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Previous ArticleNext Article

Mutant Alleles of the Drosophila trithorax Gene Produce Common and Unusual Homeotic and Other Developmental Phenotypes

Thomas R. Breen
Genetics May 1, 1999 vol. 152 no. 1 319-344
Thomas R. Breen
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    Figure 1.

    —Characterized mutations within the trx transcription unit. (A) The map depicts 32 kb containing the trx transcribed region. It is derived from previously published reports (Mozer and Dawid 1989; Mazo et al. 1990; Breen and Harte 1991; Sedkov et al. 1994; Stassen et al. 1995). The thin line with vertical tick marks represents an EcoRI map of the region. Above it are nine rectangles that indicate regions encoding exons. Unfilled areas depict 5′- and 3′-untranslated sequences; filled areas show translated sequences. Connectors between the exons represent splicing alternatives. The M’s on the 5′ sides of the third and fourth exons label positions of likely initiation codons. The TRXII isoform of 3726 amino acids is translated from mRNAs that contain the third exon. The TRXI isoform of 3358 amino acids initiates within the fourth exon. The tick marks labeled “... AAA” show the positions of alternatively used polyadenylation signals. The positions of the point mutations associated with the trxZ11 and trxZ16 alleles are indicated above the exon rectangles, as is the approximate location of a rearrangement breakpoint associated with the trxJY16 allele. The gradient shaded boxes show the approximate sizes and locations of deletions associated with the trxE3 and trxB11 alleles. The proximal breakpoint of Df(3R)redP6 is located within the region represented by the open box labeled redP6. The rightward arrow indicates that Df(3R)redP6 deletes distally beyond the extent of the map. The inverted triangle depicts the approximate position of the 9-kb insert associated with the trx1 allele. The open box labeled trx1 indicates the region of uncertainty within which the insert is located; the base of the triangle represents the size of the insert. (B) TRXII and TRXI mutant isoforms are depicted. The C termini of these protein representations are to the left, consistent with the orientation of the transcription unit in A. The trxZ11 allele is associated with a missense mutation causing a G- to S-substitution at amino acid 3601 in the conserved SET domain (lightly shaded region). The trxZ16 allele is associated with a missense mutation causing an R- to W-substitution at amino acid 1753 in the conserved Cys-rich, PHD finger domain (medium gray region). The black region labeled DBD shows the region with similarity to DNA-binding domains of steroid receptors. The trxE3 allele is associated with an in-frame deletion that leads to the removal of 271 amino acids from both isoforms. The region removed is indicated by the gradient shaded box. The trxB11 allele is associated with an 833-bp deletion that encodes truncated isoforms with 83 novel, C-terminal residues (shaded boxes at left of B11 isoforms). The trxJY16 allele is associated with a rearrangement (possibly a small inversion) breakpoint that occurs in the region encoding the third exon. The resulting fusion gene must be transcribed as determined in this analysis. Fusion mRNAs encode normal TRXI. A fusion form of TRXII is also possible that would have the N-terminal ca. 172–276 amino acids replaced by residues encoded by the fusion partner.

  • Figure 2.
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    Figure 2.

