: : Molecular map of P (W. R. Engels) TRANSPOSABLE ELEMENTS by: D. J. Finnegan ____________________________________________________________________ At least ten percent of the genome of Drosophila melanogas- ter is made up of transposable elements. These are all moderately repeated sequences. There are about fifty families of such elements and these may be divided into groups accord- ing to their DNA topologies and putative mechanisms of tran- sposition. The largest group contains the copia-like elements, named after one of the first elements of this type to be discovered. They are similar to retroviral proviruses and have long termi- nal direct repeats, LTRs, and a long open reading frame that encodes an amino acid sequence related to viral reverse tran- scriptases. These elements are believed to transpose by a mechanism related to a retroviral life cycle. Eighteen of the elements listed below are of this type (17.6, 297, 1731, 3S18, 412, BEL, blood, copia, flea, gypsy, H.M.S. Beagle, mdg1, mdg2, micropia, NEB, opus, roo, and springer). Six elements, D, F, G, I, Doc, and jockey, are believed to be members of a second class of elements, sometimes called non-viral retroposons, that are also believed to transpose by reverse transcription of an RNA intermediate. They have an A-rich sequence at the 3' end of one strand, but no terminal repeats, and encode putative reverse transcriptases. These elements are variable in length and are often truncated at the 5' end of the strand with the A-rich sequence. P, pogo, hobo, and HB elements have short terminal inverted repeats and are believed to transpose directly from DNA to DNA. The same may be true of FB and BS elements that have long terminal inverted repeats. The information given below relates to specific elements, more general discussions can be found in the review by Finne- gan and Fawcett [1986, Oxford Surveys of Eukaryotic Genes (N. McClean, ed.). Oxford University Press, Oxford, vol. 3, pp. 1-64] or in articles in "Mobile DNA" [1989, (Berg and Howe, eds.). American Society for Microbiology, Washington]. The restriction maps, terminal sequences and lengths of target- site duplications are given to aid in the identification of elements encountered during chromosome walks or in the analysis of molecular lesions associated with particular muta- tions. At least half of all spontaneous mutations in Droso- phila melanogaster are due to insertions of transposable ele- ments. The terminal sequences shown for an element that is variable in length may not be found at the ends of all copies of that element. # 17.6 length: 7.4 kilobases (Saigo et al., 1984). target site duplication: Four base pairs (Kugimya et al.; Inouye et al.). copy number: Forty (Kugimya et al.; 1983). references: Saigo, Millstein, and Thomas, 1981, Cold Spring Harbor Symp. Quant. Biol. 45: 619-28. Kugimya, Ikenaga, and Saigo, 1983, Proc. Nat. Acad. Sci. USA 80: 3193-97. Saigo, Kugimya, Matsuo, Inouye, Yoshioka, and Yuki, 1984, Nature 312: 659-61. Inouye, Yuki, and Saigo, 1986, Nature 310: 332-33. comments: First described by Saigo et al. as a sequence inserted into histone genes and hybridizing to 297 elements. The sequence of the LTR shown here was reported by Kugimya et al.. A complete 17.6 element has been sequenced by Saigo et al. (1984); the map shown here is derived from this sequence. There are no sites for the enzymes AvaI, KpnI, SacI, SmaI, or XbaI. The sequences of the LTRs of 17.6 and 297 elements are similar. Heteroduplexes between 17.6 and 297 elements show a 1.7 kb region of homology between their right-hand ends (Kugi- mya et al.). All insertions studied so far are associated with duplications of the sequence ATAT. left end: AGTGACATAT TCACATACAA AACCACATAA CATAGAGTAA 40 right end: AATAGACTCA AAACTATTTA TTGCAACCAT TTATTTGCAA TT 512 restriction map (17.6): # 297 length: 7 kilobases (Inouye et al.). target site duplication: Four base pairs (Ikenaga and Saigo; Spradling and Rubin). copy number: Approximately 30 (Potter et al.). references: Potter, Brorein, Dunsmuir, and Rubin, 1979, Cell 17: 415-27. Ikenaga and Saigo, 1981, Proc. Nat. Acad. Sci. USA 79: 4143- 47. Spradling and Rubin, 1981, Ann. Rev. Genet. 15: 219-64. Kugimya, Ikenaga, and Saigo, 1983, Proc. Nat. Acad. Sci. USA 80: 3193-97. Inouye, Yuki, and Saigo, 1986a, Eur. J. Biochem. 154: 417-25. Inouye, Saigo, Yamada, and Kuchino, 1986b, Nucl. Acids Res. 14: 3031-43. comments: 297 elements were first described by Potter et al. but were originally identified by Wensink and Rubin as being complementary to abundant polyA RNA in tissue-culture cells. The sequence of an LTR shown below was reported by Ikenaga and Saigo. A complete element has been sequenced by Inouye et al. (1986a) and the restriction map shown here is based on that sequence. There are no sites for enzymes BamHI, PstI, SalI, SmaI or XhoI. Insertions are preferentially at the sequence ATAT (Spradling and Rubin). The sequences of the LTR's of 297 and 17.6 elements are similar, and heteroduplexes between these elements show a region of 1.7 kb of homology at the right-hand ends of each (Kugimya et al.). Inouye et al. (1986b) have identified a serine tRNA as the probable primer for reverse transcription. left end: AGTGACGTAT TTGGGTGGAC CAAACCAGCC ACTTCCATTA 40 right end: TAGTTCAGAC TCATACATAA AACAACAATT TTACT 415 restriction map (297): # 412 length: 7.6 kilobases (Shepherd and Finnegan). target site duplication: Four base pairs (Will et al.). copy number: 40 (Will et al.). references: Rubin, Finnegan, and Hogness, 1976, Progress in Nucl. Acid Research. (Cohen and Volkin, eds.). Academic Press, New York, Vol. 19, pp. 221-26 Finnegan, Rubin, Young, and Hogness, 1978, Cold Spring Harbor Symp. Quant. Biol. 42: 1053-63. Will, Bayev, and Finnegan, 1981, J. Mol. Biol. 153: 897-915. Shepherd and Finnegan, 1984, J. Mol. Biol. 180: 21-40. Chang, Wisely, Huang, and Voelker, 1986, Mol. Cell. Biol. 6: 1520-28. Yuki, Ishimaru, Inouye, and Saigo, 1986a, Nucl. Acids Res. 14: 3017-29. Yuki, Inouye, Ishimaru, and Saigo, 1986b, Eur. J. Biochem. 