# bx: see BXC # bxD: see Ubx in BXC # Bx: Beadex location: 1-59.4. phenotype: Male and homozygous female with Beaded-like wings; long, narrow, and excised along both margins; fully viable. Heterozygous female less extreme and overlaps wild type. Some venation abnormality. Development studied by Goldschmidt [1935, Biol. Zentralbl. 55: 535-54 (fig.)]. According to Waddington (1940), embryological effect is same as that of vg. RK2 (RK3 as Bx/+). alleles: allele origin discoverer ref ( mol. biol. | ___________________________________________________________________________ Bx1 spont Bridges, 23a3 2, 3, 9, 13, 17 8.5 kb (roo) Bx2 / spont Mohr, 24l29 2, 3, 10, 14, 16 gypsy Bx3 / spont Gershenson, 1927 2, 3, 6 10.3 kb (roo) Bx9 P Engels 13 -1.2 kb Bx15 P Engels 13 -2.0 kb Bx32e X ray Moore, 32e 2 Bx46 13 4.2kb (copia) *Bx59h spont T.J. Lee, 59h 3, 12 *BxC spont Catcheside 39c3 1, 2 *Bxin spont Mohr, 24d4 2, 15 BxJ / heat? Jollos, 1930 2, 3, 4, 5, 13 6.2 kb (3S18) *BxL spont Lancefield 2, 13 BxM spont Muller 12-16 kb (in Winscy) Bx0 spont Oster, 1964 (in C(1)Dx) Bxr / spont Ives, 35k 2, 3, 8, 9, 11 Bxr49k / spont Mossige, 49k22 2, 3, 10, 17 ( 1 = Catcheside, 1939, DIS 12: 49; 2 = CP552; 3 = CP627; 4 = Jollos, 1933, Naturwissenschaften 21: 831-34; 5 = Jol- los and Waltsky, 1937 DIS 8: 9; 6 = Gassinovitsch and Gershenson, 1928, Biol. Zentralbl. 48: 385-87 (fig.); 7 = Gottschewski, 1935, DIS 4: 7, 14, 16; 8 = Green, 1952, Proc. Nat. Acad. Sci. USA 38: 949-53; 9 = Green, 1953, Genetics 38: 91-105 (fig.); 10 = Green, 1953, Z. Indukt. Abstamm. Vererbungsl. 85: 435-39 (fig.); 11 = Ives, 1937, DIS 7: 6; 12 = Lee, 1964, DIS 39: 60; 13 = Mattox and Davidson, 1984, Mol. Cell. Biol. 4: 1343-53 (fig.); 14 = Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. USA 80: 1678-82; 15 = Mohr, 1927, Hereditas 9: 178; 16 = Mohr, 1927, Nyt. Mag. Natur. 65: 265-74; 17 = Morgan, Bridges, and Sturtevant, 1925, Bibliogr. Genet. 2: 219; 18 = Mossige, 1950, DIS 24: 61. | Size of DNA insert in Bx region. / Phenotypes described below. cytology: Placed in 17C2-3 based on the position of breakpoints of hybrid-dysgenesis-induced hdp mutants (Engels and Preston, 1981, Cell 26: 421-28). molecular biology: 49kb, including the Bx locus, cloned and restriction mapped by Mattox; 0 coordinate defined as SmaI site within a 1.8 kb Bam HI fragment within or very close to the Bx coding sequence; positive values to the right. Six mutants differ from wild type in having different segments of DNA inserted into the same 0.4kb restriction fragment (-2.0 to -1.6). Bx2 has two gypsy elements inserted in opposite orien- tation at coordinates -0.5 and -1.5. Hybrid-dysgenesis- induced mutations, Bx9 and Bx15, are imprecise excisions of the P factor, which is inserted at coordinate -0.8 in the TT2 X chromosome and is without phenotypic effect. Bx9 deletion includes 1.2kb of flanking DNA including -0.8 to -2.0, and Bx15 deletion of 2.0kb includes -1.3 to +0.4 (Mattox and Davidson, 1984, Mol. Cell. Biol. 4: 1343-53). other information: Interpreted by Lifschytz and Green (1979, Mol. Gen. Genet. 171: 153-59) as mutation in cis-acting con- trol element causing overproduction of hdp-a gene product. Tandem duplication of Bx+ and hdp-a+ has recessive Bx effect (e.g., Bxr); tandem triplication and quadruplication have dom- inant Bx effects in combination with a normal X, but not in combination with hdp-a or a Bx deficiency (Lifschytz and Green, 1979). Amorphic or extreme hypomorphic Bx mutations and deficiencies for Bx act as trans suppressors of Bx. Suppression used by Lifschytz and Green to select null alleles or deficiencies from treated + or Bx3 chromosomes; seven derivatives of Bx3 and those of Bx+ described; all have hdp-a effects as well. Bx2: Beadex-2 Edith M. Wallace, unpublished. # Bx2 phenotype: Wings of males and homozygous females narrowed by marginal excision. Wings often bubbly and ragged. Homozygous female fully viable. Bx2/+ less extreme; overlaps wild type. Classifiable in a single dose in triploids (Schultz, 1934, DIS 1: 55). RK1 (RK3 as Bx2/+). # Bx3 phenotype: Extreme allele usually without the bubbles in the wing. Shortened L5 a constant character (few Bx2 show this). Wings more pointed than Bx2 and hairs at tip of wing clumped. Third-instar larvae show 20-40 degenerating cells in area of wing disk corresponding to future wing margin (D. Fristrom, 1969, Mol. Gen. Genet. 103: 363-79). Scalloping visible in prepupal wing bud [Waddington, 1940, J. Genet. 41: 75-139 (fig.)]. Bx3 in heterozygous combination with a Bx deficiency or hdp-a has normal wing phenotype (Lifschytz and Green, 1979, Mol. Gen. Genet. 171: 153-59). Bx3/+ fully separable. RK1. # BxJ: Beadex of Jollos phenotype: Wings reduced to slender strip; only posterior cell present at tip. BxJ/+ have half and BxJ/BxJ one third the normal number of cells in membrane of wing. Femur shortened or legs otherwise abnormal, especially third pair. Halteres abnormal. Homozygous female viable. Interacts with bi to give more nearly normal wings. The only dominant Bx allele not suppressed by a Bx deficiency [e.g., In(1)ClLy4R] or hdp (Lifschytz and Green, 1979, Mol. Gen. Genet. 171: 153-59). Embryology like Bx [Goldschmidt, 1935, Biol. Zentralbl. 55: 535-54; Waddington, 1940, J. Genet. 41: 75-139 (fig.)]. Clonal analysis of wing disk development indicates massive cell loss during third larval instar. Clones of Bx+ cells in BxJ/+ wings that reach the margin but are confined to the dor- sal or ventral surface often cause reconstitution of both sur- faces and appearance of marginal elements derived from both surfaces (Santamaria and Garcia-Bellido). RK1. 1975, Wilhelm Roux' Arch. Entwicklungsmech. Organ. 178: 233-45. # Bxr: Beadex-recessive phenotype: Bxr/+ is normal. Male and homozygous female show less extreme narrowing of wings than Bx. Anterior crossvein short and thickened and that region blistered. May overlap wild type in old crowded cultures at 25, more extreme at 19. RK3A. cytology: Associated with Dp(1;1)Bxr = Dp(1;1)17A;17E-F (Green, 1953, determined by E.B. Lewis). Recessive Bx effects are due not to an altered gene but to increased dosage of the normal allele. other information: Bx/Dp(1;1)Bxr produces recombinants of geno- type Bx+Bx and BxBx+, which are more extreme than Bx. Same holds for Bx2/Dp(1;1)Bxr. Bxr49k: Beadex-recessive 49k From Green, 1953, Z. Indukt. Abstamm. Vererbungsl. 