ptg # pep: peppercorn (T. Schupbach) location: 2-{104}. origin: Induced by ethyl methanesulfonate. references: Schupbach and Wieschaus. phenotype: Female sterile; homozygous females contain many small egg chambers in their ovaries, which seem blocked in early stages of oogenesis. Follicle cells nevertheless syn- thesize a very small, round chorion around these egg chambers, giving them the appearance of small round peppercorns. alleles: pepQW = pep1. cytology: Placed in 59D8-60A7, since uncovered by Df(2R)bw-S46 = Df(2R)59D8-11;60A7. # Pepck: Phosphoenolpyruvate-carboxykinase references: Gundelfinger, Hermans-Borgmeyer, Grenningloh, and Zopf, 1987, Nucleic Acids Res. 15: 6745. phenotype: Structural gene for the enzyme phosphoenolpyruvate- carboxykinase in Drosophila melanogaster. molecular biology: A cDNA clone of Pepck has been isolated and found to encode a polypeptide that is 64% identical to the rodent and 62% identical to the avian enzyme precursors. The predicted Drosophila protein consists of 747 amino acid resi- dues. # peppercorn: see pep # per: period (J.C. Hall; M. Young) location: 1-1.4 (between z and w). origin: Induced by ethyl methanesulfonate or nitrosoguanidine. discoverer: Konopka. references: Konopka and Benzer, 1971, Proc. Nat. Acad. Sci. USA 68: 2112-16. Young and Judd, 1978, Genetics 88: 723-42. Handler and Konopka, 1979, Nature (London) 279: 236-38. Kyriacou and Hall, 1980, Proc. Nat. Acad. Sci. USA 77: 6729- 33. Smith and Konopka, 1981, Mol. Gen. Genet. 183: 243-51. Kyriacou and Hall, 1982, Anim. Behav. 30: 794-801. Smith and Konopka, 1982, Mol. Gen. Genet. 185: 30-36. Bargiello, Jackson, and Young, 1984, Nature (London) 312: 752-54. Bargiello and Young, 1984, Proc. Nat. Acad. Sci. USA 81: 2142-46. Reddy, Zehring, Wheeler, Pirrotta, Hadfield, Hall, and Ros- bash, 1984, Cell 38: 701-10. Zehring, Wheeler, Reddy, Konopka, Kyriacou, Rosbash, and Hall, 1984, Cell 39: 752-54. Shin, Bargiello, Clark, Jackson, and Young, 1985, Nature (Lon- don) 317: 445-48. Young, Jackson, Shin, and Bargiello, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 865-75. Cote and Brody, 1986, J. Theoret. Biol. 121: 487-503. Hamblen, Zehring, Kyriacou, Reddy, Yu, Wheeler, Zwiebel, Konopka, Rosbash, and Hall, 1986, J. Neurogenet. 3: 249-91. James, Ewer, Reddy, Hall, and Rosbash, 1986, EMBO J. 5: 2313-20. Kyriacou and Hall, 1986, Science 232: 494-97. Jackson, Bargiello, Yun, and Young, 1986, Nature (London) 320: 185-88. Reddy, Jacquier, Abovich, Peterson, and Rosbash, 1986, Cell 46: 53-61. Bargiello, Saez, Baylies, Gasic, Young, and Spray, 1987, Nature (London) 328: 686-91. Baylies, Bargiello, Jackson, and Young, 1987, Nature (London) 326: 390-92. Citri, Colot, Jacquier, Yu, Hall, Baltimore, and Rosbash, 1987, Nature (London) 326: 42-47. Dowse, Hall, and Ringo, 1987, Behav. Genet, 17: 19-25. Dowse and Ringo, 1987, J. Biol. Rhythms 2: 65-76. Hall and Rosbash, 1987a, Trends Genet. 3: 185-91. 1987b, Bio Essays 7: 108-12. 1987c, J. Biol. Rhythms 2: 153-78. Konopka, 1987, Life Sci. Adv. Series 5: 47-49. Yu, Colot, Kyriacou, Hall, and Rosbash, 1987a, Nature (London) 326: 765-69. Yu, Jacquier, Citri, Hamblen, Hall, and Rosbash, 1987b, Proc. Nat. Acad. Sci. USA 84: 784-88. Crossley, 1988, Anim. Behav. 36: 1098-1109. Ewing, 1988, Anim. Behav. 36: 1091-97. Hall and Rosbash, 1988, Ann. Rev. Neurosci. 11: 373-93. Kyriacou and Hall, 1988, Anim. Behav. 36: 1110. Liu, Lorenz, Yu, Hall, and Rosbash, 1988, Genes Dev. 2: 228- 38. Saez and Young, 1988, Mol. Cell Biol. 8: 4588-99. Young, Bargiello, Baylies, Saez, and Spray, 1988, Cellular and Neuronal Oscillators, (M. Dekke, ed.). pp. 507-20. Hamblen-Coyle, Konopka, Zwiebel, Colot, Dowse, Rosbach, and Hall, 1989, G. Neurogenet. 5: 229-56. phenotype: The per gene is essential for biological clock func- tions and determines the period length of circadian and ultra- dian rhythms. The per mutants are characterized by aberrant rhythms involving eclosion and locomotor activity (Konopka and Benzer, 1971) and may change the rhythmic component of the male courtship song (Crossley, 1988; Ewing, 1988; Kyriacou and Hall, 1980, 1986, 1988). These mutants also affect the rhythm of the larval heartbeat (Dowse, Ringo, and Kyriacou; Living- stone, 1981, Neurosci. Abstr. 