158: 403-10. Micard, Couderc, Sobrier, Girard, and Dastugue, 1988, Nucl. Acids Res. 16: 455-70. comments: First described as being complementary to abundant poly(A)+ RNA in tissue culture cells (Rubin et al.). The sequence of the LTR shown here was reported by Will et al.; rare 412 elements have 571 base-pair LTRs, the first 482 base pairs of which correspond to the sequence presented (Will et al.). The map shown here is adapted from that published by Shepherd and Finnegan; there are no sites for the enzymes BamHI, SacI, or SalI. The sequence of a complete element has been reported by Yuki et al. (1986 a and b). Fourteen of the 18 bases of the putative primer binding sites of 412 and mdg1 elements are identical, as are 27 bases adjacent to their left-hand LTRs (Will et al.). Yuki et al. (1986b) have sug- gested that an arginine tRNA may serve as the primer for reverse transcription of 412 RNAs. Finnegan et al. and Micard et al. have reported that the majority of 412 transcription is from right to left in tissue culture cells. This would pro- duce antisense RNAs. Prosser and Finnegan have found that both strands of 412 are represented in polyA RNA from adults. Micard et al. have shown that the level of 412 transcription in tissue-culture cells is decreased in the presence of 20- hydroxyecdysone. The phenotypes of some mutations associated with 412 insertions are affected by su(s) mutations (Yuki et al., 1986a). left end: TGTAGTATGT GCCTATGCAA TATTAAGAAC AATTAAATAA 40 right end: TTAAAACGGA CTTGTGTTCT GAATTGGAGT TCATCATTAC A 481 restriction map (412): # 1731 length: 4.6 kilobases (Peronnet et al.). target site duplication: Five base pairs (Peronnet et al.). copy number: Ten (Peronnet et al.). references: Peronnet, Becker, Becker, d'Auriol, and Best- Belpomme, 1986, Nucl. Acids Res. 14: 9017-33. Fourcade-Peronnet, d'Auriol, Becker, Galivert, and Best- Belpomme, 1988, Nucl. Acids Res. 16: 6113-25. comments: The first 1731 element was identified because its transcription in tissue-culture cells is reduced in the pres- ence of 20-hydroxyecdysone (Peronnet et al.). The map, and LTR sequence shown here are taken from Peronnet et al.; the sequence of a complete 1731 element has been reported by Fourcade-Peronnet et al.; the coding capacity of this element is more closely related to that of copia than of longer copia-like elements such as 17.6. Reverse transcription of 1731 RNA may be primed by a fragment of the initiator methionine tRNA (Fourcade-Peronnet et al.). left end: TGTTGAATAT AGGCAATGCC CACATGTGTG TTGAATATAG 40 right end: TGTTCCACAC TTGGAGCACC TTTTCAATAA ACAACA 336 restriction map (1731): # 3S18 length: 6.5 kilobases (Bell et al., 1985). target site duplication: Five base pairs (O'Hare et al.). copy number: Approximately 15 (Bell et al., 1985). references: Fabijanski and Pellegrini, 1982, Nucl. Acids Res. 10: 5979-91. Mattox and Davidson, 1984, Mol. Cell. Biol. 4: 1343-53. O'Hare, Murphy, Levis, and Rubin, 1984, J. Mol. Biol. 180: 437-55. Bell, Bogardus, Schmidt, and Pellegrini, 1985, Nucl. Acids Res. 13: 3861-71. comments: First identified as an insertion within the non- transcribed spacer of an rDNA repeat (Bell et al.; Fabijanski and Pellegrini). Restriction and Southern hybridization data suggest that this element is flanked by direct repeats about 500 base pairs long (Bell et al.). A 3S18 probe hybridized to twelve euchromatic sites and the chromocenter of polytene chromosomes from a cross between gt1 and gtX11 strains. The map shown here as been taken from those published by Bell et al. and Mattox and Davidson. There are no sites for enzymes BglII, SmaI, or XbaI. The sequences at the ends of the 3S18 and BEL elements are the same suggesting that these elements are closely related if not the same (O'Hare, unpublished). The terminal sequences are from the element associated with the wzm mutation (O'Hare et al.). left end: TGTTTATAAA TAAAACCGCC AGTGTTACGT TTAATTTTCAT right end: GTGACTTGTT CGCGTATACA GGGTGTCTCG TTCCCAAACA restriction map (3S18): # B104: see roo # BEL length: 7.3 kilobases. copy number: Twenty five. references: Goldberg, Sheen, Gehring, and Green, 1983, Proc. Nat. Acad. Sci. USA 80: 5017-21. comments: First described as an insertion associated with the wa4 mutation. In situ hybridization experiments indicate that BEL elements are located at about twenty five sites throughout the genome, and that their distribution differs from one strain to another. The ends of this element hybridize to each other. Goldberg et al. have suggested that it is a copia-like elements, although it is not known whether the terminal repeats are direct or inverted. The sequences at the ends of BEL and 3S18 elements are the same, suggesting that these ele- ments are closely related if not the same (O'Hare, unpub- lished). restriction map (BEL): # blood length: 6 kilobases. target site duplication: Four base pairs. copy number: Nine to fifteen. references: Bingham and Chapman, 1986, EMBO J. 5: 3343-51. comments: First identified as an insertion associated with the mutation wbl. The putative primer binding site is similar to those for 412 and mdg1 elements, suggesting that the primer may be an arginine tRNA. left end: TGTAGTATGT GCATATATCG AGGGTACACT GTACCTATAA 40 right end: ACACGTGTTC TCAATTGGTG GCATATATTG GTTTATTACA 400 restriction map (blood): # BS length: 8 kilobases. copy number: Fifteen. references: Campuzano, Balcells, Villares, Carramolino, Garcia-Alonzo, and Modolell, 1986, Cell 44: 303-12. comments: First described as a sequence inserted within the gypsy element associated with the Hw1 mutation. It has inverted terminal repeats of 2.5 kb. These have an outer domain made up of tandem repeats about 130 base pairs long and a nonrepetitious inner domain. The sequence of the internal domain is well conserved in the genome (Livingstone and Finne- gan). restriction map (BS): # Calypso length: 7.2 kilobases (Bender). copy number: Ten to twenty (Bender). comments: First described as an insertion associated with the ry301 mutation. Three other copies have been cloned; they are identical to the ry301 element as judged by heteroduplex analysis, but have some small variations in their restriction maps. restriction map (Calypso): # copia length: 5 kilobases (Emori et al.; Mount and Rubin). target site duplication: Five base pairs (Dunsmuir et al.). copy number: Sixty (Finnegan et al.; Potter et al.). references: Finnegan, Rubin, Young, and Hogness, 1978, Cold Spring Harbor Symp. Quant. Biol. 42: 1053-63. Potter, Brorien, Dunsmuir, and Rubin, 1979, Cell 17: 415-27. Dunsmuir, Brorien, Simon, and Rubin, 1980, Cell 21: 576-79. Levis, Dunsmuir, and Rubin, 1980, Cell 21: 581-88. Shiba and Saigo, 1983, Nature 302: 119-24. Emori, Shiba, Kanaya, Inouye, Yuki, and Saigo, 1985, Nature 315: 773-76. Mount and Rubin, 1985, Mol. Cell. Biol. 5: 1630-38. Kikuchi, Ando, and Shiba, 1986, Nature 323: 824-26. Miller, Rosenbaum, Zbrezna, and Pogo, 1989, Nucl. Acids Res. 17: 2134. Sneddon and Flavell, 1989, Nucl. Acids Res. 17: 4025-35. Yoshioka, Honma, Zushi, Kondo, Togashi, Miyake, and