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FB2026_01
,
released March 12, 2026
bx, pbx, Cbx, bxd, bithorax
transcription factor - homeodomain - Antp class - Mutations of Ubx result in transformation of the dorsal and ventral appendages of the third thoracic segment (the haltere and third leg) into their counterparts on the second thoracic segment (wing and second leg).
Please see the JBrowse view of Dmel\Ubx for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.54
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.41
Gene model reviewed during 5.55
4.3, 3.2 (northern blot)
None of the polypeptides share 100% sequence identity.
The QA motif is able to mediate transcriptional repression.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Ubx using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: in the 4th to 7th pairs of alary muscles
Comment: expressed from mesothoracic segment to abdominal segment 5
Comment: expressed from mesothoracic segment to abdominal segment 5
The major domain of Ubx expression in the embryonic CNS is parasegment 6, with weaker expression in parasegment 5 (posterior T2 and anterior T3) and an isolated cluster of neurons in the midline of parasegment 4. Posterior to A1, Ubx expression is weak and spotty but still occurs in some neurons through A7. Within parasegment 6, the great majority of the neurons show strong Ubx expression.
Ubx expression begins in NB5-6A at embryonic stage 11, and is subsequently expressed in earlier born cells in this lineage in segment A1-A7.
Larval expression of Ubx protein is observed in the presumptive capitellum (haltere pouch), and in the third leg disc.
The Ubx protein is expressed in the nuclei of larval fat body cells with an anterior boundary of around T3 and a posterior limit near A6/A7. Expression occurs in all nuclei of this region and specific labeling of polytene chromosome bands can be mapped.
Ubx protein is expressed in all cells of the peripodial epithelium of the wing disc.
Protein is detected in the midsection of the embryonic dorsal vessel. The protein is expressed in cardioblasts of abdominal segments A2-A5. Low level expression of Ubx is also observed in pericardial cells of these segments. The cardiac segment of the dorsal vessel contains barely detectable levels of Ubx protein.
Ubx protein is expressed at low levels in all cells of the dorsal vessel between abdominal segment 2 and the posterior tip of the embryonic heart.
Ubx expression is low in the cardiac tube compared to the gut and ectoderm. Within the cardiac tube, expression is strongest in the cardial and pericardial cells of the aorta from segment A2 to the middle of segment A5.
Antp protein is first detected at germ band retraction stage in a 6-7 cell width stripe in the midgut visceral mesoderm and the ectoderm of parasegment 7.
The Ubx expression domain is twice as wide in homozygous ftz mutant embryos as in wild type. Embryos homozygous for eve3 showed no Ubx staining but there is some staining in embryos homozygous for eve4. Normal homeotic gene function is seen in embryos homozygous for en59, en54, en55, wgl-17, opa1, h41, odd5, prd4 and runB102. No Ubx gene expression is seen in ftz,prd double mutant embryos, some staining is seen in opa,prd double mutant embryos and there is normal staining in odd,eve double mutant embryos. The Ubx domain is in the right position in KrB206 mutants, shifted posteriorly in kni mutants and shifted anteriorly in hb mutants.
Comment: 12-14 hr AEL
JBrowse - Visual display of RNA-Seq signals
View Dmel\Ubx in JBrowse
3-59
3-58.8
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
Haploinsufficient locus (not associated with strong haplolethality or haplosterility).
DNA-protein interactions: genome-wide binding profile assayed for Ubx protein in 0-12 hr embryos; see mE1_TFBS_Ubx collection report.
During embryonic development Ubx produces mRNAs with distinct 3' UTRs that harbour different sets of miRNA targets in different tissues. The differential distribution of Ubx mRNAs bearing specific 3'UTR sequences is established independently of miRNA regulation, indicating that it is not the result of miRNA-mediated transcript degradation but instead the consequence of an "in-built" RNA processing system that remodels Ubx 3'UTRs according to developmental context.
The QA motif is preferentially required for repression of postnotal tissue.
Ubx modulates the shape and size of the third leg by a range of both cell autonomous and non-autonomous mechanisms, and is required at different times.
Ubx is required to confer an aorta identity on cardiomyocytes in the developing embryo.
Ubx blocks the development of apical and sternopleural bristles on the T3 leg.
Ubx protein present before pupation is sufficient to control the normal differences in behaviour that distinguish wing and haltere cells much later, between 24 and 48 hours after puparium formation.
The modulation of Hox gene activation and repression functions can account for segment-specific morphological differences.
Ubx has distinct spatial roles during maintenance of cell fate and patterning in the halteres.
Expression of Ubx in the haltere D/V boundary down-regulates its D/V organizer signalling compared to that of the wing D/V organizer.