    —trithorax mutant phenotypes. All flies shown have combinations of trx alleles that are lethal by the end of pupal development. Because these flies did not eclose, their wings and halteres partially transformed to wings are not expanded. Flies in A–E are trxJY21/trxZ16, the fly in F is trxZ16/trxE3, flies in G and I are trx3/trxZ11, and the fly in H is trx6.1/trxM17. (A) The arrow indicates ventral T3 with mesosternal bristles normally found only in T2. Mesosternal bristles are also visible in ventral T1. Above the arrow is a haltere partially transformed to a wing. Anterior sternites fail to fuse at the ventral midline. (B) The arrow indicates a transformation of dorsal T3 to mesonotum typical of T2. The A3 tergite is not fused at the dorsal midline. (C) The lower arrows show sternopleural bristles in T1 and T3. These are normally found only in T2. The upper arrow indicates wing tissue that developed in association with a T1 spiracle. The A6 spiracle has unusual material protruding from it. (D) The labels 6 and 7 indicate sixth and seventh tergites of this male. Males normally have fully pigmented fifth and sixth tergites and no seventh tergite. This male has his external genitalia transformed to a leg complete with terminal claws not visible in this focal plane. (E) The arrow shows a T3 leg with a large anterior preapical bristle normally found only on T2 legs. (F) The arrow indicates the presence of a right ocellus and ocellar bristle and the absence of left and center ocelli and a left ocellar bristle. The dorsal anal plate of this female is incomplete. The posterior border of the A1 tergite has Uab-like large bristles and dark pigmentation. (G) Arrows show A2 tergites with patches of small bristles normally found only in A1 tergites. Similar patches are also found in the A3 tergites of these flies. The left fly has Uab-like dark pigmentation and large bristles at the posterior of its A1 tergite. The right fly has a small head and anterior thorax compared to the one on the left. (H) Top arrow indicates a mirror image duplication of the right eye. The lower arrow shows several abnormal bristles on the lateral labellum. (I) Ventral view of same flies as G. The right fly has complete complements of T1 sternopleural bristles. Almost all of its ventral T1 is transformed to ventral T2. The maxillary palps of the right fly did not develop. Its antennae have dpp-like abnormal outgrowths and reduced aristae.

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    Figure 3.

    —Mutant penetrance and expressivity of hemizygous hypomorphs. Vertical bars show the percentage of flies with the indicated number of transformed structures associated with reduced expression of Scr, Ubx, abd-A, or Abd-B. The number of transformed structures for a category measures its expressivity. The percentage of flies with transformed structures in a category measures its penetrance. Transformation penetrance and expressivity infer a level of trx function affecting homeotic gene expression specifying cell fate identity. Scr group transformations. Decreased Scr function causes development of T1 structures with T2 identity. T1 to T2 leg transformations (L1/L2) include development of an anterior preapical bristle, a posterior apical bristle, or both (a.b.) on the distal tibia of one or two T1 legs and reduced numbers of sex comb teeth in males only (Scr ♂♂) on one or two legs. Other ventral transformations of T1 to T2 include development of one or two sets of T1 sternopleural bristles (T1sp) and one or two T1 mesosternal bristles (T1ms). Ubx group transformations. Decreased Ubx function leads to development of T3 structures with T2 identity. Dorsal T3 to T2 transformations include development of one or two halteres to wing (h/w) and one or two hemimetanota to hemimesonota (d3/d2). Ventral T3 to T2 transformations include development of one or two sets of T3 sternopleural bristles (T3sp), an anterior preapical bristle, a posterior apical bristle, or both on the distal tibia of one or two T3 legs (L3/L2), and one or two T3 mesosternal bristles (T3ms). abd-A group transformations. Decreased abd-A function results in development of A2–A7 structures with A1 identity. Dorsal transformations are evidenced by development of small hairs typical of an A1 tergite in more posterior tergites (An/A1, n = 2–7). So few A6 tergites were transformed, the category was excluded. Vertical bars show the percentage of each transformed tergite. Transformation of more posterior tergites correlates with increased expressivity. Abd-B group transformations. Decreased Abd-B function causes development of posterior abdominal segments with more anterior abdominal identities. Transformation phenotypes include anterior abdominal pigmentation in A5 and A6 tergites in males (A5/A4 ♂♂) and enlargement of A7 tergites (A7/A6). These phenotypes were scored for penetrance only. The genotype and number of flies examined are indicated at the top left of each chart. The chromosome indicated to the left of the slash was maternally inherited. The trxM17 allele supplies significant function at the target genes examined except Ubx in ventral structures. Other transformations can be attributed to haploinsufficiency. The trxZ32 allele is a weak hypomorph at the four loci examined. The trx1 allele is a strong hypomorph at the loci examined. It has a noticeably greater effect on abd-A expression than the other hypomorphs. This effect is also seen when trx1 is paternally inherited. The trxE3 allele is a moderate hypomorph at the loci examined. Few trxE3 hemizygotes develop to the pharate stage. Of those that do, most have unchitinized cuticles and fail to evert head structures. The trxZ16 and trxZ11 alleles are strong hypomorphs at the loci examined. trxZ16 has some residual function at Scr and Ubx compared to trxZ11.