Shiba, 1990, EMBO J. (in press). comments: First described by Finnegan et al. as a sequence com- plementary to abundant polyA+ RNA in tissue culture cells. The map is taken from the sequence of Mount and Rubin, and the sequence of the LTR is from Levis et al. The sequences of complete copia elements have been published by Mount and Rubin and by Emori et al. Virus-like particles containing full length copia RNAs have been found in tissue culture cells by Shiba and Saigo. The major protein in these particles is translated from a 2 kb spliced mRNA (Yoshioka et al.). The sequence of this mRNA has been determined by Miller et al. This protein is released from the primary translation product by autocatalytic cleavage (Yoshioka et al.). Kikuchi et al. have shown that a fragment of the initiator methionine tRNA acts as a primer for reverse transcription of copia RNA in these particles. Sequences essential for copia expression are located on either side of the major transcriptional start sites (Sneddon and Flavell). left end: TGTTGGAATA TACTATTCAA CCTACAAAAG TAACGTTAAA 40 right end: TATTAAGAAA GGAAATATAA ATTATAAATT ACAACA 276 restriction map (copia): # D length: Probably variable. target site duplication: Probably variable. copy number: 30 to 100 (Pittler and Davis). references: Pittler and Davis, 1987, Mol. Gen. Genet. 208: 325-28. comments: Only one D element has been reported. This was found at the 3' end of the dunce locus. It was 380 base pairs long, had an A-rich sequence at the 3' end of one strand, and was flanked by fourteen base-pair target-site duplications. left end: TTATTACACC CCAACAGCCT AGCAAGGAAG CTAGGAACTG 40 right end: TGATCAAATA ATAAAAACAT CATCGTAATC GAAAAAAAAA 380 # Delta88 length: 7 kilobases. references: Karch, Weiffenbach, Peifer, Bender, Duncan, Cel- nicker, Crosby, and Lewis, 1985, Cell 43: 81-96. comments: Only one Delta88 element has been described. This is associated with the iab8,9tuh3 mutation. It is a moderately repeated element. restriction map (Delta88): # Doc length: Variable, up to 5 kilobases (Schneuwly et al.). target site duplication: six to thirteen kilobases (Schneuwly et al.; O'Hare et al.). references: Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hogness, 1983, Science 221: 23-29. O'Hare, Levis, and Rubin, 1983, Proc. Nat. Acad. Sci. USA 80: 6917-21. Schneuwly, Kuroiwa, and Gehring, 1987, EMBO J. 6: 201-06. Driver, Lacey, Cullingford, Mitchelson and O'Hare, 1989, Mol. Gen. Genet. 220: 49-52. comments: First described as an insertion in the BXC region on a chromosome carrying the bx3 mutation, although it is not responsible for the mutant phenotype (Bender et al.). The map shown here is of this element. Schneuwly et al. have found that Doc elements lie at both break points of the Antp73b inversion; these elements lie in inverted orientation, and the inversion probably resulted from recombination between them. The element reported by O'Hare et al. as being associated with the w1 mutation is probably a Doc element. Driver et al. have cloned seven Doc elements and have determined the sequences at their termini; their 5' ends are variable, but their 3' ends are conserved. left end: CATTCGGCAT TCCACAGTCT TCGGGTGGAG ACGTGTTTCT right end: ATTCAATAAA TAATAAAAAT TAAAAAAAAA AAAAAAAAAA restriction map (Doc): # F length: Variable up to that of consensus element of 4.8 kb (Di Nocera et al.). target site duplication: 8-22 base pairs (Di Nocera et al.). copy number: Fifty (Di Nocera et al.). references: Dawid, Olong, Di Nocera, and Pardue, 1981, Cell 25: 399-408. Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hog- ness, 1983, Science 221: 23-29. Di Nocera, Digan, and Dawid, 1983, J. Mol. Biol. 168: 715-27. Di Nocera and Casari, 1987, Proc. Nat. Acad. Sci. USA 84: 5843-47. comments: First described by Dawid et al. as an element within a copy of the type I 28S rDNA insertion sequence. The termini shown here are of 101F, the longest F element to have been cloned (Di Nocera et al.). The map is the consensus for F elements (Di Nocera et al.). There are no sites for the enzymes ClaI, PvuI, or XhoI. The complete base sequence of a 3.5 kilobase element, Fw, has been reported by Di Nocera and Casari. The element Jiminy, which was identified within the BXC by Bender et al., is probably an F element. left end: ATGAAGCATT TCGATCGCCG ACGTGTGAAG ACGTTTTTAT 40 right end: ATTCAATAAA TAAAAGTAAA GTAAAAAAAA AAAAAAAAAA G 811 restriction map (F): # FB length: Variable (Truett et al.). target site duplication: Nine base pairs (Truett et al.). copy number: Thirty (Truett et al.). references: Ising and Ramel, 1976, The Genetics and Biology of Drosophila (M. Ashburner and E. Novitski, eds.). Academic Press, London, Vol. 1b, pp. 947-54. Potter, Truett, Phillips, and Maher, 1980, Cell 20: 639-47. Truett, Jones, and Potter, 1981, Cell 24: 753-63. Levis and Rubin, 1982, Cell 30: 543-50. Potter, 1982, Nature 297: 201-204. Paro, Golberg, and Gehring, 1983, EMBO J. 2: 853-60. Smyth, Templeton and Potter, 1989, EMBO J. 8: 1887-91. comments: First described as elements containing inverted repeat sequences (Potter et al., 1980). The inverted repeats at the ends of FB elements vary in length; they are made up of different numbers of tandemly repeated sequences, with a max- imum repeat length of 155 base pairs (Truett et al.; Potter et al., 1982). The DNA between the inverted repeats also varies. The element FB4 has been sequenced entirely (Potter et al., 1982). Its restriction map and terminal sequences are shown. The only HinfI and TaqI sites marked, are those that lie in the inverted repeats. There are no sites for the enzymes AvaI, BamHI, EcoRI, HpaI, PstI, SacI, SalI, SmaI, or XhoI. Potter et al. (1982) have suggested that another transposable element, HB1, lies between coordinates 1.1 and 2.75 of FB4. The sequence of the central region of an FB element related to FB-wc, the element responsible for the wc mutation, has been determined (Smyth, Templeton and Potter). It contains two long open reading frames in one strand, and these authors sug- gest that they may encode functions required for transposition of FB elements. They have evidence that the product of the first open reading frame is a 71 kd polypeptide present in early embryos and egg chambers. FB elements have been found at the ends of the TE elements (Ising and Ramel; Paro et al.). The smallest known element of this type is associated with the mutation wDZL (Levis and Rubin). left end: AGCTCAAAGA AGCTGGGGTC GGAAAAATCG AATTTTTGAA 40 right end: TCAAAAATTC GATTTTTCCG ACCCCAGCTT CTTTGAGCT 4089 restriction map (FB): # flea length: 5.6 kilobases (Kidd and Young). target site duplication: Six base pairs (Kidd and Young). references: Kidd, Lockett. and Young, 1983, Cell 34: 421-33. Kidd and Young, 1986, Nature 323: 89-91. comments: First described associated with four different fa mutations. The map shown here is the reverse of that published by Kidd and Young. There are no sites for the enzyme BglII. These are copia-like elements and Kidd and Young have reported sequences from the ends of the LTRs. The elements in the N locus have inserted in target sites within the consensus ATG/GTAT. left end: GTAACATGGA GTAAGGC... .......... .......... 