7: 351), the level of tyrosine decarboxylase [Livingstone and Tempel, 1983, Nature (London) 303: 67-70], and fluctuations in membrane potentials in lar- val salivary glands (Weitzel and Rensing, 1981, J. Comp. Phy- siol. 143: 229-35), modulate intercellular junctional commun- ication (Bargiello et al., 1987), and alter the location of neural secretory cells in the brain (Konopka and Wells, 1980, J. Neurobiol. 11: 411-15). In wild-type flies the period length is about 24 hr. In general, increases in per+ dosage lead to shortened circadian rhythms and decreases lead to lengthened circadian rhythms (Baylies et al., 1987; Cote and Brody, 1986; Hamblen et al., 1986; Smith and Konopka, 1981, 1982; Young et al., 1985). Females heterozygous for per+ and a deletion of the locus or a per0 allele show longer-than-normal periods. per flies can be classified on the basis of their circadian rhythms as: (1) Cryptic period mutants (per0, per-) which have a 10-15 hr (ultradian) period and appear arrhythmic except in special algorhythmic tests (Dowse et al., 1987); (2) Long period mutants (perL), 29 hr; (3) Long-period variable mutants (perLvar), which in homozygotes or heterozy- gotes are arrhythmic but in combination with certain partial deletions of the per locus result in a 30-34 hr period. (Konopka, 1987); (4) Short period mutants (pers), 19 hr; (5) Short period variable mutants (persvar), some flies having a 20 hr period and the others a normal 24 hr period for locomo- tor activity. In temperature-change experiments on pers and perL1, the locomotor activity periods were found to be nearer to 24 hr at low temperatures, but to diverge further from normal upon heating (Konopka, Pittendrigh, and Orr; Hamblen, Ewer, and Hall). perL2 shows lengthening of the periods at high tem- peratures. The mutant types affecting circadian rhythms (per0, perL, and pers) may cause similar kinds of changes in the rhythmic fluctuations in courtship song interpulse intervals (IPIs) of the male (Crossley, 1988; Ewing, 1988; Kyriacou and Hall, 1980, 1986, 1988). per0 mutants show nonrhythmic variations in the interval between pulses of wing vibration. Neural studies show that transplantation of pers brains into per01 adult hosts causes some of the hosts to be "rescued"; i.e. to show short-period circadian rhythms for locomotor activity (Handler and Konopka, 1979). Octopamine synthesis occurs at subnormal rates in per01 brains, with a correspond- ing decrease in the enzyme tyrosine decarboxylase (Livingstone and Tempel, 1983); less severe decrements in tyrosine decar- boxylase are found in pers and perL1 flies. Physiological studies show that per mutations can affect the level of gap junctional communication among cells in a tissue (Bargiello et al., 1987). In salivary glands the per0 and perL1 mutations cause a lowering of the level of junctional communication, while pers gives a level of communication higher than wild type. Because electrical synapses are com- posed of gap junctions, per may influence circadian behavioral rhythms through altered conductances at the synapse (Bargiello et al., 1987). Mosaic analysis of pers mutants indicates that the gene influences the brain with respect to aberrant locomotor rhythms (Konopka, Wells, and Lee, 1983, Mol. Gen. Genet. 