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    Figure 4.

    —trxJY21 may be a weak antimorph. Bar graphs are as in Figure 3. Compare hypomorph/trxJY21 profiles to those of the same hypomorphic hemizygotes in Figure 3. Penetrance and expressivity are higher in heteroallelic combinations with trxJY21. trxE3/trxJY21 is pupal lethal and not available for comparison. Note that trxJY21 impairs the already decreased function of trx1 at abd-A. trxM18 is a stronger hypomorph than trxZ11. It may be a near amorph in imaginal cells at the loci examined.

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    Figure 5.

    —trx1/hypomorph heterozygotes. Bar graphs are as in Figure 3. Compare trx1/hypomorph profiles to those of hemizygous hypomorphs in Figure 3. Penetrance and expressivity are lower in heteroallelic combinations with trx1. Thus, trx1 retains significant function. The effect shown here is almost the same as when trx1 is paternally inherited. The maternal effect of trx1 is more pronounced when penetrance and expressivity of trx1/amorph heterozygotes from trx1 homozygous mothers to amorph/trx1 heterozygotes from amorph/trx+ mothers are compared (Table 2). Amorph/trx + mothers supply more trx function to eggs than trx1/trx1 mothers. trxJY16 hemizygotes die as small, third instar larvae. trxJY16 is a strong imaginal hypomorph as seen when it is heterozygous with other strong hypomorphs (Figure 6 and Table 2). trx3 is an amorph when paternally inherited, but slightly antimorphic when maternally inherited (Table 2). Assuming trx1 reduces the amount of normal TRXI and TRXII made, Abd-B and Scr functions in developing T1 legs are most easily affected by reduced levels of these proteins.

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    Figure 6.

    —Penetrance and expressivity of hypomorphs heterozygous with a strong hypomorph, trxZ11. Bar graphs are as in Figure 3. Compare with profiles in Figures 3 and 4. Hypomorphs other than trx1 and trxE3 proportionally have a greater effect on Ubx expression in developing T3 legs than at the other loci examined in other tissues. Compare the profile for trx1/trxZ11 to those of trx1/trxJY21 heterozygotes and trx1 hemizygotes. trxZ11 supplies substantial trx function to the loci examined. Weaker hypomorphs, trxM17, trxZ32, trx1, and trxE3 complement trxZ11 to an extent expected on the basis of their penetrance and expressivity when hemizygous and in combination with trxJY21. trxZ16 complements trxZ11 more than expected on the basis of the same comparisons, suggesting it has true functional complementation of trxZ11 at Scr, Ubx, and abd-A. This effect is only seen when trxZ16 is maternally inherited. All hypomorph/trxZ11 genotypes have nearly wild-type function at abd-A.

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    Figure 7.