40 right end: .......... .......... ...GCCTTAC TCCATGTTAC restriction map (flea): # G length: Variable, up to four kilobases (Di Nocera and Dawid). target site duplication: Nine base pairs (Di Nocera and Dawid; Di Nocera). copy number: Ten to twenty (Di Nocera et al.). references: Dawid, Olong, Di Nocera, and Pardue, 1981, Cell 25: 399-408. Di Nocera and Dawid, 1983, Nucl. Acids Res. 11: 5475-82. Di Nocera, Graziani, and Lavorgna, 1986, Nucl. Acids Res. 14: 675-91. Di Nocera, 1988, Nucl. Acids Res. 16: 4041-52. comments: First described by Di Nocera and Dawid as a sequence inserted within an F element. G elements have been found in tandem arrays in the non-transcribed spacer sequences of rDNA units. Their chromosomal distribution is fairly stable, as assayed by Southern transfer experiments, and they are concen- trated in chromocentric regions (Di Nocera et al.). No poly(A)+ RNA complementary to G elements has been found in embryos, larvae, pupae, or adults (Dawid et al.). The com- plete base sequence of a 4.3 kb G element, G3A has been reported by Di Nocera (1988). Its termini are shown here. The map is of the element G1 (Di Nocera and Dawid). There are no sites for the enzyme SmaI. left end: ACAGTCGCGA TCGAACACTC AACGAGTGCA GACGTGCCTA 40 right end: TTAATACATA GATCGCTAAA AAAAAAAAAA AAAAAA 4346 restriction map (G): # gypsy length: 7.3 kilobases (Yuki et al.; Marlor et al.). target site duplication: Four base pairs (Kulguskin et al.). copy number: Ten (Bayev et al.; Freund and Meselson). synonym: mdg4. references: Ilyin, Chmeliauskaite, and Georgiev, 1980, Nucl. Acids Res. 8: 3439-57. Tchurikov, Ilyin, Skyrabin, Ananiev, Krayev, Zelentsova, Kulguskin, Lyubomirskaya, and Georgiev, 1981, Cold Spring Harbor Symp. Quant. Biol. 45: 655-65. Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hog- ness, 1983, Science 221: 23-29. Modolell, Bender, and Meselson, 1983, Proc. Nat. Acad. Sci. USA 80: 1678-82. Bayev, Lyubomirskaya, Dzhumagliev, Ananiev, Amiantova, and Ilyin, 1984, Nucl. Acids Res. 12: 3707-23. Freund and Meselson, 1984, Proc. Nat. Acad. Sci. USA 81: 4462-64. Mattox and Davidson, 1984, Mol. Cell. Biol. 4: 1343-53. Marlor, Parkhurst, and Corces, 1986, Mol. Cell. Biol. 6: 1129-34. Yuki, Inouye, Ishimaru, and Saigo, 1986, Eur. J. Biochem. 158: 403-10. Geyer, Green, and Corces, 1988, Proc. Nat. Acad. Sci. USA 85: 8593-97. Peifer and Bender, 1988, Proc. Nat. Acad. Sci. USA 85: 9650- 54. Spana, Harrison, and Corces, 1988, Genes Dev. 2: 1414-23. Mazo, Mizrokhi, Karavanov, Sedkov, Krichevskaja, and Ilyn, 1989, EMBO J. 8: 903-11. comments: First described by Ilyin et al. (1980) as mdg4, a sequence complementary to double stranded RNA from tissue cul- ture cells, and by Bender et al. (1983) as an insertion asso- ciated with mutations bx3, bx34e, bx55i, and bx51j. Modolell et al. have shown by in situ hybridization that gypsy inser- tions are associated with many mutations suppressed by su(Hw). The su(Hw) product binds to an enhancer-like sequence within gypsy, and this may affect the expression of adjacent genes as well as of gypsy itself. This is alleviated by su(Hw) muta- tions (Geyer et al.; Peifer et al.; Spana et al.; Mazo et al.). The phenotypes of some mutations caused by gypsy inser- tions are affected by su(f) mutations. The LTR sequence shown here was reported by Bayev et al.. Freund and Meselson have reported an equivalent sequence of 482 base pairs. The sequences of complete elements have been reported by Yuki et al. and Marlor et al.. The map shown here is based on those of Bayev et al. and Mattox and Davidson. There are no sites for the enzymes BamHI or SalI. left end: AGTTAACAAC TAACAATGTA TTGCTTCGTA GCAACTAAGT 40 right end: AAATAACATA ACTCTGGACC TATTGGAACT TATATAATT 479 restriction map (gypsy): # Harvey length: 7.2 kb (Bender). comments: First described as an insertion associated with the bx8 mutation. The results of whole genome Southern transfer experiments indicate that this element is repeated within the genome, and that the internal SalI fragment is conserved in length. The ends of the element hybridize to each other. restriction map (Harvey): # HB length: 1.6 kilobases (Potter, Brierly, and Potter). target site duplication: Possibly 8 bp (Potter, Brierly, and Potter). copy number: Twenty (Brierly and Potter). references: Potter, 1982, Nature 297: 201-4. Brierly and Potter, 1985, Nucl. Acids Res. 13: 485-501. Harris, Bailie, and Rose, 1988, Nucl. Acids Res. 16: 5991-98. Henikoff and Plasterk, 1988, Nucl. Acids Res. 16: 6234. comments: The first HB element was found as the loop sequence within the FB element FB4 (Potter). Brierly and Potter have shown that HB sequences are rarely associated with FB sequences and have suggested that they constitute a separate transposable element. The chromosomal distribution of these elements is fairly stable as assayed by Southern transfer experiments. There are 29 bp inverted repeats at the ends of the two elements that have been sequenced, but part of these may comprise target site duplications (Brierly and Potter). If there is an 8 bp target site duplication then the length of the terminal repeat is 20 bp. The sequence of HB1 contains an open reading frame of 444 bp (Potter). There is about 25% sequence identity between the amino acid sequences encoded by HB1 and the Tcl transposable element of Caenorhabditis elegans (Harris et al.; Henikoff and Plasterk). This map is taken from the sequence of HB1. There are no sites for the enzymes BamHI, EcoRI, SacI, SalI and XhoI. left end: TACAGCTGTG TTCAGAAAAA TAGCAGTGCG AAGGAAACTA right end: TGAAGTCCAA AGCACTGCTA TTATTCTGAA CACAGCTGTA restriction map (HB): # H.M.S. Beagle length: 7.3 kb. target site duplication: Four base pairs. copy number: 50. references: Snyder, Kimbrell, Hunkapiller, Hill, Fristrom, and Davidson, 1982, Proc. Nat. Acad. Sci. USA 79: 7430-34. comments: First