Whenever a Hox gene functions as a repressor in the dpp enhancer it prevails over others that function as activators.
The detailed regulation of Ubx patterns trichomes on the posterior femur of the second leg. Evolution of this regulation has contributed to divergence among closely related species.
The Ubx promoter and nearby sequences are not required to establish a normal late embryonic pattern.
Formation of the Ubx HD-DNA complex is associated with significantly greater water release than that of the Dfd HD-DNA complex. No influence of pH in water release was detected for either homeodomain. Chimeric Ubx-Dfd homeodomains demonstrates the C terminal region of the Ubx HD is the primary determinant for the greater water release associated with DNA binding for the protein.
A wg response sequence (WRS) is identified in the visceral mesoderm enhancer from Ubx. WRS is a binding site for Mmus\Lef1. Mmus\Lef1 can form a stable complex with arm protein on the Ubx WRS and function in vivo depends on arm. The ability of Mmus\Lef1 to stimulate transcription requires dpp signalling, implying Mmus\Lef1 has a crucial function in coordinating multiple signalling inputs.
Ubx 5' UTR contains an internal ribosome entry site (IRES). The IRES exhibits a high degree of developmental regulation.
Ectopic expression of Ubx, abd-A and Abd-B cause similar transformations in the appendages (antenna and wing) but different transformations in the main body axis. abd-A, and to some extent Abd-B, can form haltere-like tissue in the absence of Ubx. Although exd product affects wing development the presence of exd fails to modify the wing to haltere transformation caused by ectopic expression of either Ubx or abd-A.
Flies have been artificially selected for differential sensitivity to the induction of bithorax phenocopies by ether vapour.
Increased sensitivity to ether correlates with loss of expression of Ubx in the third thoracic imaginal discs.
Transvection effects have been analysed in terms of rates of transcription from both Ubx homologues in various combinations. The results suggest that transvection is not simply a case of the enhancer of one homologue regulating transcription of the other homologue, but indicate a more complex level of trans regulation that may have implications for the aetiology of genetic disorders that are influenced by chromosome rearrangements.
Despite the absence of a syncytium in C.floridanum embryos monoclonal antibodies to en, Ubx and abd-A demonstrate their cognate proteins are expressed in a conserved pattern in the post-gastrulation stages of development. The expression of the eve cognate protein is not completely conserved and lacks a pair rule phase to its expression.
The Ubx gene has redundant cis-regulatory elements, which apparently contain binding sites for factors that share the function of the z gene product. z and Trl have an overlapping function in regulating Ubx. The z product binds at equal levels to Ubx promoter constructs (which it activates) as to the endogenous Ubx gene (which it redundantly regulates).
Expression of the 2218R6 enhancer element, found in the bxd region, begins after gastrulation and is dependent on wg. H1 and H3 elements are only activated in the later embryo and direct expression in the imaginal discs.
Pc associates with multiple sites in the bithorax complex and these sites all contain maintenance element.
Ubx expression can induce gonad formation.
Highly selective interactions exist between exd and certain isoforms of Ubx and with the abd-A protein. The Ubx sequences critical for the interaction have been mapped to the homeodomain and a 15 residue N-terminal extension of the homeodomain that includes the YPWM sequence. The region between the homeodomain and YPWM influences the interaction.
The transcription unit that produces the noncoding bxd transcript has been identified.
Ubx fragments that bind hb protein in vitro contain parasegmental enhancers active in the embryo in specific parasegmental patterns. Three new embryonic enhancer elements have been defined. Imaginal disc expression of Ubx is not determined by the embryonic enhancers but by a distinct set of imaginal disc enhancers. They are active in thoracic and head imaginal discs. Positional information is conveyed to them through the Pc-group response element, which in turn depends on the state of activity of the parasegmental enhancers.
Heat shock induced expression of mouse Hox genes in Drosophila embryos deficient for homeotic genes demonstrates that functional hierarchy is a universal property of the homeobox genes. Correlations exist between the expression patterns of the mouse Hox genes along the antero-posterior body axis of mice and the extent of their effect along the antero-posterior body axis of flies.
Ubx expression in the ectoderm and mesoderm of the posterior abdomen is regulated by co-operative cis regulatory elements. At least some of these regulatory elements are germ layer specific and not parasegment specific.
The region -20 to -30kb upstream of the Ubx promoter carries an element the responds to the Pc group genes, this forms a complex with products of the Pc group genes and is able to maintain the repressed state of enhancers present in its vicinity throughout development. This regulatory element is called the Pc-G response element of PRE.
