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A Genetic Screen of the Drosophila X Chromosome for Mutations That Modify Deformed Function
Brian Florencea and William McGinnisaa Department of Biology, University of California, San Diego, California 92093
Corresponding author: William McGinnis, Department of Biology 0349, 4305 Bonner Hall, 9500 Gilman Dr., University of California, San Diego, CA 92093-0349., wmcginnis{at}ucsd.edu (E-mail).
Communicating editor: T. C. KAUFMAN
| ABSTRACT |
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We have screened the Drosophila X chromosome for genes whose dosage affects the function of the homeotic gene Deformed. One of these genes, extradenticle, encodes a homeodomain transcription factor that heterodimerizes with Deformed and other homeotic Hox proteins. Mutations in the nejire gene, which encodes a transcriptional adaptor protein belonging to the CBP/p300 family, also interact with Deformed. The other previously characterized gene identified as a Deformed interactor is Notch, which encodes a transmembrane receptor. These three genes underscore the importance of transcriptional regulation and cell-cell signaling in Hox function. Four novel genes were also identified in the screen. One of these, rancor, is required for appropriate embryonic expression of Deformed and another homeotic gene, labial. Both Notch and nejire affect the function of another Hox gene, Ultrabithorax, indicating they may be required for homeotic activity in general.
HOMEOTIC (Hox) genes of the Antennapedia and Bithorax Complexes of Drosophila encode transcriptional regulators that bind DNA through a 60-amino-acid homeodomain (![]()
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Understanding how the Hox proteins differentially specify regulatory targets and, thus, determine unique segmental identity has been problematic. The Hox homeodomains are highly related, causing different Hox proteins to have similar or identical monomeric DNA-binding specificity (![]()
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Screens for genetic modifiers of homeotic functions have constituted one method for identifying regulatory factors that interact with the Hox system. Previous Hox modifier screens have identifed many members of the repressive Polycomb Group (PcG) or activating trithorax Group (trxG) genes (reviewed in ![]()
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Another class of Hox-interacting genes (extradenticle, teashirt, homothorax, and cap'n'collar) fall into a class that we call the Hox modulators. These genes can mutate to give homeotic transformations, but they appear to act in parallel to Hox proteins, in contrast to the upstream regulatory functions of the PcG and trxG (![]()
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We have previously screened the second and third chromosomes of Drosophila for genes that show dose-sensitive interactions with the Hox gene Deformed (Dfd; ![]()
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The X chromosome presents practical difficulties in modifier screens, and it has been relatively neglected when screening for mutations that interact with homeotic genes. We present here a screen of the X chromosome of Drosophila for genes involved in Dfd function. We have screened >2000 lethal chromosomes, isolating 14 alleles that show dose-sensitive interactions with Dfd hypomorphic alleles. These alleles map in seven different complementation groups. Three of these groups correspond to previously characterized X-chromosome genes involved in either cell-cell signaling (Notch) or transcriptional regulation (nejire and extradenticle). Another gene identified in the X-chromosome screen corresponds to a previously isolated but uncharacterized locus, l(1)6Ee (![]()
| MATERIALS AND METHODS |
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Drosophila strains:
P{cosP479BE}7-20, N+ was obtained from S. Artavanis-Tsakonas (![]()
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Mutagenesis:
EMS mutagenesis was performed according to standard protocols (![]()

where N is the number in each class, and IS is the interaction strength shown in Table 2. For potentially positive lines, this interaction test was repeated at least twice with three initial vials.
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Determining map positions:
Recombinant map positions of the Dfd interactors were determined by mapping against isogenic, viable y+ cv v g2 f or y+ sn3 wy car chromosomes. Appropriately marked chromosomes from these crosses were kept to provide "clean" chromosomes. Cytological positions were determined by crossing lines to flies carrying appropriate deficiencies and duplications (see Table 1). Complementation tests were performed between appropriate lines and available genes having the same map position. No duplication that covered the lethality of UC119 was found.
Lethal phase and lethal cuticular phenotype:
Embryos were collected on standard apple juice agar plates for 12 hr. These were washed and evenly distributed on clean agar plates. Yeast was added around the edges of the plate to attract larvae. After 3648 hr, egg cases and dead embryos were counted. A line was considered embryonic lethal (E) if >75% of the expected number died before hatching and embryonic/larval lethal (E/L) if 2575% died. Hemizygous males of the remaining lines, which did not reach pupal stages, were considered larval lethal (L).