    —Model of TRX activation through signal transduction. The model is based on experimental findings on UBX and DPP regulatory interactions in the visceral mesoderm and DPP receptor functions in imaginal discs (see discussion). UBX with other factors (Sun et al. 1995) initiates dpp transcription. DPP may signal the cell from which it came (autocrine, shown in model) or nearby cells (exocrine). DPP signals through receptor heterodimers. Each receptor heterodimer consists of one TGF-β type I subunit and one TGF-β type II subunit. In Drosophila, thickvein and saxophone proteins (TKV and SAX) are type I receptors and punt protein (PUNT) is a type II receptor. DPP signaling through undetermined intermediates may lead to phosphorylation (*) of CREB bound to a promoter proximal CRE (Eresh et al. 1997). Phosphorylated CREB recruits CBP (Chrivia et al. 1993) to the promoter proximal region where it may participate in histone acetylation that may form transcriptionally permissive chromatin (Bannister and Kouzarides 1996; Ogryzko et al. 1996). DPP signaling may additionally act through chromosomal trxG proteins including TRX to boost Ubx expression. Upstream elements of this signaling cascade may include the known DPP-signaling intermediate, MAD, and perhaps nonchromosomal trxG proteins. Signaling may affect any combination of chromosomal trxG proteins that would subsequently interact in an unknown way to augment Ubx transcription. Other known chromosomal trxG proteins include ASH1 (Tripoulas et al. 1996), GAGA factor (Farkas et al. 1994), and perhaps BRM (Dingwall et al. 1995), which is at least nuclear. These may work cooperatively or in parallel. They may be components with TRX of a signal response pathway, or they may function independently to prepare Ubx for elevated transcription. TRX transcriptional augmentation appears to operate in cells where Ubx was previously activated. PcG proteins silence Ubx transcription in cells where there is no Ubx transcription when PcG proteins are activated during germ band elongation. Therefore, TRX mediates DPP-signaled elevation of Ubx transcription in cells where Ubx is previously activated and its previous activation prevents PcG silencing. Other target genes in other cells may similarly use TRX to respond to DPP and other signal transduction pathways. The TRX-mediated signaling response of a cell may be quantitatively controlled by the concentration of a signaling ligand within its gradient distribution and by the number of TRXs recruited to a target gene’s regulatory elements.

Tables

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  • TABLE 1

    trithorax alleles

    AlleleHemizygous phenotypeaHeterozygous penetrancebMolecular lesioncReferencesd
    trxM17 ts, viable at 22°0.000 (1255)Unknown1
    trxZ32 ts, viable at 22°0.000 (799)Unknown1
    trx1 Viable, ts ↑ P&E0.008 (1698)~9-kb insert in region encoding first intron2, 3
    trxE3 Pupal lethal0.016 (1135)Causes a 271-aa in-frame deletion from aa 21303–7
    trxZ16 Pupal lethal0.000 (1017)Causes R to W at aa 1753 in Cys-rich domain1, 8
    trxZ11 Pupal lethal0.013 (668)Causes G to S at aa 3601 in SET domain1, 8
    trxM18 Pupal lethal0.007 (534)Unknown1, 23
    tr XJY16 Larval lethal0.199 (1139)Breakpoint within region encoding aa's 172–2763
    trx6.1 Embryonic lethal0.082 (514)Unknown9
    trxD Embryonic lethal0.067 (390)Unknown10–16
    trxB11 Embryonic lethal0.045 (222)Causes truncated protein after aa 6591, 3, 6, 7, 17
    trxA7 Embryonic lethal0.019 (368)Unknown1, 23
    trxM14 Embryonic lethal0.015 (334)Unknown1, 23
    trxZ15 Embryonic lethal0.102 (422)Unknown1
    trxJY25 Embryonic lethal0.155 (161)Unknown, a T(Y;3) not in trxThis study
    trx7. 1 Embryonic lethal0.097 (527)Unknown9
    trxZ44 Embryonic lethal0.052 (192)Unknown1, 23
    trx3 Embryonic lethal0.208 (525)Unknown15, 18, 19
    trxJY21 Embryonic lethal0.136 (309)UnknownThis study
    Df(3R)redP52 Embryonic lethal0.105 (500)Deletes trx, removes 88A4 to 88B4-51, 3, 12, 18, 20, 21
    Df(3R)redP6 Embroynic lethal0.331 (136)Breakpoint in second intron, removes 88B1 to 88B3-C21, 3, 22

    The top-to-bottom organization of the alleles reflects their relatively increasing contribution to the penetrance and expressivity of the homeotic transformations examined in this study (see Table 2). The exception to this organization is that trx3 and trxJY21 cause a slightly more transformed phenotype than the two deficiencies that are listed at the bottom for convenient reference.

    • ↵a Phenotypes are for animals heterozygous for the trx mutant chromosome and a Df(3R)redP52 chromosome. ts, temperature sensitive; ts ↑ P&E, increasing penetrance and expressivity with increasing temperature.