190: 284-88); per01 and per02 (and, to a lesser degree, pers) are said to cause anomalous photonegative behavior in light- response tests (Palmer, Kendrick, and Hotchkiss, 1985, Ann. N.Y. Acad. Sci., pp 323-24), but in general are not defective in visual responses (phototaxis tests, optomotor behavior, and electroretinogram) according to Dushay and Hall. alleles: Ten mutant alleles of per are described in the table below. per01, per02, and per03 may be the same allele ori- ginating at different times, (all three carry the same non- sense or stop codon); per04 is a different allele. See rear- rangement section for T(1;4)JC43 which shows circadian rhythms with a long period. alleles origin discoverer ref ( comments molecular data ____________________________________________________________________________________________________________________________________ per- | 1-7, 9, 25 multiple periods; short deletion of 10 kb ultradian rhythms; hyperactive flies per01 / EMS Konopka, Benzer 1-10, 12-14, 16-27 multiple periods; short nonsense mutation ultradian rhythms in exon 4 per02 EMS Smith, Konopka 5-7, 19, 23, 26 multiple periods; short same nonsense codon ultradian rhythms as per01 per03 EMS Konopka 6, 7, 26 multiple periods; short same nonsense ultradian rhythms codon as per01 per04 EMS/NNG Konopka 6, 21, 26 multiple periods; short per01 nonsense ultradian rhythms; codon absent hyperactive flies perL1 ` EMS Konopka, Benzer 3, 4, 6, 7, 10-13 circadian rhythms; nucleotide substitution 16, 23, 26 long period in exon 3 perL2 ` EMS Orr 9, 23 circadian rhythms; long period perLvar EMS/NNG Konopka 7, 11 circadian rhythms; variable long period pers EMS Konopka, Benzer 3, 4, 6, 8, 10, 12, 13 circadian rhythms; nucleotide substitution 15, 16, 23, 26 short period in exon 5 persvar NNG Konopka 7 circadian rhythms; variable short period ( 1 = Bargiello, Jackson, and Young, 1984, Nature (London) 312: 752-54; 2 = Bargiello, Saez, Baylies, Gasic, Young, and Spray, 1987, Nature (London) 328: 686-91; 3 = Bargiello and Young, 1984, Proc. Nat. Acad. Sci. USA 81: 2142-46; 4 = Baylies, Bargiello, Jackson, and Young, 1987, Nature (London) 326: 390-92; 5 = Dowse, Hall, and Ringo, 1987, Behav. Genet. 17: 19-35; 6 = Hall and Rosbash, 1987, J. Biol. Rhythms 2: 153-78; 7 = Hamblen, Zehring, Kyriacou, Reddy, Yu, Wheeler, Zwiebel, Konopka, Rosbash, and Hall, 1986, J. Neurogenet. 3: 249-91; 8 = Handler and Konopka, 1979, Nature (London) 279: 236-38; 9 = Jackson, Bargiello, Yun, and Young, 1986, Nature (London) 320: 185-88; 10 = Jackson, Gailey, and Siegel, 1983, J. Comp. Physiol. 151: 545-52; 11 = Konopka, 1987, Life Sci. Adv. Series C5: 47-49; 12 = Konopka and Benzer, 1971, Proc. Nat. Acad. Sci. USA 68: 2112-16; 13 = Konopka and Orr, 1980, Develop- ment and Neurobiology of Drosophila (Siddiqi, Babu, Hall, and Hall, eds.). Plenum Press, New York, pp. 409-16; 14 = Konopka and Wells, 1980, J. Neurobiol. 11: 411-15; 15 = Konopka, Wells, and Lee, 1983, Mol. Gen. Genet. 190: 284-88; 16 = Kyriacou and Hall, 1980, Proc. Nat. Acad. Sci. USA 77: 6729-33; 17 = Livingstone, 1981, Neurosci. Abstr. 7: 351; 18 = Livingstone and Tempel, 1983, Nature (London) 303: 67-70; 19 = Palmer, Kendrick, and Hotchkiss, 1985, Ann. N.Y. Acad. Sci. 323-24; 20 = Reddy, Zehring, Wheeler, Pirrotta, Hadfield, Hall, and Rosbash, 1984, Cell 38: 701-10; 21 = Siwicki, Eastman, Petersen, Rosbash, and Hall, 1988, Neuron 1: 141-50; 22 = Smith and Konopka, 1981, Mol. Gen. Genet. 183: 243-51; 23 = Smith and Konopka, 1982, Mol. Gen. Genet. 185: 30-36; 24 = Weitzel and Rensing, 1981, J. Comp. Physiol. 143: 229-35; 25 = Young, Jackson, Shin, and Bargiello, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 865-75; 26 = Yu, Jacquier, Citri, Hamblen, Hall, and Rosbash, 1987, Proc. Nat. Acad. Sci. USA 84: 784-88); 27 = Zehring, Wheeler, Reddy, Konopka, Kyriacou, Rosbash, and Hall, 1984, Cell 39: 369-76. | Includes deficiencies for the per locus such as Df(1)TEM202/Df(1)64j4 or Df(1)62d18/Df(1)64j4. / per0 listed as per in many references. ` Synonym: perL1 = perl; perL2 = perl2. cytology: Located in 3B1-2 since per0 mutations are uncovered by a variety of deletions in the zeste-white region, including Df(1)64j4 = Df(1)3A8-9;3B1-2, Df(1)62d18 = Df(1)3B1-2;3C6-7, Df(1)64f1 = Df(1)3A9-B1;3B2-3 and Df(1)TEM = Df(1)3B1-2;3C3-5 and are covered by w+Y and Dp(3;1)w+67k27. The 3B1-2 break- point of T(1;4)JC43 = T(1;4)3B1-2;3E3-4;102D "partially" inac- tivates per+, making