85: 435-49. # Bxr49k phenotype: Slight scalloping of posterior wing margin only; overlaps wild type. RK3A. cytology: Associated with Dp(1;1)Bxr49k = Dp(1;1)17A;17C (E.B. Lewis). other information: This duplication undergoes unequal crossing over readily and forms triplications and quadruplications. Duplication is recessive; triplication is dominant. Pheno- typic interaction with Bx same as for Bxr. # BXC: Bithorax Complex (I. Duncan) The bithorax complex (BXC) is a gene cluster that functions to assign unique identities to body segments in the abdomen and posterior thorax (Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hogness, 1983, Science 221: 23-29). Most, perhaps all, BXC functions are expressed within paraseg- ments, metameric units composed of the posterior compartment of one segment and the anterior compartment of another. Com- plementation studies indicate that the BXC is organized into three large functionally integrated regions, known as the Ultrabithorax (Ubx), abdominal-A (abd-A), and Abdominal-B (Abd-B) domains. Apparent point mutations have been recovered that totally inactivate each of these domains. The Ubx domain functions primarily to assign identities to parasegments 5 and 6 (PS5 and PS6), the abd-A domain functions in PS7-PS13, and the Abd-B domain functions in PS10-PS14. Each BXC domain con- tains subregions that are responsible for the assignment of identities to specific compartments or parasegments. The Ubx domain contains two major subregions. These are the anterobithorax-bithorax (abx-bx) region, which specifies PS5 identities, and the bithorax-postbithorax (bxd-pbx) region, which specifies PS6 identities. Molecular studies indicate that most or all Ubx domain functions are executed by a family of homeodomain-containing Ubx proteins. The abx-bx and bxd- pbx subregions appear to cis-regulate the expression of these proteins in PS5 and PS6, respectively. abd-A and Abd-B func- tions are also executed by homeodomain-containing proteins. The abd-A and Abd-B domains each contains parasegment- or segment-specific subregions which have been named infra- abdominal (iab) regions. Each iab region is named according to the anterior compartment of the segment or parasegment whose identity is specifically abolished by mutations in that region. For example, iab2 mutations cause a transformation of the anterior second abdominal segment (A2) toward A1, and iab3 mutations cause transformations of anterior A3 (and more pos- terior segments) toward A2. The iab2, iab3, and iab4 subre- gions are contained within the abd-A domain whereas the iab5 through iab9 regions are located within the Abd-B domain. Some evidence suggests that the bxd-pbx region and some of the iab regions may be bifunctional and affect the expression of both adjacent BXC domains. Remarkably, the order of subre- gions wihin the complex is the same as the order of the parasegments or segments that each affects. Although it is not known whether this correlation has functional signifi- cance, two mutations (Uab1 and Cbx1) that change the relative order of BXC regions alter the spatial expression of BXC pro- ducts. # abd-A: abdominal-A (I. Duncan) location: 3-58.5 (to the right of iab2; to the left of iab3). references: Lewis, 1978, Nature 276: 565-70. Morata, Botas, Kerridge, and Struhl, 1983, J. Embryol. Exp. Morphol. 78: 319-41. Sanchez-Herrero, Vernos, Marco, and Morata, 1985, Nature 313: 108-13. Sanchez-Herrero, Casanova, Kerridge, and Morata, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 165-172. Tiong, Bone, and Whittle, 1985, Mol. Gen. Genet. 200: 335-42. Karch, Wieffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Duncan, 1987, Annual Review of Genetics 21: 285-319. Cumberledge, Zaratzian, and Sakonju, 1990, Proc. Nat. Acad. Sci. USA 87: 3259-63. phenotype: Null alleles are recessive lethal. Homozygous lar- vae show transformations of the ventral and dorsal setal belts of A2 through A8 toward A1. These transformations are com- plete in A2 through A4, but are incomplete more posteriorly. Partial Keilin's organs composed of monohairs occur variably on all segments from A1 through A7. In the adult cuticle, homozygous abd-A mitotic recombination clones are completely transformed to A1 in segments A2 through A4 and show charac- teristics of A1 to A4 in segments A5 to A7. alleles: molecular allele origin discoverer synonym cytology biology ( _____________________________________________________________________ abd-A39 ENU R.H. Baker Habrev28390.39 abd-A41 ENU R.H. Baker Habrev28390.41 abd-A517 X ray R.H. Baker iab231616.517 T(2;3)34-35;41; 40-45 kb 78;83-84;89E abd-AC26 X ray Crosby iab2C26 normal 34.5-36 kb deleted abd-AC51 X ray Crosby HabrevC51 In(3LR)80;89E 41.5-43 kb iab2C51 abd-AC53 X ray Crosby HabrevC53 normal undetected iab2C53 abd-AD24 EMS Duncan iab2D24 normal undetected abd-AM1 EMS Morata not reported not studied abd-AM3 abd-AMX1 X ray Morata T(2;3)40;89E 54-56 kb abd-AMX2 X ray Morata normal 55-58.5 kb deleted abd-AP10 X ray Shaw iab2P10 Tp(3;2)29A-C; 35-36 kb T(2;3)P10 89C1-2;89E1-2 abd-AS2 X ray Tiong 50-55 kb ( Coordinates of rearrangement breakpoints unless otherwise indicated: Karch, Wieffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96. # Abd-B: Abdominal-B (I. Duncan and S. Celniker) location: 3-58.8 (to the right of iab7; to the left of iab8,9). references: Karch, Wieffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96. Sanchez-Herrero, Casanova, Kerridge, and Morata, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 165-172. Sanchez-Herrero, Vernos, Marco, and Morata, 1985, Nature 313: 108-13. Tiong, Bone, and Whittle, 1985, Mol. Gen. Genet. 