    • ↵b Numbers on the left are the frequency of appearance of at least one transformation phenotype in adults heterozygous for the trx mutant chromosome and TM1 or TM6B balancers. Numbers of adults examined are in parentheses.

    • ↵c See Figure 1 for more detailed descriptions.

    • ↵d Numbers refer to the following list: 1, Mortin et al. (1992); 2, Ingham and Whittle (1980); 3, Breen and Harte (1991); 4, Kennison and Tamkun (1988); 5, Mozer and Dawid (1989); 6, Mazo et al. (1990); 7, Sedkov et al. (1994); 8, Stassen et al. (1995); 9, Tripoulas et al. (1994); 10, Lewis (1968); 11, García-Bellido and Capdevila (1978); 12, Capdevila and García-Bellido (1981); 13, Duncan and Lewis (1982); 14, Botas et al. (1982); 15, Ingham (1985a); 16, Capdevila et al. (1986); 17, Kuzin et al. (1994); 18, Ingham (1981); 19, Ingham (1983); 20, Lewis (1981); 21, Parkhurst et al. (1988); 22, Gans et al. (1980); 23, D. B. Bailey and P. J. Harte (unpublished results).

  • TABLE 2

    Heteroallelic penetrance and expressivity

    ♂/♀trxM17trxZ32trx1trxE3trxZ16trxZ11trxM18trxJY16
    trxM17 Larva0 (75)0.30 (45)0.35 (37)0.55 (11)1.18 (49)0.18 (22)3.83 (33)b
    trxZ32 0 (48)Larva2.07 (95)0.95 (155)1.36 (36)4.19 (21)b2.95 (12)d2.68 (30)
    trx1 0.01 (89)2.11 (75)7.16 (105)4.82 (125)3.20 (38)2.56 (72)1.90 (50)3.51 (105)
    trxE3 0.12 (65)0.80 (85)4.40 (112)Embryo5.89 (11)c7.90 (79)b6.75 (40)bPupa
    trxZ16 0.25 (44)1.20 (66)2.29 (159)3.08 (36)aLarva9.41 (26)d9.50 (4)e14.07 (27)e
    trxZ11 0.27 (l07)a2.63 (94)b2.75 (125)4.21 (51)a7.36 (28)d14.69 (31)e13.30 (10)e15.13 (16)c
    trxM18 0.42 (12)3.91 (22)c3.55 (80)5.78 (20)d10.58 (4)c16.39 (14)eLarva17.50 (32)e
    trxJY16 1.86 (29)2.47 (56)a3.40 (55)Pupa11.82 (25)d13.32 (34)e16.40 (22)eLarva
    trx6.1 2.37 (56)5.62 (8)c1.36 (157)Pupa18.87 (8)e19.50 (2)e22.20 (10)eLarva
    trxD 0.50 (6)6.12 (8)b12.36 (41)Pupa17.00 (2)ePupaLarvaLarva
    trxB11 2.30 (l0)a4.19 (7)a8.86 (50)Pupa15.29 (7)ePupa14.00 (1)eLarva
    trxA7 1.00 (16)5.34 (31)e8.54 (103)a13.00 (1)e21.00 (3)eLarvaLarvaLarva
    trxM14 1.54 (45)b5.29 (12)e9.14 (34)aPupa18.10 (10)e17.00 (2)eEmbryoLarva
    trxZ15 3.16 (64)7.19 (39)e13.23 (75)Pupa15.75 (4)ePupaEmbryoLarva
    trxJY25 4.37 (8)a3.29 (7)d11.35 (77)Pupa17.74 (8)ePupa21.00 (2)eLarva
    trx7.1 2.06 (31)a5.56 (34)d12.08 (112)aPupa20.67 (9)e23.00 (3)e21.00 (2)eLarva
    trxZ44 3.40 (5)e5.73 (45)e10.24 (34)dPupa17.00 (1)ePupaLarvaLarva
    trx3 2.93 (14)a6.33 (6)c12.27 (59)Pupa19.50 (2)e21.70 (5)e25.00 (1)eLarva
    trxJY21 3.31 (78)a7.79 (32)e17.41 (30)aPupa22.45 (9)e22.33 (3)e23.29 (11)eLarva
    redP52 1.25 (9)a5.96 (14)13.20 (117)11.33 (3)d18.15 (10)e21.74 (7)d26.00 (1)eLarva
    redP6 3.82 (41)b5.86 (7)12.26 (28)Pupa20.14 (14)e22.60 (3)eEmbryoLarva
    ♂/♀trx6.1trxDtrxB11trxA7trxM14trxZ15trx7.1trxZ44trx3trxJY21redP52redP6
    trxM17 6.75 (31)b3.60 (20)b3.60 (60)d2.88 (8)b4.00 (7)e5.67 (10)e5.60 (5)b5.82 (26)d7.60 (10)c6.39 (46)b5.35 (52)4.88 (11)b
    trxZ32 5.90 (67)a5.42 (12)a4.08 (52)b4.93 (7)e4.72 (28)c6.70 (5)c7.58 (13)e6.15 (17)e8.95 (13)a7.27 (23)e6.19 (14)7.01 (18)a
    trx1 1.51 (83)3.46 (30)6.74 (75)2.05 (57)4.60 (20)6.90(209)9.25 (76)Larva6.51 (62)5.86(195)7.01 (45)8.69 (23)
    trxE3 PupaPupaPupaPupaPupaPupaPupaPupaPupaPupaPupaPupa
    trxZ16 17.97 (11)e16.50 (14)c16.64 (22)e18.17 (6)d17.97 (6)e18.43 (50)e17.61 (22)e17.25 (4)e21.33 (12)e20.22 (18)e20.50 (6)e16.67 (6)e
    trxZ11 20.80 (5)e18.70 (10)e20.00 (6)eLarva18.67 (3)e19.00 (1)e22.20 (5)e21.00 (1)e23.40 (5)e22.49 (11)e23.00 (10)e18.83 (6)e
    trxM18 20.50 (4)eLarva20.00 (1)eLarvaEmbryoEmbryoLarvaLarvaLarva23.84 (6)eLarvaEmbryo
    trxJY16 LarvaLarvaLarvaLarvaLarvaLarvaLarvaLarvaLarvaLarvaLarvaLarva