Two types of silencers restrict the activity of imaginal disc enhancers from Ubx to the Ubx domain in imaginal discs; embryonic silencers with hb protein binding sites and at least one silencer (BXD) which lacks such sites. Silencing by BXD requires Pc. Silencing in imaginal discs requires cooperation between hb and Pc target sites within the two types of silencers.
Antp, Ubx and Dfd protein homeodomain regions bind preferentially to a core sequence which differs from the binding sequence of Abd-B. N-terminal amino acid differences are responsible for the sequence specificity difference between Abd-B and Ubx. Antp and Ubx homeodomains display indistinguishable preferences outside the core, while Ubx differs.
Ubx and abd-A have equivalent functions in promoting the formation of particular muscle precursors in the abdominal segments, while Abd-B suppresses these same myogenic cells in the posterior region of the abdomen. Either Ubx or abd-A can override the inhibitory effect of Abd-B, when expressed in the same mesodermal cells. Homeotic cues specific to both the mesoderm and ectoderm cooperate to specify the pattern of muscle attachment sites.
Naturally occurring binding sites for the Ubx protein contain multiple, individual recognition sequences. Ubx protein complexes are progressively stabilised by increasing numbers of individual recognition sequences. This cooperative stabilisation can extend to sites separated by as much as 200bp. Cooperative binding requires amino acid sequences outside the homeodomain.
There is a strong correlation between chromosomal location of breakpoint or insertional mutation at Ubx and clustering of S1 nuclease sensitive sites. Prominent S1 sites colocalise with unusual DNA sequences and transcription factor(s) putative binding sites.
In the absence of the bithorax complex, Scr is derepressed in the posterior compartments of the thorax and abdomen, but only in the epidermis.
Transformed metathorax of Ubx adult mutants has a functional, duplicated neural pathway for the escape-jump response. That transformation of the corresponding flight muscles is rare indicates that the presence of a motor neuron is not always sufficient to induce or determine the development of its target muscle.
The bithorax complex genes are regulated by the Pc group of genes, acting via 'Pc group response elements' (PREs), that can work even when removed from the normal the bithorax complex context.
The first Ubx splicing event is cotranscriptional.
Ubx homeodomain binds optimally to a distinct DNA sequence.
Different homeotic genes have specific local effects on Dfd expression.
Analysis of Dfd-Ubx chimeric coding regions identifies specific amino acid residues at the amino end of the Ubx homeo domain that are required to specifically regulate Antp transcription. In the context of Dfd protein, these amino-end residues are sufficient to switch from Dfd- to Ubx-like targeting specificity.
Ubx is a member of the bithorax complex. The bithorax complex is a gene cluster that functions to assign unique identities to body segments in the abdomen and posterior thorax. Most, perhaps all, the bithorax complex functions are expressed within parasegments, metameric units composed of the posterior compartment of one segment and the anterior compartment of another. Complementation studies indicate that the bithorax complex is organized into three large functionally integrated regions, known as the Ultrabithorax (Ubx), abdominal-A (abd-A), and Abdominal-B (Abd-B) domains. The Ubx domain functions primarily to assign identities to parasegments 5 and 6.
Mutations in Ubx fall into several classes including the bithorax (bx), bithoraxoid (bxd), anterobithorax (abx), postbithorax (pbx), Contrabithorax (Cbx) classes. Ubxabx-1 homozygotes show variable transformations of the anteriormost portion of the third thoracic segment (T3) toward the corresponding part of T2. Homozygotes also show variable transformations of posterior T2 to posterior T1. The latter effect is enhanced by low temperature. Ubxabx-1 partially complements and shows transvection with Ubxbx-1, Ubxbx-3 and Ubxbx-34e. Ubxabx-1/Ubxpbx-1 has the posterior portion of the distal segment of the haltere very slightly transformed into wing tissue; Ubxabx-1/Ubxpbx-2 is similar if heterozygous for a rearrangement that suppresses transvection. Ubxbx-1 homozygotes have anterior portion of third thoracic segment (T3) transformed toward corresponding region of second (T2). The extent of this transformation is allele-dependent and is most extreme in Ubxbx-3 and weakest in Ubxbx-4. Although the transformations caused by most bithorax alleles are uniform, those caused by Ubxbx-1 and Ubxbx-34eprv are highly variable. At 17oC several bithorax alleles show weak and variable transformations of posterior T2 to posterior T1. Ubxbx-3, Ubxbx-8 and Ubxbx-G over Ubxpbx-1 show a very slight Ubxpbx-1 effect (as described for Ubxabx-1) if heterozygous for a rearrangement that suppresses transvection. Ubxbxd-1 