Cuticles of unhatched larva were fixed for 3 hr in 1:4 glycerol:acetic acid and then mounted in 1:2 Hoyer's mountant:lactic acid. Aberrant cuticular structures were scored in ~20 cuticles from the embryonic lethal lines. Defects observable in
80% of the animals are listed as part of the phenotype. Other defects that were not as penetrant are also listed but qualified as such, e.g., often or less often observed.
Ubx interaction:
UbxM1/TM6B males carrying an isogenic UbxM1 chromosome were crossed to females of FM7c balanced lines. Flies were allowed to lay eggs for 3 days at 25° and then discarded. All B+ Tb+ female flies were collected from each vial and preserved in ethanol. After collections, 20 females were randomly selected. Their halteres were dissected, mounted in Hoyer's, and scored for ectopic bristles. The experiment was repeated at least once, and the total number of ectopic bristles from each experiment was used to determine an average. When standard errors of the mean >25% were obtained, a third experiment was performed. Pc4, trx5C4, and the parental y2·YL chromosomes were used as controls.
In situ staining:
Lines to be analyzed molecularly were placed over FM7c carrying an actin:lacZ transgene (FM7c, P{w+mC = act-lacZ.B}GD-1 P{w+mC = act-lacZ.B}GD-2; ![]()
| RESULTS |
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We have screened the X chromosome of Drosophila for mutations that show dominant interactions with the homeotic gene Dfd. This was done using a slightly modified version of earlier screens (![]()
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65% of the expected Dfd adult female hypomorphs survived. Potentially interacting chromosomes were rescreened at least twice to confirm the interaction. In all, 2048 lethal chromosomes were screened, resulting in 17 chromosomes that consistently showed an interaction with Dfd. Lethals on these chromosomes were mapped by meiotic recombination. Four chromosomes had multiple lethals that individually failed to show an interaction with Dfd, and those will not be discussed. The remaining 14 chromosomes carried lethals that interacted with Dfd. These mutations were mapped against appropriate deficiencies and duplications to obtain cytological map positions (Table 1). Lethal phases were also determined (see MATERIALS AND METHODS; Table 2). If suitable duplications were available, appropriate lines were tested for complementation. The screen led to the identification of three known and four novel genes that genetically influence the function of Dfd (Table 2; Figure 2). Given that a single allele was isolated for four genes, it is likely that the screen was not saturating.
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The three known complementation groups are Notch (N), nejire (nej), and extradenticle (exd). Each group displayed a range of Dfd interaction strengths (IS, Table 2) that did not notably change when alleles were placed on unmutagenized chromosomes (data not shown). Notch was originally identified as a neurogenic gene and was found to encode an epidermal growth factor repeat transmembrane receptor (reviewed in ![]()
The largest number of interacting alleles were isolated in nej, which encodes a member of the CBP/p300 family of transcriptional adaptor molecules (![]()
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The four novel or uncharacterized loci are, proximally to distally, WC1, stout, rnc, and UC119. Only stout has multiple alleles, and these showed a strong interaction with Dfd. The three remaining loci, WC1, rnc, and UC119, showed intermediate interactions with Dfd.
Genetic interactions with other homeotics:
Although these loci were identified by their ability to interact with the gnathal homeotic Dfd, they might also have a general role in Hox-mediated patterning. We and other researchers have investigated such relationships by observing the genetic modification of the Pc phenotype, particularly the number of ectopic sex combs in adult males (![]()
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Heterozygotes for Ubx display ectopic bristles on the haltere, an indication of a partial transformation toward wing. Heterozygosity at a locus required for Ubx function could potentially enhance this phenotype. Conversely, heterozygosity for a locus that normally represses Ubx haltere function would be expected to suppress the Ubx phenotype. The Dfd-interacting alleles were placed in a UbxM1 heterozygous background, and the number of bristles on ~80 halteres was scored for each line. Only nej mutations showed an enhancement of the Ubx phenotype, while Notch alleles strongly suppressed ectopic bristle formation (Figure 3). The remaining Dfd-interacting alleles showed no effect, nor did the Pc4 and trx5C4 mutations (data not shown).