circadian eclosion arrhythmic (Smith and Konopka, 1981; Young and Judd, 1978); in regard to circadian locomotor activity; however, some T(1;4)JC43/per0 females are weakly rhythmic and have a long period while the rest are arrhythmic. A synthetic deletion of the X between 3B1-2 and 3C2 (the 4PXD segment of T(1;4)JC43 and the XP2D segment of T(1;2)RC45) leads to the same array of long-period/arrhythmic individuals when heterozygous with per01 (Smith and Konopka, 1981). molecular biology: The per locus and its environs have been cloned by chromosomal walking/jumping (Bargiello and Young, 1984) and by micro-excision (Reddy et al., 1984) and the genomic per DNA sequenced (Citri et al., 1987; Jackson et al., 1986) Sequencing data and immunochemical studies suggest that the gene product is a proteoglycan (Bargiello et al., 1987; Jackson et al., 1986; Reddy et al., 1986; Shin et al., 1985). Four types of transcripts have been reported (4.5 kb, 0.9 kb, 2.7 kb, and 1.7 kb) from the region of the per locus. The 4.5 kb transcript class is complex, comprising three messages pro- duced by differential splicing which differ in their 3' sequences (Yu et al., 1987b). The 4.5 kb transcript class almost certainly codes for the per gene product (Bargiello et al., 1984; Bargiello and Young, 1984; Bayles et al., 1987; Citri et al., 1987; Hamblen et al., 1986; Young et al., 1985; Yu et al., 1987a,b). Three types of cDNA (A, B, and C), corresponding to three species of 4.5 kb RNA, have been cloned and their sequences compared (Citri et al., 1987). In type A cDNA (the eight-exon type and the most abundant), the first (5'-most) and the last exon (to the right of the stop codon) are noncoding; exon 5 encodes a Threonine-Glycine repeat with 17-23 pairs of alternating Thr-Gly residues (Citri et al., 1987; Jackson et al., 1986; Reddy et al., 1986; Shin et al., 1985) and is polymorphic in different wild-type strains (Yu et al., 1987a); in vitro-effected deletion of the Thr-Gly repeat in transformation experiments does not appear to affect cir- cadian rhythms, but causes shorter than normal song rhythm periods (Yu et al., 1987a). 4.5 kb RNA has been found in the brain and ventral ganglia of developing per+ individuals (James et al., 1986; Liu et al., 1988; Lorenz, Hall, and Ros- bash; Saez and Young, 1988) as well as in adult heads (Bar- giello et al., 1987; James et al., 1986; Liu et al., 1988; Saez and Young, 1988); it can also be detected in the salivary glands of per+ embryos and larvae (Bargiello et al., 1987), but is not found in individuals that lack the per locus. The per gene product has been demonstrated immunologically in per+ embryos in the midline of the nervous system, in salivary glands, in per+ pupae in the optic lobes of the brain and thoracic gland/corpora allata, and, in per+ adults, in the brain, eyes, gut, male and female reproductive tissues, Mal- pighian tubules, and most appendages (Bargiello et al., 1987; Liu et al., 1988; Saez and Young, 1988; Siwicki, Eastman, Petersen, Rosbash, and Hall, 1988, Neuron 1: 141-50). Stu- dies involving anti-per antibodies show that per01 embryos, larvae, pupae, and adults are "null" at the protein level [in that peptides used to generate the antibodies were downstream of the relevant stop codon (Bargiello et al., 1987; Saez and Young, 1988; Siwicki et al., 1988)]; per04 adults are antigen- ically null, whereas perL1 adults stain poorly and pers adults stain normally (Siwicki et al., 1988). Expression of per in adults (embryonic expression bypassed) has been studied by temporal manipulation experiments in which a Hsp70 promoter has been fused to the per gene and the fusion gene turned on in adults only [Ewer, Rosbash, and Hall, 1988, Nature (London) 333: 82-84]. Inducing the expression of per after develop- ment is completed is necessary for the manifestation of the phenotype; earlier induction of the gene is not necessary or helpful. Circadian rhythmicity can be restored to some of the per- and per0 