200: 335-42. Casanova, Sanchez-Herrero and Morata, 1986, Cell 47: 627-36. Duncan, 1987, Annual Review of Genetics 21: 285-319. Sanchez-Herrero, and Crosby, 1988, EMBO J. 7: 2163-73. Celniker, Keelan, and Lewis, 1989, Genes Dev. 3: 1425-37. Zavortnik and Sakonju, 1989, Genes Dev. 3: 1969-81. DeLorenzi and Bienz, 1990, Development 108: 323-29. phenotype: Heterozygotes for null alleles show weak anteriorly-directed transformations of A5, A6, and A7. In the male, this results in the presence of a tiny extra tergite in A7 and a loss of pigmentation on the A5 tergite. Heterozy- gotes are partially to completely sterile in both sexes, but are fertile if a duplication for the BXC [such as Dp(3;5)P5 or Dp(3;1)P68] is present. Hemizygotes and homozygotes are lethal; embryos lack posterior spiracles and filzkorper, have the ventral setal bands of A6, A7 and A8 transformed toward A5 or A4, and develop rudimentary chitinized plates in posterior A8. alleles: molecular allele origin discoverer synonym biology _______________________________________________________ Abd-BD3 DEB Duncan iab7D3 undetected Abd-BD16 EMS Duncan iab7D16 undetected Abd-B297 ENU Lewis iab7297 undetected Abd-BM1 EMS Morata not examined # abx: anterobithorax (E.B. Lewis) location: 3-58.8 (to the right of Cbx3; to the left of bx). references: Lewis, 1978, Nature 276: 565-70. Lewis, 1980, DIS 55: 207-08. Lewis, 1981, Developmental Biology Using Purified Genes (Brown and Fox, eds.). Academic Press, New York, pp. 189-208. Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hog- ness, 1983, Science 221: 23-29. Casanova, Sanchez-Herrero, and Morata, 1985, Cell 42: 663-69. Peifer and Bender, 1986, EMBO J. 5: 2293-2303. phenotype: Homozygotes show variable tranformations of the anteriormost portion of the third thoracic segment (T3) toward the corresponding part of T2. Homozygotes also show variable tranformations of posterior T2 to posterior T1. The latter effect is enhanced by low temperature. Partially complements and shows transvection with bx1, bx3, and bx34e. abx/pbx has the posterior portion of the distal segment of the haltere very slightly transformed into wing tissue; abx/pbx2 is simi- lar if heterozygous for a rearrangement that suppresses transvection. alleles: allele origin discoverer synonym molecular biology ( _____________________________________________________________________ abx1 X ray Lewis, 59i bx7 -79 to -73 kb deleted abx2 X ray Kerridge bxSK, abxsk -79.0 to -77.5 kb deleted abxCAC4 dysgenesis Adler, 1984 -80 to -66 kb deleted, with Hobo element inserted at point of deletion. ( Peifer and Bender, 1986, EMBO J. 5: 2293-2303. bx: bithorax From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 152. # bx: bithorax (E.B. Lewis) location: 3-58.8 (to the right of abx; to the left of Cbx1.) references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. 327: 137. Morgan, Bridges, and Sturtevant, 1925, Bibliogr. Genet. 2: 79. Lewis, 1951, Cold Spring Harbor Symp. Quant. Biol. 16: 159- 74. Lewis, 1963, Am. Zool. 3: 33-56. Finnegan, Rubin, Young, and Hogness, 1978, Cold Spring Harbor Symp. Quant. Biol. 42: 1053-63. Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. USA 80: 1678-82. Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hog- ness, 1983, Science 221: 23-29. Casasnova, Sanchez-Herrero, and Morata, 1985, Cell 42: 663- 669. Peifer and Bender, 1986, EMBO J. 5: 2293-2303. phenotype: Homozygote has anterior portion of third thoracic segment (T3) transformed toward corresponding region of second (T2). The extent of this transformation is allele dependent and is most extreme in bx3 and weakest in bx4. Although the transformations caused by most bx alleles are uniform, those caused by bx1 and bx34eprv are highly variable. At 17C several bx alleles show weak and variable transformations of posterior T2 to posterior T1. bx3, bx8, and bxG over pbx show a very slight pbx effect (as described for abx) if heterozy- gous for a rearrangement that suppresses transvection. alleles: allele origin discoverer molecular biology ( ___________________________________________________________________ bx1 spont Bridges, 1915 412 at -60 kb bx3 spont Stern, 1925 gypsy at -57 kb; doc at -53 kb bx4 spont Lewis undetected bx8 EMS Lewis, 1965 harvey at -59.5 kb bx9 spont Kuhn, 1981 gypsy at -64 kb bx34e spont Schultz, 1934 gypsy at -63.5 kb bx34eprv X ray Lewis -66.5 to -57 kb deleted bxAF spont Lewis identical to bx34e bxAF2 spont Lewis identical to bx34e bxAV spont | Rosenfeld gypsy at -66 kb bxF31 spont Adler, 1982 I factor at -74 kb bxG spont Gans gypsy at -66 kb bxIS spont Ising identical to bx1 bxKa spont Kuhn, 1983 gypsy at -61.5 kb bxKb spont Kuhn, 1983 gypsy at -55 kb bxX spont Lewis identical to bx34e ( Peifer and Bender, 1986, EMBO J. 5: 2293-2303. | Probably spontaneous. # bxd: bithoraxoid (E.B. Lewis) location: 3-58.8 (to the right of Ubx1; to the left of pbx1). references: Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. 327: 137. Morgan, Bridges, and Sturtevant, 1925, Bibliogr. Genet. 2: 79. Lewis, 1951, Cold Spring Harbor Symp. Quant. Biol. 16: 159- 74. Lewis, 1955, Am. Nat. 89: 73-89. Lewis, 1963, Am. Zool. 3: 33-56. Kerridge and Sang, 1981, J. Embryol. Exp. Morphol. 61: 69-86. Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hog- ness, 1983, Science 221: 23-29. Peattie and Hogness, 1984, Genetics 107: s81. Bender, Weiffenbach, Karch, and Peifer, 1985, Cold Spring Har- bor Symp. Quant. Biol. 50: 173-80. Lipshitz, Peattie, and Hogness, 1987, Genes Dev. 1: 307-22. phenotype: Homozygotes show transformation of the anterior first abdominal segment (A1) to the corresponding region of the third thoracic segment (T3). In addition, bxd homozygotes have posterior T3 and posterior A1 transformed toward poste- rior T2. Hemizygotes for the stronger bxd alleles show (with variable expression) formation of one or a pair of well- developed thoracic legs and, rarely, an extra haltere on A1; the frequency of these abdominal halteres is greatly enhanced in hemizygotes for bxd9 iab2K. The A1 legs in bxd hemizygotes contain underdeveloped posterior compartments, indicating that posterior A1 is partially transformed toward thorax. alleles: See table on the following page for allele informa- tion. bxd: bithoraxoid From Bridges and Morgan, 1923, Carnegie Inst. Washington Publ. No. 327: 225. # Cbx: Contrabithorax (E.B. Lewis) location: 3-58.8. references: Lewis, Proc. Int. Congr. Genet. 9th, 1954, 1: 100-05. Lewis, 1963, Am. Zool. 3: 33-56. Lewis, Proc. Int. Congr. Genet. 12th, 1968, 2: 96-97. Morata, 1975, J. Embryol. Exp. Morphol. 34: 19-31. Lewis, 1978, Nature 276: 565-70. Capdevila and Garcia-Bellido, 1978, Wilhelm Roux's Arch. Dev. Biol. 185: 105-26. Lewis, 1981, Developmental Biology Using Purified Genes (Brown and Fox, eds.). Academic Press, New York, pp. 189-208. Lewis, 1982, Embryonic Development: Genes and Cells (Burger, ed.). Alan Liss, Inc., New York, pp. 269-88. Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, allele origin discoverer synonym cytology molecular biology ( type | _____________________________________________________________________________________________________ bxd1 spont Bridges normal gypsy at -21 kb I bxd9 spont Kuhn and normal gypsy at -19 kb I Lewis bxd55i spont Green normal gypsy at -23 kb I bxd51j spont Lewis normal gypsy at -17.5 kb I bxd68 X ray Baker bxd1068 T(2;3)41;89E III bxd100 X ray Lewis Tp(3;3)66;89B5-6; I 89E bxd101 X ray Lewis T(3;4)89E;101F I bxd106 X ray Lewis In(3LR)72D11-E2; I 89E bxd110 X ray Lewis bxd107 Tp(3;3)89E;91D1-2; I 92A2-3 bxd111 X ray Lewis bxd23240.1 Tp(3;1)4D;89E; II 90B2 bxd113 X ray Lewis In(3LR)69C3-4; I 89E bxd114 X ray Lewis bxd3978.114 In(3R)89E;94 I bxd121 X ray Lewis normal -15 kb to +60-65 kb ? deleted bxd123 X ray Crosby T(2;3)41;89E ? bxd125 ENU Chiang bxd27830.C5A, In(3R)89B;89E I bxdC5A bxd127 X ray Lewis bxd29315.4G, T(2;3)59C;89E + II bxd54G In(3R)88C-D;92 bxd183 EMS Lewis bxd17756.83 In(3R)89C;89E I bxd194 X ray Lewis bxd19409.2X, In(3LR)80F;89E II bxd92 bxd266 X ray Tung bxd24032.266 T(2;3)40;89E III bxd657 EMS Lewis bxd16765.7 In(3R)81;89E I bxdDB1 X ray D. Baker T(2;3)41;89E I bxdDB3 X ray D. Baker T(2;3)48;89E II bxdDB4 X ray D. Baker T(2;3)32;89E ? bxdDB5 X ray D. Baker bxdB231 T(2:3)41;89E ? bxdDB6 X ray D. Baker T(2;3)22A;43A-C; II 60D;84;89E;92F bxdDB7 X ray D. Baker T(Y;3)89E ? bxdDB9 X ray D. Baker Tp(3;3)80;89E ? bxdK spont (?) Kuhn normal (?) gypsy at -2.5 kb; II P-element at -6.5 kb bxdSR spont Rosenberg ? bxdUab1 EMS Lewis bxdG normal I bxdX X ray Lewis bxd22290.11X T(2;3)42B-C; ? 89E1-2 ( Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hogness, 1983, Science 221: 23-29; Bender, Weiffenbach, Karch, and Peifer, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 173-80. | Type is as described by Bender et al., 1985. I Strong bxd (Hemizygotes): Transformation of posterior portion of haltere towards wing, loss of A1 tergite, and appearance of T3 legs on A1. Ventral setal belt of A1 is transformed toward that of T3, and ventral pits appear on abdominal segments A1 to A7, inclusive. II Intermediate bxd (Hemizygotes): Transformation of poste- rior portion of haltere toward wing, replacement of A1 tergite by post-notal tissue as in (I), no extra legs. A1 setal belt is intermediate between A1 and T3 type belts. Ventral pits on all abdominal segments. III Weak bxd (Hemizygotes): Only two bxd effects remain: A1 tergite is slightly reduced in hemizygote but not in homozygote, and ventral pits are formed on A1 to A7, inclusive, in the hemizygote and on A1 in the homozygote. These weak alleles when homozygous survive to adults and appear wild type. and Hogness, 1983, Science 221: 23-29. Casanova, Sanchez-Herrero, and Morata, 1985, J. Embryol. Exp. Morphol. 90: 179-196. White and Akam, 1985, Nature 318: 567-69. phenotype: Cbx1/+ has a strong transformation of the posterior region of the second thoracic segment (T2) toward the corresponding region of the third (T3), and a weak and vari- able transformation of anterior T2 toward anterior T3. The Cbx1 homozygote differs in having a stronger, but still vari- able, transformation of anterior T2 toward T3. Cbx1/Ubx has a slight enhancement of the Ubx phenotype (see also su-Cbx). Cbx2 has both anterior and posterior regions of T2 moderately transformed toward T3. CbxHm affects only the wing, which is strongly transformed to haltere. Flies carrying two doses of CbxHm plus a normal allele have a virtually complete transfor- mation of wing to haltere (as figured in Lewis, 1982). Cbx2 and CbxHm have inseparable recessive bxd effects. Cbx3/+ transforms anterior portions of T2 variably toward anterior T3. It has no effect in posterior T2. For an overview of the effects of Cbx mutants on specific structures see Table 1: Lewis, 1982. molecular allele origin discoverer synonym cytology biology ( ______________________________________________________________________ Cbx1 X ray Bacon normal insert of -3 kb to +14 kb in inverted orientation at -44 kb Cbx2 ? Kreber In(3R)89E;91C-E +8 to +10 kb Cbx3 X ray Akam In(3R)89A;89E -110 to -103 kb CbxTwt X ray Abbot In(3R)87EF;89E -110 to -103 kb CbxHm X ray Slatis Hm T(2;3)breaks? -27.5 kb to -29.5 kb ( Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hogness, 1983, Science 221: 23-29. # Hab: Hyperabdominal (E.B. Lewis) location: 3-58.8 (between iab2 and iab3: to the right of abd- AC53). synonym: Cbxd (Contrabithoraxoid). references: Lewis, Proc. Int. Congr. Genet. 12th, 1968, 2: 96-97. Lewis, 1978, Nature 276: 565-70. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Bender, Weiffenbach, Karch, and Peifer, 1985, Cold Spring Har- bor Symp. Quant. Biol. 50: 173-80. phenotype: Hab/+ has the third thoracic segment (T3) and first abdominal segment (A1) variably transformed toward the second abdominal segment (A2), occasionally resulting in the loss of one or both metathoracic legs and one or both halteres; an A2 type tergite and sternite appear on T3; but A1 is only weakly transformed toward A2. Strongly enhanced when mother is from stock of Df(3R)red-P93, l(3)tr Sb/In(3L)P + In(3R)P18, Me Ubx. alleles: allele origin discoverer _____________________________ Hab1 EMS Bacher, 66k Hab2 EMS Duncan # iab2: infra-abdominal 2 (I. Duncan) location: 3-58.8 (to the right of pbx; to the left of abd-A). references: Lewis, 1978, Nature 276: 565-70. Kuhn, Woods, and Cook, 1981, Mol. Gen. Genet. 181: 82-86. Sanchez-Herrero, Vernos, Marco, and Morata, 1985, Nature 313: 108-13. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Duncan, 1987, Annual Review of Genetics 21: 285-391. phenotype: Adult homozygotes or hemizygotes show transforma- tions of A2 toward A1. The known alleles cause only partial transformations. Wheeler's organs (A2 structures) are reduced or absent and A2 tergite bristles are reduced in size. These alleles do not affect the larval cuticle pattern. alleles: molecular allele origin discoverer synonym cytology biology ____________________________________________________________________ iab2671 X ray Lewis T(Y;2;3)21E;26;86;89E on In(3R)81F;90C-D iab2K Spont Woods normal gypsy insert at 27.5 kb iab2S3 X ray Tiong abd-AS3 In(3R)89E;93F 24-28 kb # iab3: infra-abdominal 3 (E.B. Lewis) location: 3-58.8 (to the right of abd-A; to the left of iab4). references: Lewis, 1978, Nature 276: 565-70. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Lewis, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 155-64. Sanchez-Herrero and Akam, 1989, Development 107: 321-89. phenotype: Hemizygote and homozygote have third, fourth, fifth and sixth abdominal segments (A3, A4, A5, and A6) transformed toward the second abdominal segment (A2). The Wheelers Organ (normally only on A2) is now partially to fully developed on A3 to A6, inclusive. Hemizygotes are viable, and show a loss of gonads in both sexes. In homozygotes A1 is weakly transformed toward A2. alleles: molecular allele origin discoverer synonym cytology biology ( _______________________________________________________________________ iab333 X ray R.H. Baker iab335250.33 In(3LR)74A;89E iab386 X ray Lewis In(3R)62C;89E on In(3R)81F;90C-D iab3277 X ray D. Baker McprevB277, Tp(3;3)89E; 63-64.5 kb iab3B277, 94A;96F; iab3DB 89E on In(3R)81; 92D-E iab3999 X ray Lewis In(3R)68F;89E on In(3R)81E;90C-D iab32576 X ray Lewis T(2;3)51D-E;89E on In(3R)81E;90C-D iab3Uab4 EMS Lewis iab3Uab, In(3LR)80C; 58.5-61.5 kb Uab4 85A;89E ( Coordinates of rearrangement breakpoint (Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96). # iab4: infra-abdominal 4 (E.B. Lewis) location: 3-58.5 (to the right of iab3; to the left of Mcp). references: Karch, Weiffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96. Lewis, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 155- 64. Cumberledge, Zaratzian, and Sakonju, 1990, Proc. Nat. Acad. Sci. USA 87: 3259-63. phenotype: Both the hemizygote and homozygote are viable and have a tranformation of A4 toward A3 as well as a weak transformation of A5 toward A4 or A3. Gonads are absent in both sexes (or partially developed in some alleles). In some of the alleles, A2 transforms weakly to A3, especially in the homozygote. alleles: Eight alleles induced by X rays. molecular allele discoverer synonym cytology biology ( ___________________________________________________________________ iab445 R.H. Baker iab431616.1045, T(2;3)32;41;89E 78.5-82 kb iab411045. complex iab4125 R.H. Baker Mcprev 31125.27 T(3;4)89E;101 81-83 kb iab431125.27 iab4166 Von Der Ahe Mcprev 31166.1 In(3LR)79D-E;89E 76-83 kb iab431166.1 iab4186 Lewis In(3LR)73D-F;89E on In(3R)81F;90C-D iab4302 R.H. Baker iab431616.302 T(2;3;4)60D;81; 83-86.5 kb 89E;100F;101 iab43110 Lewis In(3R)81F;89E on In(3R)81F;90C-D iab4,5849 Lewis In(3LR)76F-G;89E on In(3R)81F;90C-D iab4,5DB D. Baker iab5DB 85-113 kb deleted ( Coordinates of rearrangement breakpoint unless otherwise indicated (Karch, Weiffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96). # iab5: infra-abdominal 5 (I. Duncan) location: 3-58.8 (to the right of iab4; to the left of iab6). references: Lewis, 1978, Nature 276: 565-70. Lewis, 1981, Developmental Biology Using Purified Genes (Brown and Fox, eds.). Academic Press, New York, pp. 189-208. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Lewis, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 155- 64. Duncan, 1987, Annual Review of Genetics 21: 285-319. phenotype: Hemizygotes show strong transformation of A5 toward A4, resulting in a loss of black pigment in the A5 tergite of the male. In addition, A6 may be weakly transformed toward A4. When homozygous, iab5301 causes a weak transformation of A3 toward A4 as well as a transformation of A5 to A4. alleles: Five alleles induced by X rays. molecular allele discoverer synonym cytology biology ( _________________________________________________________________ iab5198 Lewis In(3R)89A;89E on In(3R)81F;90C-D iab5301 R.H. Baker iab531616.301 Tp(2;3)41;86E; 95-104 kb 89E deleted iab5771 Lewis In(3LR)69E-F;89E on In(3R)81F;90C-D iab5843 R.H. Baker iab531616.843 T(2;3)24E-F; 93-99.5 kb 53F;81;89B; 89E iab5,61881 Lewis T(2;3)30D-E;89E on In(3R)81F;90C-D ( Coordinates of rearrangement breakpoint unless otherwise indicated (Karch, Weiffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96). # iab6: infra-abdominal 6 (I. Duncan) location: 3-58.8 (to the right of iab5; to the left of iab7). references: Karch, Weiffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96. Duncan, 1987, Annual Review of Genetics 21: 285-319. phenotype: Hemizygotes show strong transformations of both A5 and A6 toward A4. Males show a loss of pigment on the A5 and A6 tergites and show the development of bristles on the A6 sternite. Some alleles cause weak transformations of A4 toward A5. alleles: iab6C7 induced by ethyl methanesulfonate. The other alleles induced by X rays. molecular allele discoverer synonym cytology biology ( _________________________________________________________________________ iab611 Lewis In(3LR)72;89E 113.2-115 kb on In(3R)81F;90C-D iab675 R.H. Baker iab575 T(2;3)30A-B;89F; 103-108 kb Mcprev31075.26 31D-E;59F;89E iab6105 Lewis iab5105 T(2;3)60C;89E 108-111 kb iab6200 Lewis T(2;3)29E-F;89E 120-121.2 kb on In(3R)81F;90C-D iab61821 Hong T(2;3)30F-31A;89E 116-118 kb on In(3R)81F;90C-D iab6C1 Crosby McprevC1 T(2;3)60B;81; 108-111 kb 89E iab6C7 Crosby iab5c7, Mcprvc7 insertion of DNA from 90E at 124 kb iab6Vno E.H. Grell Vno Tp(3;3)89E;93F; 108-111 kb 97A ( Coordinates of rearrangement breakpoint unless otherwise indicated (Karch, Weiffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96). # iab7: infra-abdominal 7 (I. Duncan) location: 3-58.8 (to the right of iab6; to the left of Abd-B). references: Sanchez-Herrero, Vernos, and Morata, 1985, Nature 313: 106-13. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Sanchez-Herrero, Casanova, Kerridge, and Morata, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 165-72. Duncan, 1987, Annual Review of Genetics 21: 285-319. phenotype: Hemizygotes show strong transformations of A5, A6, and A7 toward A4. In males, the A5 and A6 tergites show a loss of pigmentation and an unpigmented A4-type tergite develops in A7. Both A6 and A7 show the development of ster- nites with bristles. Heterozygotes show a small A7 tergite in the male. Two gain-of-function alleles recorded. iab7Spth (split thorax) heterozygotes display a longitudinal furrow in the mesothorax; iab7SGA heterozygotes causes abdominal struc- tures to develop in the back of the head (Awad, Gausz, Gyurko- vics, and Parducz, 1981, Acta Biol. Acad. Sci. Hung. 32: 219-28; Kuhn and Packert, 1988, Dev. Biol. 125: 8-18). alleles: Seven alleles induced by X rays. molecular allele discoverer synonym cytology biology ( ____________________________________________________________ iab7164 Lewis In(3R)65;89E 126-128 kb on In(3R)81F;90C-D iab7770 Hong In(3LR)68;89;94 on In(3R)81F;90C-D iab73081 Charles In(3R)66;79;89 on In(3R)81F;90C-D iab7MX1 Casanova iab6MX1, T(Y;3)63A; 126-129 kb Abd-BMX1 66B;68A;72E; 89B;92A-D;97D-F; 98F;Y iab7MX2 Casanova iab6MX2, In(3LR)64A; 139.5-142 kb Abd-BMX2 89A;89E iab7SGA Gyurkovics SGA62 In(3R)88C;89E 133-139.5 kb iab7Spth Kemphues iab6Spth In(3R)89A;89E 133-139.5 kb ( Coordinates of rearrangement breakpoint unless otherwise indicated (Karch, Weiffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96). # iab8: infra-abdominal 8 (I. Duncan and S. Celniker) location: 3-54.8 (to the right of Abd-B; to the left of iab-9). references: Karch, Weiffenbach, Peifer, Bender, Duncan, Cel- niker, Crosby, and Lewis, 1985, Cell 43: 81-96. Casanova, Sanchez-Herrero, and Morata, 1986, Cell 47: 627-36. Celniker and Lewis, 1987, Genes. Dev. 1: 111-23. Duncan, 1987, Annual Review of Genetics 21: 285-319. phenotype: Hemizygous adult males show strong transformation of A5, A6, A7 toward A4. In addition, an A8 tergite develops which is half the size of a normal tergite. In these males, A5 and A6 tergites show a loss of pigmentation and an unpig- mented A4-type tergite develops in A7. A6, A7, and A8 all development sternites, the first two with bristles. alleles: molecular allele origin discoverer synonym biology _______________________________________________ iab8380 ENU Lewis iab7308 iab8D6 EMS Duncan iab7D6 iab8D14 EMS Duncan iab7D14 157-157.4 kb detected iab8D15 EMS Duncan iab7D15 # iab9: infra-abdominal 9 (I. Duncan and S. Celniker) location: 3-58.8 (to the right of Abd-B; this is the distal most region of the BXC). references: Gardner and Woolf, 1949, Genetics 34: 573-85. Lewis, 1978, Nature 276: 565-70. Kuhn, Woods, and Cook, 1981, Mol. Gen. Genet. 181: 82-86. Lewis, 1981, Developmental Biology Using Purified Genes (Brown and Fox, eds.). Academic Press, New York, pp. 189-208. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Casanova, Sanchez-Herrero, and Morata, 1986, Cell 47: 627-36. Celniker and Lewis, 1987, Genes. Dev. 1: 111-23. Duncan, 1987, Annual Review of Genetics 21: 285-319. phenotype: Adult homozygotes or hemizygotes show absent or defective genitalia and analia in both sexes. Adults homozy- gous or heterozygous for iab965 show in addition a partial transformation of A6 toward A7. Embryos hemizygous for iab9 mutations show the development of a zone of naked cuticle and a rudimentary ninth abdominal setal belt posterior to the eighth abdominal setal belt. Posterior spiracles are absent in iab965 and iab948 hemizygotes and are defective in iab9Uab1, iab9tuh-3, and iab9Tab hemizygotes. iab965 and iab948, but not the other iab9 mutations, cause transforma- tions of the A8 setal belt (located in anterior A8) toward A7. alleles: molecular allele origin discoverer synonym cytology biology _________________________________________________________________________ iab948 X ray R.H. Baker In(3R)89E; +163-166.5 kb 100C on In(3R)81;92E iab965 X ray R.H. Baker iab765 T(2;3)41;89E +163-166.5 kb iab91392 X ray Hong In(3R)63A;89E 182-187 kb on In(3R)81F;90C-D iab91645 X ray Hong T(2;3)26A;89E 182-187 kb on In(3R)81F;90C-D iab9Tab X ray Lewis Tab In(3R)89E;90D +187-188 kb iab9tuh-3 spont Woolf tuh-3 insert of Delta 88 at +200 kb iab9Uab1 EMS Lewis Uab1 inversion of -14 to +185 kb iab9x23-1 X ray Casanova x23-1 # Mcp: Miscadastral pigmentation (E.B. Lewis) location: 3-58.5 (to the right of iab4; to the left of iab6). origin: Spontaneous. discoverer: Crosby. synonym: Male chauvinist pigmentation. references: Lewis, 1978, Nature 276: 565-70. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Duncan, 1986, Cell 47: 297-309. phenotype: Mcp homozygotes have the fourth (A4) and fifth (A5) abdominal segments transformed to a state intermediate between A5 and A6. Similar, but weaker, tranformations occur in Mcp/+ heterozygotes. Mcp1 can be scored in males by dark pigmenta- tion of the A4 tergite and in females by an effect on the orientation of the lateral bristles of the A4 tergite. alleles: allele origin discoverer cytology molecular biology ( ________________________________________________________________ Mcp1 spont Crosby normal 94-97.6 kb deleted Mcp2 spont Crosby ( Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. # pbx: postbithorax location: 3-58.8 (to the right of bxd; to the left of iab2). references: Lewis, Proc. Int. Congr. Genet. 9th, 1954, 1: 100-05. Lewis, 1955, Am. Nat. 89: 73-89. Lewis, 1981, Developmental Biology Using Purified Genes (Brown and Fox, eds.). Academic Press, New York, pp. 189-208. Lewis, 1982, Embryonic Development: Genes and Cells (Burger, ed.). Alan Liss, Inc., New York, pp. 269-88. Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hog- ness, 1983, Science 221: 23-29. phenotype: Adult homozygotes and hemizygotes have posterior region of third thoracic segment (T3) transformed toward corresponding region of the second (T2). alleles: allele origin discoverer cytology molecular biology ( ___________________________________________________________________ pbx1 X ray Lewis, 1954 normal -3 to +14 kb deleted pbx2 X ray Lewis, 1980? normal 14 to +1 kb deleted ( Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hogness, 1983, Science 221: 23-29. # Sab: Superabdominal (E.B. Lewis) location: 3-58.8 (just to the right of Mcp). synonym: Uab-5Sab. references: Sakonju, Lewis, and Hogness, 1984, Genetics 107: s93. Duncan, 1986, Cell 47: 297-309. phenotype: Sab/+ adults show patchy transformations of A3 and A4 to A5. Homozygote viable and more extreme than heterozy- gote. Mcp1 Sab1 homozygotes show transformations of A3, A4, and A5 to a state intermediate between A5 and A6. alleles: allele origin discoverer synonym cytology ______________________________________________________________ Sab1 ENU Sakonju Uab4, Uab4SS normal Sab2 ENU Lewis Uab4-like, Uab4b normal Uab4-427995, Sabb # Tab: Transabdominal (E.B. Lewis) location: 3-58.8. origin: X ray induced. discoverer: E.B. Lewis. synonym: Net: Neo-ectopic tergite; Eat: Ectopic abdominal tergite; Comma-like. references: Celniker and Lewis, 1984, Genetics 107: s17. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. Celniker and Lewis, 1987, Genes Dev. 1: 111-23. phenotype: Heterozygous adults have a pair of laterally disposed longitudinal stripes of tissue on the second thoracic segment (T2) probably corresponding to tissue from the dorsal sixth (A6) and/or seventh (A7) abdominal segments. These ectopic stripes of tissue are entirely black in males but only partially pigmented in females. Tab/+ flies are virtually sterile, and have a thin seventh tergite in males. Fertility is partially restored in the presence of a duplication for BXC, such as Dp(3;1)P68. When hemizygous, Tab embryos have a reduction of the posterior spiracles and filzkorper, and a tiny ninth abdominal ventral setal belt that appears as a small row of denticles posterior to the A8 setal belt. cytology: Associated with In(3R)Tab = In(3R)89E;90D. molecular biology: The inversion puts the 90D region into the BXC at +188 kb., in the presumed iab9 region (see Karch et al., 1985). # Uab: Ultraabdominal (E.B. Lewis) location: 3-58.8. references: Kiger, 1976, Dev. Biol. 50: 187-200. Davis and Kiger, 1977, Dev. Biol. 58: 114-23. Lewis, 1978, Nature 276: 565-70. Lewis, 1982, Embryonic Development: Genes and Cells (Burger, ed.). Alan Liss, Inc., New York, pp. 269-88. Karch, Weiffenbach, Peifer, Bender, Duncan, Celniker, Crosby, and Lewis, 1985, Cell 43: 81-96. phenotype: Uab1, Uab2, and Uab4 cause A1 to transform toward A2. Uab5 causes A1 and A2 to transform toward A3. Uab1 is an intra-complex inversion with a breakpoint in the bxd region, Uab2 is associated with a Uab mutation, the Uab4 breakpoint is an iab-3 mutation, and the Uab5 breakpoint is a weak bxd muta- tion. Reversion studies show that Uab1, Uab4, and Uab5 cause abnormal expression of abd-A domain functions in A1. alleles: molecular allele origin discoverer synonym cytology biology ____________________________________________________________________ Uab1 EMS Lewis -14 kb; +185 kb inverted Uab2 X ray Lewis Uab4 EMS Lewis iab3Uab4 In(3LR)80C;85A;89E 58.5-61.5 kb Uab5 EMS N. Shaw T(1;3)1F;89E3-4 # Ubx: Ultrabithorax (E.B. Lewis) location: 3-58.8 (to the right of Cbx, to the left of bxd). synonym: bxD, bxdD, bxl. references: Bridges and Brehme, 1944, Carnegie Inst. Washington Publ. 552: 35. Lewis, 1951, Cold Spring Harbor Symp. Quant. Biol. 16: 159- 74. Lewis, 1955, Am. Nat. 89: 73-89. Lewis, 1963, Am. Zool. 3: 33-56. Akam, 1983, EMBO J. 2: 2075-84. Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hog- ness, 1983, Science 221: 23-29. Akam, Moore, and Cox, 1984, Nature 309: 635-37. Hayes, Sato, Denell, 1984, Proc. Nat. Acad. Sci. USA 81: 545-49. Struhl, 1984, Nature 308: 454-57. White and Wilcox, 1984, Cell 39: 163-71. Akam and Martinez-Arias, 1985, EMBO J. 4: 1689-1700. Beachy, Helfand, and Hogness, 1985, Nature 313: 545-51. Hogness, Lipshitz, Beachy, Peattie, Saint, Goldschmidt- Clermont, Harte, Gavis, and Helfand, 1985, Cold Spring Harbor Symp. Quant. Biol. 50: 181-94. Struhl and White, 1985, Cell 43: 507-19. Beachy, Krasnow, Gavis, and Hogness, 1988, Cell 55: 1069-81. O'Connor, Binari, Perkins, and Bender, 1988, EMBO J. 7: 435- 45. Kornfeld, Saint, Beachy, Harte, Peattie, and Hogness, 1989, Genes Dev. 3: 243-58. Mann and Hogness, 1990, Cell 60: 597-610. phenotype: Larvae homozygous and hemizygous for strong Ubx mutants, such as the Ubx1-type, have the ventral setal bands or "hooklets" of the first abdominal segment (A1) and T3 transformed toward those of T2; dorsally, the hair patterns of posterior T2 and posterior T3 are transformed toward posterior T1; Keilin organs with 2 hairs appear on A1; ventral pits appear on segments A1 thru A7; two extra sets of anterior spiracles appear, one on T3 and one on A1. Homozygotes die, usually as tiny third-instar larvae, but occasionally grow to a normal-sized third-instar larvae and may pupate. Homozy- gotes of some weaker alleles, such as Ubx61d, survive to adult stage and show weak bx, bxd, and pbx effects, especially in the haltere, and A1 is generally reduced. alleles: allele origin discoverer synonym cytology type ___________________________________________________________________________________________________________________________________ Ubx1 spont W.F. Hollander, 34 bxD, bxd1D, Bxl normal Ubx1A X ray Ubx19649.1 T(2;3)41;89E Ubx1K X ray Lewis, 64c Ubx15152.1K Ubx1U Ubx18264.1U*** T(2;3)31;89E Ubx1X EMS Smit, 71k Ubx1007.14 unusual Ubx Ubx19061X Ubx2E Ubx23240.2E Ubx2J EMS Lewis, 69g Ubx18498.2J like Ubx11 Ubx2P X ray Ubx19649.2P T(Y;2;3)39;89E1-2;91F Ubx2R EMS Bacher, 66h Ubx16612.2R like Ubx11 Ubx2V EMS Bacher, 66h Ubx16800.2V weak Ubx Ubx2W Ubx18264.2V*** like Ubx11 Ubx4 EMS Tung, 81b Ubx26074.4 Ubx4A EMS Lewis, 73k Ubx19530.4A Ubx4B Ubx3944.4 Ubx6C X ray Lewis, 64c Ubx15152.6C Ubx6Q Ubx21560.6Q In(3R)89E3-4;96F;97A Cbx-like rev. "Ubx" Ubx7L X ray Smit, 72i Ubx19286.7L In(3R)89E1-2;96A Ubx7M X ray Lewis, 64c Ubx15152.7M In(3R) Ubx8 Ubx12110.8 Ubx8A Ubx21560.8A T(1;3)5B;89E1-2 Cbx-like rev. "Ubx" Ubx8B EMS Tung, 81b Ubx26074.8 Ubx8M X ray Smit, 72i Ubx19286.8M Ubx8N X ray Lewis, 64c Ubx15152.8N In(3R) Ubx10 EMS Tung, 81c Ubx26074.10 Ubx10A ENU Chiang, 82f Ubx28510 A1 missing Ubx12 EMS Tung, 81c Ubx26074.12 Ubx12C EMS Shaw, 72a Ubx19191.12C weak Ubx Ubx13 ENU Lewis, 81i Ubx26930.13 very weak Ubx Ubx16N X ray Smit, 72i Ubx19286.16N In(3R)89E;99 Ubx16V X ray Ubx19709.16V normal Ubx18 X ray Ubx19709.18W normal like Ubx11 Ubx19 ENU Chiang, 82b Ubx27510.C9A larvae die over bxd at 2-3instar Ubx21J EMS Lewis, 73k Ubx19530.21J Ubx21R X ray Ubx19649.21R T(Y;3)89E Ubx24 Ubx18624*** Ubx24K EMS Lewis, 73k Ubx19530.24K Ubx27 EMS Lewis, 73k Ubx19530.27L Ubx30 X ray Ubx19709.30G moderate Ubx30A Ubx3966.30 In(3R)89E1-2;91B Ubx31 Ubx16184.31E 86E-F;87A Ubx34 ENU Chiang, 82d Ubx28030.C4A like Ubx11 Ubx40 X ray Ubx19709.40Z normal Like Ubx df over bx34e like weak Ubx over ss bxd Ubx43 X ray Lewis, 73f Ubx19409.43 Df(3R)89D-E1-2 (?) Ubx51 EMS Bacher, 65j Ubx16160.51P vw Ubx56 ENU Chiang, 81j Ubx26956 Ubx58 spont Lewis, 67i Ubx17358U Ubx59 Ubx3858.59 Ubx61d H. Gloor, 61d Ubx65 X ray Smit, 72i Ubx19286.65S Ubx66e