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Phenotypes:
Dfd is required for the formation of the mouth hook, ectostomal sclerite, H-piece bar, anterior lateralgräten, cirri, ventral organ, and maxillary sense organ (![]()
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Notch:
The classical dominant Notch phenotype includes notched wing margins. Although all three Dfd-interacting alleles showed notched wings in adults, their phenotypes were less severe than a Notch null, suggesting that all three alleles are hypomorphic. Mutant embryos lacking Notch have a neurogenic phenotype (reviewed in ![]()
nejire:
The extant nej3 allele has been molecularly characterized as a null (![]()
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A genetic interaction has been previously noted between nej and a dominant mutation of cubitus interruptus (ciD; ![]()
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rancor:
Cuticles of rncTA54, rncTA54/Df(1)DesiS3, and Df(1)DesiS3 embryos showed defects in derivatives of the antennal and ventral gnathal lobes, including Dfd-dependent structures. Specifically, the hypostomal sclerite and the H-piece arm were present but malformed, the base of the mouth hook was reduced, the mouth hooks were multiply serrated (Figure 4A, arrowhead), and head involution failed. The involution defect caused the maxillary and antennal sense organs to develop on the lateral aspect of the head instead of at the normal anterior-dorsal location. Less often, the H-piece cross-bar was reduced or failed to fuse medially, the dorsal-lateral or medial papillus was missing or misplaced (Figure 4A, arrow, DLP, or DMP), the ventral organ was disrupted, and the median tooth was translocated dorsally. The head involution defect is similar to that caused by mutations in another homeotic gene, labial (lab; ![]()
strung out:
Cuticles of stoutTA181 and stoutUA104 male and stoutTA181/Df(1)HA32 and stoutTA181/l(1)6Ee4 female embryos had very similar phenotypes, although the stoutTA181/l(1)6Ee4 phenotype was somewhat milder. Most striking in these mutants were the defects surrounding the dorsal sac. The dorsal bridge was diffuse and occasionally unfused. Strands of sclerotic material were "strung out" from the anterior vertical plate and ventral side of the dorsal bridge in the area between the dorsal sac and lateralgräten (white arrow in Figure 4A). Also, the H-piece lateral arm was bifurcated or widened, and the H-piece crossbar was widened or broken. The mouth hooks were of normal length, but thin, and the mouth hook bases were often reduced. The trunk of stout animals also showed narrow third thoracic denticle belts (Figure 4B, white and black arrowheads). A similar denticle phenotype was seen in mutants of another Dfd interactor, EcR (![]()
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Heterozygous stoutTA181 and stoutUA104 adults have thick aristae (Figure 6, arrows) and arced wings, and many have one or more kinked macrochaete, phenotypes that are not seen in deficiency heterozygotes for the stout locus. In addition, males carrying these alleles over two duplications that cover the stout locus [Dp(1;2)sn13a1 or Dp(1;Y)ct+y+] were sterile. The presence of these dominant phenotypes indicates that the stoutTA181 and stoutUA104 alleles are either neomorphic or antimorphic. Another extant allele of stout, l(1)6Ee4, does not exhibit these dominant phenotypes, nor does this mutant allele exhibit an interaction with Dfd in our assay.
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extradenticle:
The exdS136 allele is embryonic-larval lethal (~40% die as embryos), while exd nulls are embryonic lethal (Table 2; ![]()
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Other loci:
The novel WC1 and UC119 alleles displayed larval and embryonic-larval lethality, respectively. Animals that died as embryos showed inconsistent phenotypes in all segments. These variable phenotypes included occasional random holes, head defects, and poorly differentiated cuticle (data not shown). Because of the variable and poorly penetrant mutant defects, we did not further analyze these mutant alleles in the present study.
Molecular analysis:
Wild-type Dfd expression is initiated in the blastoderm embryo in the primordia of the mandibular and maxillary segments (![]()
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In rnc mutants, ectopic Dfd expression was often seen in the anterior mandibular lobe (Figure 7A). Because cnc is required for the repression of anterior mandibular Dfd expression (N. MCGINNIS, E. RAGNHILDSTVEIT, A. VERAKSA and W. MCGINNIS, unpublished data), one possiblity is that the ectopic Dfd seen in rnc mutants is indirectly caused by a loss of cnc expression. Figure 7A shows that cnc expression is severely reduced in the hypopharyngeal and mandibular lobes of rnc mutant embryos, suggesting that the aberrant mandibular Dfd expression is caused by reduced cnc levels. Expression of cnc in the clypeolabrum is unaffected in these mutants.