described as an insertion within the promoter region of the cuticle protein gene, Lcp3n1. The sequence shown here is the reverse complement of that published by Snyder et al.. There are no sites for the enzymes AvaI, BamHI, HindIII, or KpnI. left end: AGTTATTGCC CTGCAATTGA TTCTCTAACA TCTTGTGGTT 40 right end: TCTTCAAAAT CAAATCGATA ACTGTAATTA TTAACT 266 restriction map (H.M.S. Beagle): # hobo length: Variable, up to 3 kb (Streck et al.). target site duplication: Eight base pairs (McGinnis et al.; Streck et al.). copy number: 0-50 (McGinnis et al.; Streck et al.). references: McGinnis, Shermoen, and Beckendorf, 1983, Nucl. Acids Res. 11: 737-51. Streck, MacGaffrey, and Beckendorf, 1986, EMBO J. 5: 3615-25. Yannopoulos, Stamatis, Monastirioti, Haizopoulos, and Louis, 1987, Cell 49: 487-95. Blackman, Grimaila, Koehler, and Gelbart, 1987, Cell 49: 497-505. Lim, 1988, Proc. Nat. Acad. Sci. USA 85: 9153-57. Blackman, Macy, Koehler, Grimaila, and Gelbart, 1989, EMBO J. 8: 211-17. comments: First described by McGinnis et al. as being associ- ated with the Sgs4 allele in the strain Stromsvreten 8. The sequence and map shown are of hobo100 (Streck et al.). This element contains a single long open reading frame that reads from left to right. Blackman et al. have identified a fully functional hobo element and have used it to introduce a marked element into the genome. Some strains appear to lack hobo elements, whereas others have 10-50 copies. These are called "E" and "H" strains, respectively (Streck et al.). The fre- quency of hobo activity is elevated in some strains and in some cases is increased in the progeny of crosses between E and H strains (Yannopoulos et al.; Blackman et al.). Lim has evidence that recurring chromosome aberrations that he has found on an unstable X chromosome are due to recombination between hobo elements that lie at the breakpoints. The major- ity of strains derived from natural populations before the mid 1950's harbor few hobo homologous sequences. In contrast almost all present-day populations carry numerous hobo ele- ments and two specific deletion-derivative elements called Th1 and Th2 (Periquet, Hamelin, Bigot, and Lepissier, 1989, J. Evol. Biol. 2: 223-29). left end: CAGAGAACTG CAGCCCGCCA CTCGCACTCT ACGTCCACCC 40 right end: TGTGAGTCGA GTGGTAAAAA AGTGCCACCC TTGCAGTTCT CTG 1273 restriction map (hobo): # I length: Variable, up to 5.4 kb. target site duplication: Variable but usually about twelve base pairs (Fawcett et al.). copy number: 0-10 complete I elements plus about 30 incomplete elements (Bucheton et al.). references: Bucheton, Paro, Sang, Pelisson, and Finnegan, 1984, Cell 38: 153-63. Sang, Pelisson, Bucheton, and Finnegan, 1984, EMBO J. 3: 3079-85. Fawcett, Lister, Kellett, and Finnegan, 1986, Cell 47: 1007- 15. Crozatier, Vaury, Busseau, Pelisson, and Bucheton, 1988, Nucl. Acids Res. 16: 1999-2013. Busseau, Pelisson, and Bucheton, 1989a, Nucl. Acids Res. 17: 6939-45. Busseau, Pelisson, and Bucheton, 1989b, Mol. Gen. Genet. 218: 222-28. comments: First described by Bucheton et al. as insertions associated with w gene mutations induced by I-R hybrid dys- genesis. The base sequence of a complete I element has been determined by Fawcett et al., and the restriction map shown here is based on this sequence. There are no sites for the enzymes BamHI, EcoRI, SacI, SalI, SmaI, or XhoI. Incomplete I elements that have recently inserted in the genome have deleted varying amounts from the 5' end of the sequence of a complete element (Busseau et al., 1989a). Incomplete elements that have been in the genome for a long time are located in pericentromeric regions, and differ from complete elements by many base substitutions and internal or terminal deletions or both (Crozatier et al.). Mutations induced by I-R hybrid dys- genesis include apparent point mutations due to insertion of I elements and chromosome rearrangements due to recombination between I elements (Sang et al.; Busseau et al., 1989b). left end: CATTACCACT TCAACCTCCG AAGAGATAAG TCGTGCCTCT 40 right end: TAGTTTTGTA AACTATTCTA TCTATCATAA TAATAATAAT AA 5372 restriction map (I): # Isadora length: 8.3 kilobases. copy number: 8. references: Tsubota, Rosenberg, Szostak, Rubin, and Schedl, 1989, Genetics 122: 881-90. comments: Only one Isadora element has been studied. It was identified as an insertion at the Bar locus of a chromosome carrying the partial revertant of Bar, B3, and may be respon- sible for the altered phenotype. It is present at 8 sites on the arms of Oregon R chromosomes but not at the chromocenter. There are no sites for the enzymes BamHI, HindIII, SalI and XhoI. restriction map (Isadora): # jockey length: Variable, up to five kilobases (Priimagi et al.). target site duplication: Nine or ten base pairs (Priimagi et al.). copy number: Fifty (Ilyin). references: Mizrokhi, Obolenkova, Priimagi, Ilyin, Gerasimova, and Georgiev, 1985, EMBO J. 4: 3781-87. Mizrokhi, Georgieva, and Ilyin, 1988, Cell 54: 685-91. Priimagi, Mizrokhi, and Ilyin, 1988, Gene 70: 253-62. comments: First described by Mizrokhi et al., (1985) as an insertion within the gypsy element associated with the ctMR2pN10 mutation. The complete base sequence of a five kilobase element, j1, has been reported by Priimagi et al. The restriction map of this element and the sequences of its ends are shown here. The genome contains several jockey ele- ments that are deleted internally (Priimagi et al.; Ilyin). jockey elements are transcribed in tissue culture cells using an internal polII promoter (Mizrokhi et al., 1988). The ele- ments sancho1, sancho2, and wallaby appear to be deleted jockey elements (Mizrokhi et al., 1988; Corces). left end: AAAAATCATT CACATGGGAG ATGAGCAATC GAGTGGACGT 40 right end: GCGTTGATCA AATAATAAAA ACATCATAAA AAAAAAAAAA 5020 restriction map (jockey): # Kermit length: 4.8 kilobases. copy number: Thirty. references: Bender, Akam, Karch, Beachy, Peifer, Spierer, Lewis, and Hogness, 1983, Science 221: 23-29. comments: Only one copy of this element has been described; it was found within the 87E1-6 region in Canton S but not Oregon R DNA. It has been mapped by Bender. There are no sites for the enzymes BamHI, HindIII, or SalI, and there may be addi- tional sites for EcoRI at the ends of the element. restriction map (Kermit): # mdg1 length: 7.3 kilobases (Ilyin et al.). target site duplication: Four base pairs (Kulguskin et al.). copy number: 25 (Ilyin et al.). references: Georgiev, Ilyin, Ryskov, Tchurikov, and Yenikolo- pov, 1977, Science 195: 394-97. Georgiev, 1978, Cold Spring Harbor Symp. Quant. Biol. 42: 959-69. Ilyin, Chmeliauskaite, and Georgiev, 1980, Nucl. Acids. Res. 8: 3439-57. Ilyin, Chmeliauskaite, Kulguskin, and Georgiev, 1980, Nucl. Acids Res. 8: 5347-61. Kulguskin, Ilyin, and Georgiev, 1981, Nucl. Acids Res. 9: 3451-63. Will, Bayev, and Finnegan, 1981, J. Mol. Biol. 153: 897-915. Yuki, Inouye, Ishimaru, and Saigo, 1986, Eur. J. Biochem. 