homozygotes show transformation of the anterior first abdominal segment (A1) to the corresponding region of the third thoracic segment (T3). In addition, Ubxbxd-1 homozygotes have posterior T3 and posterior A1 transformed toward posterior T2. Hemizygotes for the stronger bithoraxoid alleles show (with variable expression) formation of one or a pair of well-developed thoracic legs and, rarely, an extra haltere on A1; the frequency of these abdominal halteres is greatly enhanced in hemizygotes for Ubxbxd-9 abd-Aiab2-K. The A1 legs in Ubxbxd-1 hemizygotes contain underdeveloped posterior compartments, indicating that posterior A1 is partially transformed toward thorax. UbxCbx-1/+ has a strong transformation of the posterior region of the second thoracic segment (T2) toward the corresponding region of the third (T3) and a weak and variable transformation of anterior T2 toward anterior T3. The UbxCbx-1 homozygote differs in having a stronger, but still variable, transformation of anterior T2 toward T3. UbxCbx-1/Ubx has a slight enhancement of the Ultrabithorax phenotype (see also su(Cbx)). UbxCbx-2 has both anterior and posterior regions of T2 moderately transformed toward T3. UbxCbx-Hm affects only the wing, which is strongly transformed to haltere. Flies carrying two doses of UbxCbx-Hm plus a normal allele have a virtually complete transformation of wing to haltere. UbxCbx-2 and UbxCbx-Hm have inseparable recessive bithoraxoid effects. UbxCbx-3/+ transforms anterior portions of T2 variably toward anterior T3. It has no effect in posterior T2. For an overview of the effects of UbxCbx-1 mutants on specific structures see Table 1 of Adult Ubxpbx-1 homozygotes and hemizygotes have posterior region of third thoracic segment (T3) transformed toward corresponding region of the second (T2). Larvae homozygous and hemizygous for strong Ubx mutants, such as the Ubx1-type, have the ventral setal bands or 'hooklets' of the first abdominal segment (A1) and T3 transformed toward those of T2; dorsally, the hair patterns of posterior T2 and posterior T3 are transformed toward posterior T1; Keilin organs with 2 hairs appear on A1; ventral pits appear on segments A1 through A7; two extra sets of anterior spiracles appear, one on T3 and one on A1. Homozygotes die, usually as tiny third instar larvae, but occasionally grow to a normal-sized third instar larvae and may pupate. Homozygotes of some weaker alleles, such as Ubx61d, survive to adult stage and show weak bithorax, bithoraxoid and postbithorax effects, especially in the haltere and A1 is generally reduced.
ftz protein acts directly as a transcriptional activator of Ubx. Some ftz binding sites are adjacent to, and some overlap, hb binding sites in the Ubx promoter, suggesting that ftz protein competes with hb protein for DNA binding and/or transcriptional activation of Ubx, to produce the sharp anterior boundary to Ubx expression.
Ubx plays a role in the formation of imaginal histoblast cells.
The bxd region does not cis-regulate abd-A.
Three Ubx key control regions, PBX, ABX and BXD confer an expression pattern mimicking certain aspects of Ubx expression. The boundaries of expression imposed by PBX or ABX on the BXD pattern are dependent on Pc function. PBX and ABX are recognized by repressors which act across large distances to suppress BXD activity.
Mutations in zygotic homeotic gene Ubx do not interact with RpII140wimp.
The bx region contains a spatially regulated enhancer element, BRE. The imaginal function of bx requires the interaction of the BRE with other control elements to produce the correct pattern in the haltere and third leg discs and to repress the expression in discs more anterior than parasegment 5. The BRE element is regulated by hb.
Homeotic gene activity programs primordia as either discs or histoblast nests by the early extended germ band stage.
Homeotic gene products can be ectopically expressed in regions where they are normally down regulated causing no phenotypic consequence in the epidermis.
Ectopic expression of Ubx causes homeotic transformation in the embryo and adult.
The C terminal homeodomain portion of Ubx is needed to generate the transformation phenotype.
Ubx mutants have been classified into "transvection groups".
A regulatory element in the abx region programs Ubx expression with a proper anterior limit in parasegment 5 and a regulatory element in the bxd region programs proper anterior limit in parasegment 6.
The position of the Ubx expression domains in the visceral mesoderm have been defined with respect to parasegment boundaries.
The homeodomain proteins encoded by Antp::Ubx can specifically activate transcription of certain promoters by acting upon a common sequence to modulate gene transcription.
Genetic analysis of transvection effects suggests that the transcription of UbxCbx-1RM and UbxCbx-2 alleles depends on RNAs of short radius of action from the homologous Ubx gene.
Mutant individuals display enlarged halteres.
Source for identity of: Ubx CG10388