Although it was not obvious from the cuticular phenotype, the altered expression patterns of Dfd and cnc suggested that the loss of rnc function may result in a partial homeotic transformation of cells in the mandibular segment to maxillary identity. If this hypothesis is correct, maxillary-specific target genes of Dfd should be inappropriately regulated in the mandibular lobe of rnc mutants. We examined the expression of the Dfd targets prd, Ser, and Dll in rnc mutants. In most rnc mutant embryos, two of these genes were expressed in maxillary-like patterns in the mandibular segment: prd being ectopically activated, and Ser inappropriately absent (Figure 7A); Dll expression was unaffected in rnc mutants (data not shown). These data are consistent with a partial transformation of the mandibular lobe toward maxillary identity.
As the rnc cuticular phenotype also had similarities to the lab phenotype, we examined the lab transcription pattern in rnc mutants. Early phases of lab expression were normal in the rnc mutant embryos (stage 10, Figure 7B). However, by stage 13/14, lab transcript abundance in the intercalary and tritocerebral primordia of the procephalic region was weaker or absent in rnc mutants than in wild-type embryos (Figure 7B). The pattern and amounts of lab transcript in the midgut of rnc mutants was comparable to wild type (![]()
| DISCUSSION |
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This is the final paper in a series uncovering genetic requirements for the function of the homeotic gene Dfd (see Figure 2 for a summary). We have isolated mutations in seven loci on the X chromosome that significantly reduced the viability of Dfd hypomorphs. The Notch, exd, and nej genes have been characterized previously, while stout and rnc are either novel or uncharacterized. Many Dfd-interacting alleles we have isolated are either hypomorphic or antimorphic and have stronger interactions with Dfd than nulls. This indicates that the interactions between Dfd and other genes may not always be caused by reduced gene dosage, but by an antagonistic function of the mutant protein on wild-type activity, perhaps by interfering with particular subfunctions of interacting factors. Therefore, molecular characterization of antimorphic or hypomorphic proteins may provide insight as to how the respective wild-type proteins modify Dfd (or Hox) function.
Embryonic lethal Deformed interactors:
Mutations in a gene crucial for embryonic Dfd function would be expected to cause defects in or loss of Dfd-dependent cuticular structures, as is seen in Notch, exd, stout, and rnc mutants. As mutations for the other genes identified in our screen do not appreciably affect the formation of the gnathal cuticle, the functions of these genes might be supplied maternally or affect the development of Dfd-dependent tissues not visible in cuticular preparations (e.g., tentorium and subesophageal ganglion). Alternatively, some may interact with Dfd only during postembryonic development. These results are similar to those from the second and third chromosome screens, where zygotic mutants for one-third of the loci did not exhibit defects in Dfd-dependent embryonic cuticular structures.
Transcription:
Only 18 of the 27 genes identified in all three Dfd interactor screens have been sequenced, and their encoded products have been published. Of these 18, 16 may be grouped according to their roles in either cell-cell signaling (Notch, Collagen type IV, viking, devenir, Vacuolar H+-ATPase 55-kD B subunit, Laminin A, Serrate, and hedgehog) or transcription (exd, nej, Ecdysone Receptor, cap'n'collar, apontic, Polycomb, trithorax, and cubitus interruptus). Because the Dfd protein is a transcription factor, it is not unexpected to have isolated a large number of genes involved in transcription. One of these, exd, is required for many homeotic functions (![]()
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The other X-chromosome Dfd interactor known to participate in transcription in nej (![]()
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Cell-cell signaling:
Nearly half of the molecularly characterized loci from all three Dfd interactor screens (see Figure 2) have functions in cell-cell signaling. Four of the Dfd-interacting loci encode transmembrane receptors (devenir and Notch) or extracellular ligands (hedgehog and Serrate). Three other lociLaminin A, Collagen type IV, and vikingencode components of the basal lamina that also provide signals that modulate cell differentiation and gene transcription (reviewed in ![]()
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1D could have a direct affect on Dfd function, as Ca2+ flux has been shown recently to have a potent affect on the function of some transcriptional activators (![]()
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The interaction of Hox proteins with the transcriptional effectors of signaling cascades has been noted previously. For example, Ubx modulates the ability of Wingless and Dpp signals, allowing appropriate activation of Dll expression in the leg primordia (![]()
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The Notch gene is expressed in every cell (![]()
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The Notch alleles that interact with Dfd are hypomorphic, with the strongest effect on viability (IS) shown by the allele with the least severe cuticular phenotype. The reason for this paradox is unclear, as is the reason why 9 of the 12 Notch alleles we tested failed to interact with Dfd. One explanation could be that the Dfd-interacting hypomorphs have levels of active Notch protein within a critical range required to observe an effect. Alternatively, the aberrations in Dfd-interacting Notch proteins could preferentially affect a Dfd- (or Hox-) specific subfunction.