158: 403-10. comments: First described by Ilyin et al. (1978) and Georgiev et al. (1978) as being complementary to abundant poly(A)+ RNA. The sequence of the LTR shown here is the reverse com- plement of that published by Kulguskin et al., and the map is the reverse of that published by Ilyin et al. (1978). The direction of major transcription is left to right (Ilyin et al.). Fourteen of the eighteen bases of the putative primer binding sites of mdg1 and 412 elements are identical, as are the 27 bases adjacent to their left-hand LTRs (Will et al.). Yuki et al. have identified an arginine tRNA as being the probable primer for reverse transcription of both mdg1 and 412 RNAs. left end: TGTAGTTAAT TTGAATTCTA ATACTTCTGA TGTAGTTAAT 40 right end: ATTATTGTTA TTATTATTGT TATTATATTC GTATATACTA CA 442 restriction map (mdg1): # mdg3 length: 5.4 kilobases (Ilyin et al., 1980a). target site duplication: Four base pairs (Bayev; Mossie et al.). copy number: 15 (Ilyin et al., 1980a). references: Bayev, Krayev, Lyubomirskaya, Ilyin, Skryabin, and Georgiev, 1980, Nucl. Acids Res. 8: 3263-3273 Ilyin, Chmeliauskaite, Ananiev, and Georgiev, 1980a, Chromo- soma 81: 27-53. Ilyin, Chmeliauskaite, Kulguskin, and Georgiev, 1980b, Nucl. Acids Res. 8: 5347-61. Mossie, Young, and Varmus, 1985, J. Mol. Biol. 182: 31-43. comments: First described by Ilyin et al. (1980a and b) as being complementary to double-stranded RNA from tissue culture cells. The sequence of the LTR shown here is the reverse com- plement of that published by Bayev et al. (1980); this was originally thought to be 268 base pairs but was subsequently found to be 267 base pairs (Bayev; Mossie et al.). The reported direction of major transcription is right to left (Ilyin, 1980a); the map shown is taken from Ilyin (1980a); there are no sites for the enzyme BamHI. left end: TGTAGTAGGC TGCTCCTTCT ACCCTCTTCC TTTACTCTTA 40 right end: TGTATTAGAA TATTAACTTC TGTAAACGGC GGCTAAA 267 restriction map (mdg3): # mdg4: see gypsy # micropia length: 5.5 kilobases. target site duplication: Four base pairs. references: Lankenau, Huijser, Jensen, Miedma, and Hennig, 1989, J. Mol. Biol. 204: 233-46. comments: First identified because it hybridizes with a copia- like element found on the Y chromosome of Drosophila hydei. Only one element from D. melanogaster has been studied in detail. The complete sequence of this element has been reported by Lankenau et al.; the map is taken from this sequence. left end: TGTCGTGGCG AAAATAATGA GTATGCGTGT AGTCGCTGTT 40 right end: GACGGACGCG AGGCCCCTGA TATTCTTAAC CCGACA 476 restriction map (micropia): # NEB length: 5.5 kilobases. references: Paro, Goldberg, and Gehring, 1983, EMBO J. 2: 853-60.. comments: Only one copy of the NEB element has been described. It was found on the large transposable element TE987A near the end carrying the rst gene. The ends of this element cross hybridize. No inverted repeats could be detected by electron microscopy, suggesting that NEB is a copia-like element. NEB elements occur at multiple dispersed sites in the genome and are located at different positions in different strains. An incomplete element has been found near one end of TE77. There are no sites for the enzymes BamHI or XhpI. restriction map (NEB): # Nijinski length: 7.6 kilobases. copy number: More than 20. references: Tsubota, Rosenberg, Szostak, Rubin, and Schedl, 1989, Genetics 122: 881-90. comments: Only one Nijinsky element has been studied. It was identified as an insertion at the Bar locus of the Basc chro- mosome. It is present at about 20 sites on the arms of Oregon R chromosomes and at the chromocenter. There are no sites for the enzymes BamHI and XhoI. restriction map (Nijinski): # opus length: 8 kilobases. target site duplication: Probably six kb. references: Kidd and Young, 1986, Nature 323: 89-91. comments: First identified as insertion associated with the mutation fa. This is a copia-like element. The map and sequences from the ends of the LTRs were reported by Kidd and Young. The only element studied so far was flanked by the sequence TATATA. This is probably the target site duplica- tion, although it could be part of the inverted repeats at the ends of the LTRs. left end: AGTTCCACTT GCATCAGGGT TCTCG..... .......... 40 right end: .......... .......... .AAGAAGAGG GTTCTTAACT restriction map (opus): # P (W.R. Engels) length: 2907 base pairs or fewer (O'Hare and Rubin). Longer elements can be produced in vitro. structure: Perfect terminal repeats of 31 base pairs plus several internal repeat structures. Defective P-elements are derived from the complete 2907 base pair sequence by internal deletions of various sizes and positions (O'Hare and Rubin). Approximately 150 base pairs at each terminus are usually intact, and are thought to be needed for mobility (Mullins et al.). target site duplication: Eight base pairs (O'Hare and Rubin). copy number and distribution: (Bingham et al.; Kidwell; Anxola- behere et al.) The older laboratory strains, dating from 1950 or earlier, have no P homologous sequences, and they are called "M strains." Most natural populations in North and South America and Africa are "P strains", i.e., they have mul- tiple copies of both complete and defective P-elements in scattered and highly variable genomic positions. The total copy number is usually 30-50. Most European and Asian popula- tions are "M' strains," meaning that they have mostly defec- tive P-elements and a different kind of regulation. The total copy number tends to be less than P strains. Australia has both P and M' strains. references: Kidwell, Kidwell, and Sved, 1977, Genetics 86: 813-33. Bingham, Kidwell, and Rubin, 1982, Cell 29: 995-1004. Rubin and Spradling, 1982, Science 218: 348-53. Rubin, Kidwell, and Bingham, 1982, Cell 29: 987-94. Kidwell, 1983, Proc. Nat. Acad. Sci. USA 80: 1655-59. O'Hare and Rubin, 1983, Cell 34: 25-35. O'Hare, Levis, and Rubin, 1983, Proc. Nat. Acad. Sci. USA 80: 6917-21. Engels and Preston, 1984, Genetics 107: 657-78. Karess and Rubin, 1984, Cell 38: 135-46. Laski, Rio, and Rubin, 1986, Cell 44: 7-19. Rio, Laski, and Rubin, 1986, Cell 44: 21-32. Engels, Benz, Preston, Graham, Phillis, and Robertson, 1987, Genetics 