mutants by P-element-mediated transformation with DNA fragments homologous to all or part of the 4.5 kb RNA species (Bargiello et al., 1984; Baylies et al., 1987; Hamblen et al., 1986; Young et al., 1985; Zehring et al., 1984). "Restored" periodicities tend to be longer than normal (Bay- lies et al., 1987), except when per0 flies are transformed with a particular 13.2 kb DNA fragment carrying all the coding information flanked by 3.7 kb of 5' and 2.0 kb of 3' sequences (Citri et al., 1987). In the latter case, the periodicity and per+ penetrance of the transformed flies resembles that of normal wild-type individuals. In the transformation experi- ments of Baylies et al., 1987, period length was shown to be correlated with abundance of per RNA. Transformed flies also show a restoration of cell-to-cell junctional communication. Levels of gap junctional communication are also correlated with abundance of per RNA (Bargiello et al., 1987). The 0.9 kb transcript, located adjacent to the 4.5 kb tran- script, does not seem to be involved in the rescue of the clock functions in per- and per0 mutants (Bargiello and Young, 1984; Bargiello et al., 1984; Hamblen et al., 1986). In per+ flies, however, this transcript shows oscillations in its abundance, being higher at midday than at midnight; in per0 mutants these oscillations do not occur (Reddy et al., 1984). Nothing is known at present about the 2.7 kb and the 1.7 kb transcripts. DNA sequences from per mutants have been com- pared and single base-pair changes found in perL (T->A; Val245->Asp), pers (G->A; Ser589->Asn), and per0 (C->T; Gln464->Amber) (Baylies et al., 1987; Yu et al., 1987b). In the per mutation associated with T(1;4)JC43 flies, the 4.5 kb transcript has been replaced by a 11.5 kb transcript (Bar- giello and Young, 1984; Jackson et al., 1986; Reddy et al., 1984). other information: per01 is complemented by l(1)3A and l(1)3B mutants nearby (Young and Judd, 1978; Smith and Konopka, 1981). The mutant per01 of D. melanogaster can be rescued (i.e. made to show rhythmic behavior) by transformation with a hybrid gene carrying the coding region of the D. pseudoobscura per gene (Peterson, Hall, and Rosbash, 1988, EMBO J. 7: 3939-47). # pers: persimmon location: 3- (left arm). origin: X ray induced. discoverer: Demerec, 37l2. references: 1940, DIS 14: 40. phenotype: Eye color dull orange. Larval Malpighian tubes colorless (Brehme, 1942, Genetics 27: 133). Viability and fertility good. RK2A. cytology: Associated with In(3L)pers = In(3L)63C2-5;73B2-5. # petit: see pe # Pfd: Pufdi location: 2-70.8. discoverer: Brierley, 1935. references: Shull, 1937, DIS 8: 10. 1938, Proc. Michigan Acad. Sci. 23: 647-49. Baker, 1950, Am. Naturalist 84: 51-70. phenotype: Wings spread; fluid often accumulates between mem- branes. Degree of wing divergence inversely correlated with temperature; wings more divergent in male. In transfers from 19 to 31, temperature-effective period begins 6-8 hr before eclosion in male and 4-6 hr before eclosion in female and ends with eclosion. In transfers from 31 to 19, the temperature- sensitive period begins 8-10 hr before eclosion and ends 2- 4 hr before eclosion (P. H. Baker, 1950). Homozygous lethal. RK2. # Pfk: Phosphofructokinase location: 2-85.2. references: Laurie-Ahlberg, Wilton, Curtsinger, and Emigh, 1982, Genetics 102: 191-206. Munneke and Collier, 1985, Biochem. Genet. 23: 847-57. genetics: Produces the glycolytic enzyme phosphofructokinase [PFK (E.C. 2.7.1.11)]. Only one electrophoretic form has been found in larvae and adults. cytology: Located at 55E. #*pg: prong location: 2-40. discoverer: Mohr, 19e. references: 1923, Z. Indukt. Abstamm. Vererbungsl. 32: 218. phenotype: Extra crossveins distal to anterior crossvein; usu- ally incomplete. Overlaps wild type in at least 10% of flies. RK3. # pg: see pig # Pgd: Phosphogluconate dehydrogenase location: 1-0.6 [between br and pn (Gvozdev et al., 1970)]. discoverer: Young. synonym: Lethal allele: l(1)2Dc. references: Kazanian, Young, and Childs, 1965, Science 150: 1601-02. Young, 1966, J. Hered. 