Notably, no obvious intermediates (e.g., kinases) between transmembrane receptors and the nucleus were isolated in our screens although others have been successful in identifying such factors (e.g., ![]()
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Hierarchical relationships of unclassified loci:
The products encoded by stout and rnc, and therefore their molecular functions, are not known. However, the morphological and molecular nature of their phenotypes gives some indication of their roles in specification by Dfd. Mutants for rnc show alterations in Dfd expression (see below), while stout mutants show no detectable alteration in Dfd expression. In addition, extant alleles of stout do not have a maternal effect (![]()
strung out:
Although the major defects in stout mutants are in Dfd-independent dorsal structures, these cuticles also have reduced mouth hooks and a malformed H-piece lateral bar, which are Dfd dependent. In addition, stout mutants have reduced third thoracic denticle belts, indicating a possible role in thoracic Hox function as well. A similar phenotype is also seen in EcR mutants (![]()
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rancor:
The similar phenotypes of rncTA54 and Df(1)DesiS3 hemizygotes suggest that rncTA54 is a strong allele. The distinctive cuticular and molecular phenotypes of rnc mutants indicate an important role for rnc in cephalic homeotic regulation and head development. Mutants for rnc have defects mainly in derivatives of the mandibular, maxillary, and labial lobes, whose structures are present but disrupted. Some of these defects are apparently caused by a partial transformation of mandibular to maxillary identity, as some genes that are regulated in a Dfd-dependent manner are regulated in a maxillary-like pattern in the mandibular segment of rnc mutants [i.e., Dfd (![]()
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Loss of rnc results in reduced levels of cnc in mandibular cells. As cnc antagonizes Dfd expression and function in the mandibular lobe (![]()
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Another rnc phenotype is a partial failure of head involution, resulting in the maxillary and antennal lobes being more posterior and lateral. The head involution defect is distinct from and more severe than that seen in Dfd mutants, but it is similar to that observed in mutants for another homeotic gene, lab (![]()
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Interactions with other homeotics:
The molecular and phenotypic analyses of our mutants suggest that they play a role in the function of homeotic genes other than Dfd. We tested this possibility by looking at their genetic interactions with Ubx. Unlike the interaction with Dfd, the Ubx test will detect interactions in only a small subset of Ubx-expressing cells (the haltere margin) during a very narrow period of time [early third instar (![]()
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The enhancement of the Ubx phenotype by nej mutations suggests that the Nej protein might be involved in either the activation of Ubx transcription or the repression of sc transcription. The role of CBP/p300 family members as transcriptional activators (reviewed in ![]()
The remaining mutant alleles from our screen did not have a significant effect on Ubx function in the haltere. For exd, this is consistent with earlier work that showed that clones of exd in the haltere pouch have no effect on Ubx expression (![]()
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| ACKNOWLEDGMENTS |
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We thank S. Artavanis-Tsakonas, in whose lab some of this work was accomplished; E. Wiellette, X. Li, N. McGinnis, and A. Veraksa for comments on this manuscript; and the Bloomington Stock Center and the many researchers who supplied the various fly strains necessary to complete this project. We would also like to thank X. Lu and M. Rosenfeld for murine CBP/GST fusion clones. Especially, we thank D. Lindsley and the late A. Schalet for many helpful discussions. This work was supported in part by a National Research Service Award GM16535-04 to B.F. and National Institutes of Health grant HD28315 to W.M.
Manuscript received June 30, 1998; Accepted for publication August 26, 1998.
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