117: 745-57. O'Kane and Gehring, 1987, Proc. Nat. Acad. Sci. USA 84: 9123-27. Simmons, Raymond, Boedigheimer, and Zunt, 1987, Genetics 117: 671-85. Anxolabehere, Kidwell, and Periquet, 1988, Mol. Biol. Evol. 5: 252-69. Cooley, Kelley, and Spradling, 1988, Science 239: 1121-28. Robertson, Preston, Phillis, Johnson-Schlitz, Benz, and Engels, 1988, Genetics 118: 461-70. Roiha, Rubin, and O'Hare, 1988, Genetics 119: 75-83. Engels, 1989, Mobile DNA (Berg and Howe, eds.). American Society for Microbiology, Washington, pp. 437-84. Mullins, Rio, and Rubin, 1989, Genes Dev. 3: 729-38. Sved, Eggleston, and Engels, 1989, Genetics (in press). transposase: Exons 0-3 (see map) encode an 87 kilodalton pro- tein needed for both transposition and excision. The 2-3 splice is germline-specific, but this intron can be artifi- cially removed to yield transposase in somatic cells (Karess and Rubin; Rio et al.; Laski et al.). insertion sites: P-elements insert at random, but their distri- bution is not uniform. There is a strong preference for euchromatin and the 5' untranslated regions of genes. They also tend to insert adjacent to other P-elements and have a slight preference for target sequences resembling GGCCAGAC. Precise insertional hotspots have been seen in several genes, suggesting that there are additional specificities not yet characterized (O'Hare and Rubin; Engels). regulation: (Engels) P strains and M' strains have relatively little transposition and excision activity, and several regu- latory mechanisms are thought to be involved. One of these, called the P "cytotype," is found only in P strains and has a partial maternal inheritance resulting in relative stability in P-elements in the progeny of P strain females crossed to M strain males. However, the elements are active in progeny from the reciprocal cross. Certain defective P-elements have been shown to encode a negative regulator of P-element activity. hybrid dysgenesis: Mobilization of P-elements results in a syn- drome of abnormal traits called hybrid dysgenesis (Kidwell et al.; Engels). This syndrome includes high frequencies of chromosome rearrangements and male recombination, both of which occur preferentially at the insertion sites of P- elements (Engels and Preston; Sved et al.). Elevated mutation rates result from insertion mutations and other genomic changes. At high temperatures there is considerable cell death either in the germline or in somatic tissues depending on the transposase source (Simmons et al.; Engels et al.). use as transformation vectors: When P-elements are injected into M strain embryos in the presence of transposase, they will jump from the injected DNA into chromosomal locations, carrying along any sequence that has been inserted into the internal portion of the element (Rubin and Spradling). Genes transformed in this way usually display approximately normal expression and regulation. However, there is usually some position effect, the degree of which depends on the particular transformed sequence. The transposase source can be a gene coinjected with the P vector such as the "wings clipped" ele- ment (Karess and Rubin) or a stable genomic source such as P[ry+__2-3](99B) (Robertson et al.). use in mutagenesis: Selecting P-element insertion mutations is useful for cloning genes through "transposon tagging" and for generating variability. The most effective approach is to mobilize defective elements with an immobile transposase source (Robertson et al.). The mobilized elements can be either naturally occurring defective P-elements or marked ele- ments introduced by transformation (Cooley et al.). use as `enhancer traps': (O'Kane and Gehring) Genes with specific expression patterns can be identified by mobilization of a P-element carrying the |-galactosidase gene fused to the transposase promoter. The spatial and developmental pattern of |-galactosidase expression appears to depend on the sur- rounding sequences. left end: CATGATGAAA TAACATAAGG TGGTCCCGTC GAAAGCCGAA 40 right end: TCTTGCCGAC GGGACCACCT TATGTTATTT CATCATG 2907 restriction map (P): # pogo length: Variable, up to at least 2.2 kb (O'Hare). target site duplication: 0 or 2 base pairs (O'Hare). references: O'Hare (unpublished). comments: First copy to be analyzed was a 190 base pair element within the w1 insertion on chromosomes carrying the white- eosin mutation. Other copies have been cloned, the longest of which is 1.1 kb. Southern transfer experiments suggest that the genome contains elements of 2.2 kb. Each element has either a 23 base pair terminal inverted repeat and no target site duplication or a 21 base pair inverted repeat flanked by duplication of the sequence TA. The map and terminal sequences are from O'Hare. left end: TACAGTATAA TTCGCTTAGC TGCCTCGAGT ACTTTGCACA 40 right end: TGCAGCTAAC TATCGATGCA GCTAAGCGAA TTATACTGTA restriction map (pogo): # roo length: 8.7 kilobases (Scherer et al., 1982). target sites duplication: Five base pairs (Scherer et al., 1982). copy: Eighty (Scherer et al., 1982). synonym: B104. references: Scherer, Telford, Baldari, and Pirrotta, 1981, Dev. Biol. 86: 438-47. Meyerowitz and Hogness, 1982, Cell 28: 165-76. Scherer, Tschudi, Perera, Delius, and Pirrotta, 1982, J. Mol. Biol. 157: 435-52. Swaroop, Paco-Larsen, and Garen, 1985, Proc. Nat. Acad. Sci. USA 82: 1751-55. comments: Described as B104 by Scherer et al. (1981; 1982) and as roo by Meyerowitz and Hogness. B104 elements were found because they are complementary to abundant poly(A)+ RNA in embryos (Scherer et al., 1981), whereas a roo element was found inserted near the Sgs3 gene (Meyerowitz and Hogness). The LTR sequence shown here was reported by Scherer et al. (1982), and the map is adapted from those of Scherer et al. (1982) and Swaroop et al.. left end: TGTTCACACA TGAACACGAA TATATTTAAA GACTTACAAT 40 right end: AAACTCAACG AGTAAAGTCT TCTTATTTGG GATTTTACA 429 restriction map (roo): # sancho1 length: 4.5 kb (Campuzano et al.). copy number: Fifty (Campuzano et al.). references: Campuzano, Balcells, Villares, Carramolino, Garcia-Alonzo, and Modolell, 1986, Cell 44: 303-312. Mizrokhi, Georgieva, and Ilyin, 1988, Cell 54: 685-91. comments: First described by Campuzano et al. as an insertion in a chromosome carrying the scD1, although it is probably not responsible for the mutant phenotype. The restriction map of sancho1 suggests that it is a deleted jockey element (Mizrokhi et al.). sancho1 hybridizes with sancho2. The 1.45 kb Hin- dIII fragment is repeated about 50 times in the genome of strains Oregon R, Canton