57: 58-60. Seecof, Kaplan, and Futch, 1969, Proc. Nat. Acad. Sci. USA 62: 528-35. Gvozdev, Birstein, and Faizullin, 1970, DIS 45: 163. Lucchesi, Hughes, and Geer, 1979, Curr. Top. Cell. Reg. 15: 143-54. Gutierrez, Christensen, Manning, and Lucchesi, 1989, Dev. Genet. (Amsterdam) 10: 155-61. phenotype: Structural gene for 6-phosphogluconate dehydrogenase [6PGD (E.C. 1.1.1.44)], the last enzyme in the oxidative part of the pentose phosphate shunt. The electrophoretic variants PgdA and PgdB have been described in Drosophila (Kazanian et al., 1965; Young, 1966), PgdA migrating faster in starch gel than PgdB. PgdA/PgdB heterozygous females produce a hybrid band of intermediate mobility. The enzyme 6PGD is a dimer. Its molecular weight was reported by Kazanian [1966, Nature (London) 212: 197-98] to be about 79,000; Williamson, Kro- chko, and Geer (1980, Biochem. Genet. 18: 87-101), using 6PGD (purified) isolated from PgdA homozygotes, found its molecular weight to be 105,000, and that it contains a mixture of equal amounts of subunits having molecular weights of 55,000 and 53,000. Enzyme activity is highest in early third instar lar- vae and lowest in late third instar larvae and 3-day old pupae, with intermediate levels in 4-day old pupae, newly eclosed adults, and 5-day old adults (Williamson et al., 1980). The enzyme is found mainly in the fat body (Cochrane and Lucchesi, 1980, Genetics 94: s20). Males with one dose of Pgd+ and females with two doses have about the same amount of 6PGD, i.e. show dosage compensation for enzyme activity (Seecof et al., 1969; Gerasimova and Ananiev, 1972, DIS 48: 93; Bowman and Simmons, 1973, Biochem. Genet. 10: 319-31; Faizullin and Gvodev, 1973, Mol. Gen. Genet. 126: 233-45). Females heterozygous for a Pgd defi- ciency show a corresponding reduction in enzyme activity, while males and females with an extra dose of Pgd+ show increased enzyme activity. A number of lethal and semilethal Pgd mutants have been induced in PgdA or PgdB (Bewley and Lucchesi, 1975, Genetics 79: 451-66; Gvozdev, Gostimsky, Gerasimova, Dubrovskaya, and Braslavskaya, 1975, Mol. Gen. Genet. 141: 269-75; Hughes and Lucchesi, 1977, Science 196: 1114-15; Gvozdev, Gerasimova, Rostovsky, Kogan, and Braslavskaya, 1978, DIS 53: 143; Luc- chesi et al., 1979). The lethals (Pgdn) show no enzyme activity unless covered by a Pgd+ duplication such as w+Y; the semilethals (Pgdlo) show low enzyme activity and are com- pletely lethal when heterozygous with Pgd lethals. Flies car- rying null alleles for both G6PD, the first enzyme in the pen- tose phosphate shunt, and 6PGD, the last enzyme, are viable, presumably because the toxic 6-phosphogluconate is not pro- duced (Lucchesi et al., 1977). Pgdn/Y males can be rescued by dietary supplements of fructose and linoleate that minimize 6-phosphogluconate production (Hughes and Lucchesi, 1978, Biochem. Genet. 16: 469-75). alleles: The following table includes electrophoretic (wild- type), semilethal and lethal alleles of Pgd. [Synonyms for Pgd+ alleles (PgdA, PgdB) use terminology for allozyme vari- ants from DIS 53: 117]. allele origin discoverer synonym ref ( genetics ________________________________________________________________________________ PgdA spont Young 6-Pgd4 6,12 viable, fertile; fast variant PgdB spont Young 6-Pgd8 6, 12 viable, fertile; slow variant PgdI Lucchesi 6-Pgd6 viable, fertile; intermediate variant Pgdlo1 | Young Pgd- 1, 2, 10 semi-lethal, female sterile, low 6PGD activity Pgdlo2 EMS Lucchesi 10 semi-lethal, female sterile, low 6PGD activity Pgdlo3 EMS Lucchesi 10 semi-lethal, female sterile, low 6PGD activity Pgdlo4 EMS Lucchesi 10 semi-lethal, female sterile, low 6PGD activity Pgdlo13 / EMS Gvozdev Pgd13 3-5 semi-lethal, low 6PGD activity Pgdlo50 / EMS Gvozdev Pgd50 3-5 semi-lethal, low 6PGD activity Pgdlo109 / EMS Gvozdev Pgd109 3-5 semi-lethal, low 6PGD activity Pgdn1 |/ EMS Bewley, l(1)Pgd-An1 