    Column headings represent maternally contributed alleles. Row headings (far left column) indicate paternally contributed alleles. Numbers are the average number of tranformations seen in adults of the genotypes determined by reading the column/row headings. Numbers in parentheses show the number of flies examined of the given genotypes. Males have a maximum of 29 transformations, females 26. The maximum average when there is a 1 male:1 female ratio is 27.5. An entry of embryo indicates that no larvae of the given genotype were seen. An entry of larva indicates that the genotype was lethal by the larval third instar stage. An entry of pupa indicates that the genotype was lethal during the pupal stage. Amorphic and antimorphic genotypes not included are embryonic lethal.

    • ↵a Between 100 and 75% of the scored adults eclosed.

    • ↵b Between 75 and 50% of the scored adults eclosed.

    • ↵c Between 50 and 25% of the scored adults eclosed.

    • ↵d Between 25% and 0 of the scored adults eclosed.

    • ↵e None of the scored adults eclosed. If no superscript, 100% eclosed.

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Volume 152 Issue 1, May 1999

Genetics: 152 (1)

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Mutant Alleles of the Drosophila trithorax Gene Produce Common and Unusual Homeotic and Other Developmental Phenotypes

Thomas R. Breen
Genetics May 1, 1999 vol. 152 no. 1 319-344
Thomas R. Breen
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Mutant Alleles of the Drosophila trithorax Gene Produce Common and Unusual Homeotic and Other Developmental Phenotypes

Thomas R. Breen
Genetics May 1, 1999 vol. 152 no. 1 319-344
Thomas R. Breen
  • Find this author on Google Scholar
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