S, and Vallecas (Campuzano et al.). restriction map (sancho1): # sancho2 length: 2.7 kilobases. copy number: Thirty (Campuzano et al.). references: Campuzano, Balcells, Villares, Carramolino, Garcia-Alonzo, and Modolell, 1986, Cell 44: 303-312. Mizrokhi, Georgieva, and Ilyin, 1988, Cell 54: 685-91. comments: First described as an insertion on a chromosome car- rying the Hw1 mutation, although it probably does not contri- bute to the mutant phenotype. The restriction map of sancho2 suggests that it is a deleted jockey element (Mizrokhi et al.). The 1.7 EcoRI-HindIII fragment is repeated about 30 times in the genome of strains of Oregon R and Vallecas. san- cho2 hybridizes with sancho1 (Campuzano et al.). restriction map (sancho2): # springer length: 8.8 kilobases (Karlik and Fyrberg). target site duplication: Probably six base pairs. copy number: Six (Karlik and Fyrberg). references: Karlik and Fyrberg, 1985, Cell 41: 57-66. Kidd and Young, 1986, Nature 323: 89-91. comments: First described by Karlik and Fyrberg as an insertion in the gene for an indirect-flight-muscle-specific tropomyosin isoform associated with the mutation Tm1. The map and sequence of an LTR were reported by Karlik and Fyrberg. There are no sites for the enzyme BamHI. This element and a copy associated with the mutation fa3 are both flanked by the sequence TATATA; this is probably the target site duplication, although it could be part of the inverted repeats at the end of the LTR. left end: AATTAATTAA ATGTATGGTG CAGGTCCCTC GCCGCGGTCT 40 right end: TGTGCGGACG ATCAGTCCGG TTAACTTAGT TAACT 405 restriction map (springer): # wallaby references: Geyer, Green, and Corces, 1988, Proc. Nat. Acad. Sci. USA 85: 3938-42. comments: This element is associated with a phenotypic rever- tant of the ym mutation. It has inserted into the gypsy ele- ment associated with ym. The sequence of its termini and its restriction map indicate that it is a jockey element. # TE The transposable elements (TE) first investigated by Ising carry the loci of w and rst flanked by foldback element sequences. The original transposition was from the normal location of w rst to 48F on 2R; secondary and tertiary tran- spositions were located both by recombination and cytologi- cally. The following table is extracted and modified from one by Ising and Block (1980, Cold Spring Harbor Symp. Quant. Biol. 45: 527-44). Here and throughout this volume we desig- nate those transposed elements whose cytological positions have been determined according to those determinations; where the cytology has not been done we retain the original numeri- cal designations but with a # sign to differentiate them from cytological positions. TE The transposable elements (TE) first investigated by Ising carry the loci of w and rst flanked by foldback element sequences. The original transposition was from the normal location of w rst to 48F on 2R; secondary and tertiary tran- spositions were located both by recombination and cytologi- cally. The following table is extracted and modified from one by Ising and Block (1980, Cold Spring Harbor Symp. Quant. Biol. 45: 527-44). Here and throughout this volume we desig- nate those transposed elements whose cytological positions have been determined according to those determinations; where the cytology has not been done we retain the original numeri- cal designations but with a # sign to differentiate them from cytological positions. symbol location origin synonym homozygote ____________________________________________________ TE#3 3-45.3 TE48F viable TE#5 2-85 TE48F lethal TE#14 2-78.9 TE48F lethal TE#21 3-69.7 TE48F lethal TE#22 3-11.8 TE48F viable TE#24 3-42.7 TE48F viable TE#37 2-53.0 TE48F viable TE#40 3-20.1 TE16B viable TE#41 3-87.9 TE48F viable TE#44 3-46.8 TE48F viable TE#46 3-10.4 TE48F viable TE#53 2-56.3 TE48F viable TE#63 2-80.6 TE48F lethal TE#64 2-58.8 TE48F viable TE#68 3-47.3 TE16B viable TE#73 2-54.2 TE48F viable TE#77 3-58.7 TE48F viable TE#91 2-79 TE#5 viable TE3C 1-1.5 TE48F TE8 viable TE7A 1-19.8 TE21EF TE100 viable TE16B 1-57.2 [TE#7] TE6 viable TE21A 2-0.1 TE21Bb TE75 lethal TE21Ba 2-0.1 TE60F TE133 lethal TE21Bb 2-0.2 TE48F? TE30 lethal TE21C 2-0.4 TE21Bb TE99 viable TE21Da 2-0.7 TE7A TE186 viable TE21Db 2-0.9 TE57Eb TE141 lethal TE21EF 2-0.8 TE48F TE61 lethal TE21F22A 2-2.4 TE48F TE90 viable TE22A 2-2.3 TE21Bb TE55 viable TE22Ba 2-1.5 TE21Bb TE56 viable TE22Bb 2-2.4 TE48F TE114 viable TE22Bc 2-2.6 TE21Bb TE57 viable TE22Bd 2-2.8 TE21Bb TE81 lethal TE23CD 2-6.7 TE48F TE52 viable TE24D 2-11.7 TE48F TE17 viable TE25D 2-19.5 TE48F TE9 lethal TE28A 2-26.4 TE48F TE62 viable TE28C 2-28.5 TE34Cb TE49 viable TE28D 2-32.9 TE21Bb TE80 lethal TE29Aa 2-31.0 TE60F TE128 lethal TE29Ab 2-31.5 TE48F TE109 viable TE29F 2-33.4 TE48F TE35 lethal TE30C 2-35.7 TE16B TE16 viable TE31A TE301 ? TE33B 2-44 TE34Cb TE150 ? TE33E34A 2-47.4 TE48F TE59 viable TE34Ca 2-48.3 TE48F TE60 lethal TE34Cb 2-48.3 TE48F TE13 lethal TE34Cc 2-48.3 TE21Bb TE94 lethal TE35A 2-49.1 TE60B TE146 viable TE35BC 2-49.8 TE48F TE36 lethal TE36A 2-50.6 TE48F TE116 lethal TE37C 2-53.3 TE48F TE42 viable TE38A 2-54.0 TE#22? TE48 viable TE44C 2-57.9 TE48F TE78 viable TE47AB 2-60.0 TE48F TE65 viable TE47BC 2-60.1 TE48F TE58 viable TE47C 2-60.1 TE16B TE96 viable TE47EFa 2-61.5 TE48F TE119 viable TE47EFb 2-62.0 TE48F TE126 viable TE48F 2-58.9 TE1 lethal TE51D 2-73.6 TE48F TE19 lethal TE54B 2-79.8 TE48F TE45 viable TE56B 2-86.7 TE48F TE124 viable TE57Ea 2-95.2 TE48F TE33 viable TE57Eb 2-97.1 TE48F TE10 lethal TE60B 2-106.7 TE48F TE47 viable TE60F 2-108.5 TE21Bb TE93 lethal TE61A 3-1.0 [TE#2?] TE23 viable TE61D 3-0.0 TE48F TE51 viable TE62DE 3-6.0 TE48F TE26 lethal TE65CD 3-22.7 TE48F TE120 viable TE65D 3-19.9 TE48F TE67 lethal TE67Ea 3-29.8 TE16B? TE31 viable TE67Eb 3-33.8 TE48F TE66 viable TE69A 3-38.0 TE48F TE32 viable TE70F 3-41.7 TE48F TE38 viable TE73C 3-44.3 TE48F TE43 viable TE76EF 3-46.6 TE48F TE4 viable TE86A 3-48.5 TE48F TE27 viable TE86F 3-50.3 TE3C TE28 viable TE87A 3-50.6 TE48F TE98 lethal TE88A 3-53.0 TE48F TE39 viable TE88Ba 3-53.5 TE48F TE71 lethal TE88Bb 3-54.1 TE48F TE72 lethal TE88Bc 3-55.5 TE48F TE34 viable TE89D 3-58.7 TE48F TE77 viable TE91E 3-66.8 TE16B TE70 viable TE94A 3-74.3 TE21Bb TE54 viable TE96D 3-87.6 TE48F TE48F viable TE96E 3-88.4 TE16B TE20 lethal TE97D 3-91.3 TE21C TE137 viable TE98Ba 3-93.9 TE62DE? TE29 viable TE98Bb 3-94.0 TE48F TE15 viable TE98F 3-97.1 TE48F TE89 viable TE100A 3-102.4 TE48F TE25 viable TE100D 3-102.9 TE16B TE69 viable TE100E 3-103.0 TE21Bb TE84 lethal TEh10-14 Y TE48F TE50 viable