1, 10 lethal; Pgd- Lucchesi Pgdn2 EMS Lucchesi 10 lethal; Pgd- Pgdn3 EMS Lucchesi 10 lethal; Pgd- Pgdn4 EMS Lucchesi 10 lethal; Pgd- Pgdn5 EMS Lucchesi 10 lethal; Pgd- Pgdn6 EMS Lucchesi 10 lethal; Pgd- Pgdn7 EMS Lucchesi 10 lethal; Pgd- Pgdn8 EMS Lucchesi 10 lethal; Pgd- Pgdn9 X ray Lefevre l(1)JE58 8 lethal; Pgd- Pgdn10 EMS Lefevre l(1)DF958 9,11 lethal; Pgd- Pgdn11 EMS Lefevre l(1)VA55 9,11 lethal; Pgd- Pgdn12 EMS Lefevre l(1)VE618 9,11 lethal; Pgd- Pgdn35 / EMS Gvozdev Pgd35 3-5 lethal; Pgd- Pgdn39 / EMS Gvozdev Pgd39 3-5 lethal; Pgd- Pgdn45 / EMS Gvozdev Pgd45 3-5 lethal; Pgd- Pgdn71 / EMS Gvozdev Pgd71 3-5 lethal; Pgd- Pgdn93 ` EMS Gvozdev Pgd93 3-5 lethal; Pgd- Pgdn94 ` EMS Gvozdev Pgd94 3-5 lethal; Pgd- Pgdn100 ` EMS Gvozdev Pgd100 3-5 lethal; Pgd- Pgdn111 / / ray Gvozdev Pgd111 3-5 lethal; Pgd- PgdnHM18 - HMS l(1)HM18 7 lethal; Pgd- ( 1 = Bewley and Lucchesi, 1975, Genetics 79: 451-66; 2 = Geer, Lindel, and Lindel, 1979, Biochem. Genet. 17: 881-95; 3 = Gvozdev, Gerasimova, Kogan, and Rostovsky, 1977, Mol. Gen. Genet. 153: 191-98; 4 = Gvozdev, Gerasi- mova, Rostovsky, Kogan, and Braslavskaya, 1978, DIS 53: 143; 5 = Gvozdev, Gostimsky, Gerasimova, Dubrovskaya, and Braslavskaya, 1975, Mol. Gen. Genet. 141: 269-75; 6 = Kazanian, Young, and Childs, 1965, Science 150: 1601- 02; 7 = Kramers, Schalet, Paradi, and Huiser-Hooteyling, 1983, Mutat. Res. 107: 187-201; 8 = Lefevre, 1981, Genetics 99: 461-80; 9 = Lefevre and Watkins, 1986, Genetics 113: 869-95; 10 = Lucchesi, Hughes, and Geer, 1979, Curr. Top. Cell. Reg. 15: 143-54; 11 = Perrimon, Engstrom, and Mahowald, 1985, Genetics 111: 23-41; 12 = Young, 1966, J. Hered. 57: 58-60. | Pgdlo1/Pgdn1 females are lethal; Pgdn1/Y males are lethal, except for a few escapers. / Induced in PgdA. ` Induced in PgdB. - HMS = hycanthon methanesulfonate. cytology: Located in 2D3 or 2D4 (Gerasimova and Ananiev, 1972, DIS 48: 93; Gvozdev, Gostimsky, Gerasimova, Dubrovskaya, and Braskavskaya, 1975, Mol. Gen. Genet. 141: 269-75; Slobodyan- yuk and Serov, 1983, Mol. Gen. Genet. 191: 372-77) based on the following: (1) Pgd is uncovered by Df(1)Pgd-kz = Df(1)2D3-4;2F5 but not by Df(1)2D6;3C2 (Lefevre; Seecof et al., 1969) and is covered by w+Y (2D1;3D4 inserted in Y); (2) It maps to the left of pn (located by Lefevre in 2D5-6). Whereas PgdA/PgdB heterozygotes show three isozyme bands on starch gels, deficiency heterozygotes show only one band and their 6PGD level is correspondingly reduced (Gerasimova and Ananiev, 1972; Gvozdev et al., 1975). molecular biology: Using a cDNA clone of the rat 6PGD as a probe, Christensen and Lucchesi (1984, Genetics 107: s20; Gutierrez et al., 1989) isolated a Drosophila clone (14.7 kb fragment) hybridizing to 2D6, the approximate cytological location of Pgd. Another clone hybridizing to 2C1-E3 was obtained by Brock. The lethal Pgd- phenotype was rescued by germline transformation (Gutierrez et al., 1989). A single Pgd+ gene transduced to an autosomal site showed higher enzyme activity in males than in females, as would be expected if sequences responsible for dosage compensation had been trans- duced into the Pgd- host. # Pgi: Phosphoglucose isomerase location: 2-58.6 (Voelker et al., 1980). references: Lee, 1979, J. Biol. Chem. 254: 6375. Voelker, Langley, Leigh-Brown, and Ohnishi, 1978, DIS 53: 200. Voelker, Langley, Leigh-Brown, Ohnishi, Dickson, Montgomery, and Smith, 1980, Proc. Nat. Acad. Sci. USA 77: 1091-95. Laurie-Ahlberg, Williamson, Cochrane, Wilton, and Chasalow, 1981, Genetics 99: 127-50. Langley, Voelker, Leigh-Brown, Ohnishi, Dickson, and Montgomery, 1981, Genetics 99: 151-56. Laurie-Ahlberg, Wilton, Curtsinger, and Emigh, 1982, Genetics 102: 191-206. Burkhart, Dickson, Montgomery, Langley, and Voelker, 1984, Genetics 107: 295-306. phenotype: Structural gene for the glycolytic enzyme phospho- glucose isomerase [PGI (E.C. 5.3.1.9)]. There are two elec- trophoretic variants (fast and slow); also a deficiency for the locus which is CRM negative and probably homozygous lethal (Lee, 1979). alleles: Two Pgi+ alleles [Pgi4 (fast) and Pgi2 (slow)] and one Pgi- allele (PginNc80) have been reported. Out of a total of 716 alleles collected in North Carolina, one null allele was recovered (Langley et al., 1981). # Pgk: Phosphoglycerate kinase location: 2-5.9 (between al and dp) (Voelker et al., 1979). references: Chew and Cooper, 1973, Biochem. Genet. 