EMS Bacher, 66e Ubx16516.115 R(Ubx) Ubx67b X ray Bacher, 67b normal Ubx80 EMS Bacher, 66h Ubx16800.75Z In(3R)87F-88A;89E Ubx88 EMS Bacher, 66h Ubx16800.88B Ubx98 EMS Lewis, 68a Ubx17756.98G very weak Ubx Ubx101 X ray Lewis, 47 In(3LR)80;89E1 Ubx102 EMS Lewis, 68a Ubx17756.102H normal like Ubx11 lethal over TM1 Ubx105 Lewis T(2;3)53C;89E1-2 Ubx106 EMS Lewis, 68a Ubx17756.106 like Ubx11 Ubx109 Lewis Df(3R)89D1-2-89E1-2 Ubx115 Lewis unknown Ubx125 X ray Lewis In(3R)81;89E Ubx130 X ray Lewis, 51l In(3LR)61A-C;74;89E;93B;96A Ubx145 EMS Lewis, 68g Ubx18136.145 weak Ubx Ubx147 EMS Lewis, 68g Ubx18136.147 weak Ubx Ubx149 EMS Lewis, 68g Ubx18136.149 normal like Ubx11; 7-legged over bxd Ubx154 EMS Lewis, 68a Ubx17756.154 like Ubx11 Ubx159 EMS Lewis, 68a Ubx17756.159 like Ubx11 Ubx159A EMS Lewis, 68g Ubx18136.159 like Ubx11 or weaker Ubx175 EMS Lewis, 68a Ubx17756.175 like Ubx1X Ubx180 EMS Lewis, 68a Ubx17756.180 like Ubx11 Ubx195 EMS Lewis, 68a Ubx17756.195 like Ubx11 Ubx196 X ray R.H. Baker, 84a Ubx31616.196 In(3LR)81;89E;90D1 ? x Ubx223 (D.virilis) Ubx311 Ubx549 X ray R.H. Baker, 84d Ubx31616.549 normal 1 Ubx757 X ray R.H. Baker, 84h Ubx31616.757 89E;96-94;96-98;47-60 x Ubx765 X ray R.H. Baker, 84h Ubx31616.765 normal 1 Ubx780 EMS Lewis Ubx849 EMS Lewis normal Ubx895 X ray R.H. Baker, 84k Ubx31616.895 Tp(3;2)2R;89E;90A x Ubx961 In(3R)89E;96 Ubx1069 X ray R.H. Baker, 85a Ubx31616.1069 T(2;3)41A;89E x Ubx1343 X ray R.H. Baker, 85d Ubx31616.1343 T(Y;3)89E x Ubx5754 UbxA X ray Schalet, 59 10+ breaks UbxAD Dowsett UbxAR Robertson Ubx28729Z UbxB1A EMS Bacher, 65i Ubx16160.1A normal UbxB1Q EMS Bacher, 66h Ubx16612.1Q like Ubx61d UbxB3 EMS Bacher, 65i Ubx16160.3B like Ubx11 UbxB5 EMS Bacher, 65i Ubx16160.5C like Ubx11 UbxB6 EMS Bacher, 65i Ubx16160.6D weak UbxB7 EMS Bacher, 65i Ubx16160.7E variable Ubx UbxB11 ENU Chiang, 82b Ubx27510.C1G like Ubx11 UbxB17 EMS Bacher, 65i Ubx16160.17H extreme Ubx UbxB18 EMS Bacher, 65i Ubx16160.18J T(2;3)21D1-2;89E UbxB18W EMS Bacher, 66h Ubx16800.18W UbxB19 EMS Bacher, 66h Ubx16800.19X weak Ubx UbxB22 EMS Bacher, 65i Ubx16160.22 normal like Ubx11 UbxB36 EMS Bacher, 65i Ubx16160.36 T(2;3)41F;89E UbxB41 EMS Bacher, 65j Ubx16160.41N like Ubx161d UbxB49 EMS Bacher, 66h Ubx16800.49Y weak Ubx UbxB54 EMS Bacher, 65j Ubx16160.54 like Ubx11, but weaker UbxB57 EMS Bacher, 66k Ubx16160.57 UbxB58 EMS Bacher, 65k Ubx16160.58V like Ubx161d UbxB61 EMS Bacher, 65k Ubx16160.61W normal UbxB78 EMS Bacher, 66h Ubx16800.78A like Ubx11, but weaker UbxB104 EMS Bacher, 65k Ubx16160.104 like Ubx11 UbxB123 EMS Bacher, 65l Ubx16160.123 weak Ubx UbxB127 EMS Bacher, 65l Ubx16160.27 UbxB160 EMS Bacher, 66b Ubx16412.160L weak Ubx UbxB203 EMS Bacher, 66a Ubx16160.2003 89E1-2;89E3-4 UbxB300 EMS Bacher, 66a Ubx16160.300, Ubx1U In(3LR)61F-62A;89E UbxC1 like Ubx61d UbxC12 ENU Chiang, 82b Ubx27510.C2G weak Ubx UbxC33 ENU Chiang, 82d Ubx27830.C3A weak Ubx UbxC34 ENU Chiang, 82c Ubx27630.C4G like Ubx11 UbxC37 ENU Chiang, 82d Ubx27830.C7G like Ubx161d UbxC38 ENU Chiang, 82c Ubx27630.C8G weak Ubx UbxC43 ENU Chiang, 82c Ubx27740.C3G Haltere winglike UbxC46 ENU Chiang, 82c Ubx27740.C6G Haltere winglike UbxC48 ENU Chiang, 82c Ubx27740.C8G Haltere winglike UbxC51 ENU Chiang, 82c Ubx27695.1 weak Ubx, very weak pbx effect UbxC52 ENU Chiang, 82b Ubx27475.C2A very weak Ubx UbxC63 ENU Chiang, 82c Ubx27560.C3A like Ubx11 UbxC64 ENU Chiang, 82d Ubx28060.C4A A1 missing UbxC65 ENU Chiang, 82d Ubx28060.C5G A1 missing UbxC82 ENU Chiang, 82b Ubx27480.C2G Halteres anteriorly wing-like UbxC90 ENU Chiang, 82d Ubx27990 UbxC91 ENU Chiang, 82a Ubx27290.C1G like Ubx11 UbxC92 ENU Chiang, 82a Ubx27290.C2A like Ubx11 UbxC93 ENU Chiang, 82f Ubx28590.C3G bxd mutant? UbxC95 ENU Chiang, 82a Ubx27290.C5A like Ubx11 UbxC101 ENU Chiang, 82d Ubx27910.C1G bxd mutant? UbxC104 ENU Chiang, 82d Ubx28477D mosaic? Ubx27910.C4G UbxD1 T(2;3)41;89E1-2 UbxE10 X ray Crosby Ubx21368E.10 UbxE12 X ray Crosby Ubx21368E.12 UbxG2 X ray Lewis, 72i Ubx19286, Ubx1Uab-2 normal UbxJ Rasmuson Ubx23823J UbxK X ray Kaufman Cbx+R1 In(3R)89E;92A Ubx12.5 X ray Kerridge & Morata, 1982 In(3R)88B;89E1-2 Ubx8.8 X ray Kerridge & Morata, 1982 normal Ubx5.12 X ray Kerridge & Morata, 1982 normal Ubx5.22 X ray Kerridge & Morata, 1982 In(3R)88F;89E1-2 Ubx9.22 X ray Kerridge & Morata, 1982 normal Ubx5.2326 X ray Kerridge & Morata, 1982 normal Ubx6.26 X ray Kerridge & Morata, 1982 T(2;3)59E;75C;89E1-2 Ubx6.28 X ray Kerridge & Morata, 1982 normal Ubx4.30 X ray Kerridge & Morata, 1982 T(2;3)34;89E1-2 Ubx8.82 EMS Kerridge & Morata, 1982 UbxP18 Lewis In(3R)81F;91F-92 UbxP20 Tp(3;3)68A;68E;89E like UbxX UbxR3 X ray Ramey Cbxprev-R17.3C UbxR5 X ray Ramey Cbxrev-R17.5E In(3R)89E;92A UbxR6 X ray Ramey Cbxrev-R17.6F In(3R)87;89E UbxR10 X ray Ramey Cbxprev-R17.10K T(2;3)41;89D-E UbxR13 X ray Ramey Cbxrev-R17.13N Df(3R)89D1-2;89E1-2 like Ubx1109 UbxR14 X ray Ramey Cbxrev-R17.14P, In(3R)87D-E;89E Ubx21987A UbxR16 X ray Ramey Cbxrev-R17.16R In(3LR)80B;89E UbxR17 X ray Ramey Cbxrev-R17.17S T(2;3)22B1-2;89E1-2 UbxR20 X ray Ramey Cbxrev-R17.20V, In(3R)87B-D;89E Ubx21988B UbxR22 X ray Ramey Cbxrev-R17.22X T(2;3)41;89E UbxR29 X ray Ramey Cbxrev-R17.29E Df(3R)89D;89E UbxR31 X ray Ramey Cbxrev-R17.31G like Ubx161D UbxR32 X ray Ramey Cbxrev-R17.32H Df(3R)89C;89D-E UbxR34 X ray Ramey Cbxrev-R17.34K T(2;3)41;89E dom. Ubx UbxR40 X ray Ramey Cbxrev-R17.40R T(3;4)89E;101 UbxR42 X ray Ramey Cbxrev-R17.42T In(3LR)70D;89E UbxR49 X ray Ramey Cbxrev-R17.49A T(1;3)20F;89E Cbx, bxd1(V) UbxU X ray Bacher Ubx300 In(3LR)62A2-3;89E1-2 UbxR79 X ray Ramey UbxX X ray Lewis In(3R)89E;98B-C UbxX-A T(1;3)20;89E UbxX-type Lewis T(2;3)52A-C;89E # bxd: see BXC # bxdD: see Ubx in BXC #*Bxd: Beadexoid location: 1-45. origin: Spontaneous. discoverer: Goldschmidt. references: 1945, Univ. Calif. (Berkeley) Publ. Zool. 49: 507, 520. phenotype: Like a strong Bx. RK2. # Bxl: see Ubx in BXC # by: blistery location: 3-48.7. origin: Spontaneous. discoverer: Glass, 33a. references: 1934, DIS 2: 8. phenotype: Wings blistered in subterminal region; wing surface dusky and warped. Thorax humpy. RK1. alleles: *by46h (CP627) like by but without thoracic effect. cytology: Placed in 85D11-E3 based on its inclusion in Df(3R)by62 = Df(3R)85D11-14;85F6 and Df(3R)by416 = Df(3R)85D10-12;85E1-3 (Kemphues, Raff, and Kaufman, 1983, Genetics 105: 345-56). # bz: see malbz