8: 267-70. Voelker, Ohnishi, and Langley, 1979, Biochem. Genet. 17: 769-83. Voelker, Langley, Leigh-Brown, Ohnishi, Dickson, Montgomery, and Smith, 1980, Proc. Nat. Acad. Sci. USA 77: 1091-95. Langley, Voelker, Leigh-Brown, Ohnishi, Dickson, and Montgomery, 1981, Genetics 99: 151-56. Laurie-Ahlberg, Wilton, Curtsinger, and Emigh, 1982, Genetics 102: 191-206. phenotype: Structural gene for 3-phosphoglycerate kinase [3-PGK (E.C. 2.7.2.3)]. Three electrophoretic variants (fast, intermediate, slow) isolated by Chew and Cooper (1973), the heterozygotes showing no hybrid band; two electrophoretic variants isolated by Volker et al. (1979). alleles: Three Pgk+ alleles, Pgk3 (fast), Pgk2 (intermediate), Pgk1 (slow) of Chew and Cooper (1973). No null alleles reported out of a total of 702 alleles collected in North Carolina (Langley et al., 1981). cytology: Located between 22D and 23C since included in the 2D segregant of T(Y;2)G146 = T(Y;2)h23;23B-C but not of T(Y;2)R136 = T(Y;2)h3;h7;22D. # Pgm: Phosphoglucomutase location: 3-43.4 (between th and st; Hjorth, 1970) or 3-43.6 (between Gl and st; Trippa et al., 1970, 1971). references: Hjorth, 1970a, DIS 45: 39. 1970b, Hereditas 64: 146-48. Trippa, Santolamazza and Scozzari, 1970, Biochem. Genet. 4: 665-67. Trippa, 1971, DIS 46: 42. Trippa, Scozzari, and Santolamazza, 1971, DIS 46: 44. Trippa, 1972, DIS 49: 35. Trippa, Danieli, Costa, and Scozzari, 1977, DIS 52: 74. Voelker, Ohnishi, and Langley, 1979, Biochem. Genet. 17: 769-83. phenotype: Structural gene for the glycolytic enzyme phospho- glucomutase [PGM (E.C. 2.7.5.1)], a monomeric protein of 56,000 daltons. Two frequently-occurring electrophoretic vari- ants were isolated and studied by Hjorth (1970a,b) and Trippa et al. (1970, 1971). Later five low-frequency variants were found by Trippa's group (see references in table of alleles). One null allele found in a total of 431 alleles collected in Great Britain (Langley, Voelker, Leigh-Brown, Ohnishi, Dick- son, and Montgomery, 1981, Genetics 99: 151-56). alleles: The seven Pgm+ alleles identified by Trippa's group are listed in the following table. The most common allele has been designated Pgm4 in accordance with the convention of Voelker et al. (1979). The slower-migrating alleles are given superscript numbers below four while the faster-migrating alleles have numbers above four. allele synonym ref ( comments _________________________________________________________________ Pgm1 | PgmE; Pgm0.55 2, 3, 5 slowest migration on gel Pgm2 | PgmB; Pgm0.70; Pgm2 1-6 frequency 0.8 - 20.7% Pgm3 PgmF; Pgm0.85; 2, 3, 5 Pgm4 / PgmA; Pgm1.00; Pgm1 1-6 frequency 79.3 - 99.2% Pgm5 PgmG; Pgm1.10; 4, 5 Pgm6 | PgmC; Pgm1.20; 2, 3, 5 Pgm7 PgmD; Pgm1.50; 2, 3, 5 fastest migration on gel ( 1 = Hjorth, 1970, DIS 45: 39; 2 = Trippa, 1972, DIS 49: 35; 3 = Trippa, Barberio, Loverre, and Santolamazza, 1972, DIS 49: 42; 4 = Trippa, Danieli, Costa, and Scozzari, 1977, DIS 52: 2; 5 = Trippa, Danieli, Costa, and Scozzari, 1977, DIS 52: 74; 6 = Trippa, Santolamazza, and Scozzari, 1970, Biochem. Genet. 4: 665-67. | Enzyme heat-sensitive [Loverre and Carmody, 1985, Biochem. Genet. 23: 29-36; Trippa, Loverre, and Catamo, 1976, Nature (London) 260: 42-44; Trippa, Catamo, Lombardozzi and Ciccheti, 1978, Biochem. Genet. 16: 299-305]. / Enzyme may be heat-sensitive or heat-resistant (Trippa et al., 1976, 1978). cytology: Located in 72D1-5 since Pgm included in Df(3L)th117 = Df(3L)72A1;72D5 but not in Df(3L)th113 = Df(3L)72A2;72D1-2 (Voelker et al., 1978; Burkhart, Dickson, Montgomery, Langley, and Voelker, 1984, Genetics 107: 295-306.)