l(3)j14A6, trxG, l(3)s5452, Rg-bx, Trx-C
histone methyltransferase activity (H3-K4 specific), transcription factor - zinc finger - trithorax group - maintains activity of homeotic genes - regulates systemic signaling during Drosophila imaginal disc regeneration - a positive regulator of global gene expression, modulates transcriptional pausing and organization of upstream nucleosomes
Please see the JBrowse view of Dmel\trx for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.48
14.205, 13.756, 12.968, 12.519, 10.941 (sequence analysis)
15, 12, 10 (northern blot)
12.445 (compiled cDNA)
15, 12, 10, 3 (northern blot)
405, 365 (kD predicted)
3726 (aa); 368 (kD)
3759 (aa)
Interacts (via SET domain) with ash1 (via SET domain) (PubMed:10454589, PubMed:10656681). Interacts with Nup98 (PubMed:25310983).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\trx 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: maternally deposited
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reference states 2-4 hr AEL
Comment: reference states 11-15 hr AEL
trx transcript is localized to the apical tip of the adult testis.
trx transcript ME is present in 0-1hr embryos and adult females suggesting that it is maternally deposited. It is also present in 2-4hr embryos where the ratio of ME to E1 to E2 is 11:3:1 . ME is also detected in 11-15hrs as a minor component. ME is detected by in situ hybridization in the syncytial blastoderm. The major site of expression is the ventral region of the posterior half of the embryo in cells fated to become mesoderm.
trx transcript E1 is detected in 2-4hr embryos. The ratio of ME to E1 to E2 at this stage is 11:3:1 . Transcript E1 is detected by in situ hybridization in the presumptive mesoderm at the syncytial blastoderm stage. It is then expressed in a broad domain that resolves into four pair-rule-like stripes in the posterior half of the embryo. Stripes 1,2 and 4 are stronger than stripe 3. By mapping relative to ftz, the stripes were located at parasegments 6, 8, 10, and 12. Stripes persist until early stage 8.
trx transcript E2 is a minor species detected in 2-4hr embryos. The ratio of ME to E1 to E2 at this stage is 11:3:1 . Transcript E2 appears to be expressed throughout the early embryo.
trx transcript L is expressed transiently in 11-15hr embryos. It becomes very abundant in early pupae, and is the major species in adult males. Transcript L is detected in late embryos by in situ hybridization. Strong staining is observed in the suboesophageal and supraoesophageal ganglia, and in the ventral nerve cord. Weaker staining is seen in the head, the clypeolabrum and the antennomaxillary complex.
The trx protein accumulates in the region of the bithorax complex genes on polytene chromosomes from central and posterior regions of larval fat bodies where the homeotic genes are expressed.
JBrowse - Visual display of RNA-Seq signals
View Dmel\trx in JBrowse





3-55
3-53.0
3-54.2
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.
ChEST reveals this is a target of Mef2.
trx protein is associated with the nuclear matrix.
Identification: Enhancer trap expression pattern survey for loci expressed in the ring gland.
Mutants are isolated in an EMS mutagenesis screen to identify zygotic mutations affecting germ cell migration at discrete points during embryogenesis: mutants exhibit germ cell migration defects.
trx is required for a subset of somatic gonadal precursors (SGPs) to maintain their identity and to maintain their association with germ cells.
Maintenance but not initiation of en gene expression in the embryo requires trx, which is also required to maintain stable long-term expression of the homeotic genes throughout development. trx is required for normal en expression in the wing imaginal disc. trx-dependent loss of en expression in the dorsal fat body is correlated with female sterility.
Proper regulation of both trx and Pc can be established by transient assays with a haploid cell line expressing Ubx promoters fused to a Ecol\lacZ reporter gene. This system has been used to map the regulatory sequences in the Ubx promoter to a 440bp region. The Ubx proximal promoter is essential for trx-dependent activation.
trx exerts its effect by binding directly or indirectly to specific DNA sequences in its target genes.
The negative autoregulation of ph-p starts at the blastoderm stage and is partly mediated by a transvection effect. As the number of functional copies of ph-p increases a concomitant reduction of the transcription in each copy is observed. This regulation is ensured positively by the trx group and negatively by the Pc group gene products.
The anterior and posterior boundaries of trx expression are set up by hb and tll. trx expression is altered in Kr and kni mutant embryos but not in gt or pair rule mutant embryos. dl is involved in the activation of trx and sna activity is required after cellularization to maintain trx expression in the ventral domain.
Dvir\trx is cloned and the gene structure and expression pattern are determined. Many aspects of trx structure and expression are conserved between D.melanogaster and D.virilis. In particular a distinct expression pattern in early embryos previously implicated in maintenance of BX-C expression is also found in D.virilis, suggesting that it is an important feature of trx function.
trx gene product binds to at least 16 sites on larval salivary gland polytene chromosomes. The intensity of binding is strongly decreased in larvae carrying mutations in ash1 and E(z). trx gene product binds within an 8.4kb regulatory region that directs fkh expression in several embryonic tissues. These results demonstrate that trx maintains expression of target genes by interaction with their regulatory regions and this interaction depends on the presence of at least some trx and Pc group proteins.
Proper expression of genes in the Bithorax and Antennapedia complexes is maintained by products of different trx RNAs at different times in embryogenesis.
trx is required for the activation of the homeotic genes within the BXC and ANTC, mutations in trx suppress Pc and Pcl mutations.
trx is required for normal expression of homeotic genes within the BXC and ANTC. trx is necessary for normal levels of Antp, Ubx and abd-A protein accumulation.
trx cDNA has been cloned and sequenced.
Genetic tests were used to confirm that ash1 and ash2 belong a functionally related class of genes, mutations in which cause a wide variety of homeotic transformations that are similar to the transformations caused by trx. Homozygous clones of lethal alleles do not express the transformation of posterior abdominal segments to anterior abdominal segments.
22-52% of double heterozygotes involving a null allele of Ash-1 and the trx deficiency, Df(3R)red-P93, show partial transformations of halteres to wings and/or partial transformations of third (and sometimes first) legs to second legs, whereas in single heterozygotes no transformations are shown (Shearn, 1989). Heterozygosis for null alleles of trx suppresses the extra sex combs phenotype of +/Df(3L)Pc-MK, and increases penetrance of the maternal-effect homeotic phenotype of fs(1)h. trx function seems to be necessary for optimal expression of Scr- (Sato, 1988).
The presence of trx+ is required throughout embryonic and larval development for the appropriate differentiation in the adult of segments in the head, thorax, and abdomen (Ingham and Whittle, 1980; Ingham, 1981), the primary effect being in the thoracic segments. Mutants show transformations of the first and the third thoracic segments to the second thoracic segment as well as transformations in the abdomen (Mozer and Dawid, 1989). The gene seems to be involved in the positive regulation of the BXC and the ANTC (Duncan and Lewis, 1982). The viable mutant combinations trx1/trx1 and trxD/+ show variable segmental transformations in adults, as do heterozygous deficiencies <up>Df(3R)red-P52/+, for example</up>. The frequency of homeotic transformations in adults and, to some extent, in larvae of such genotypes varies inversely with the dosage of the BXC (Duncan and Lewis, 1982; Sato and Denell, 1987). A similar dosage effect has been proposed for the ANTC (Sato and Denell, 1987). When the mutant allele or deficiency is maternal in origin, the frequency of transformations is higher in adults (but not in larvae). The alleles trx2, trx3 and trxD are larval or pupal lethals as homozygotes, transheterozygotes, or deficiency heterozygotes and may show weak homeotic transformations in larvae or in homozygous clones in adults (Capdevila and Garcia-Bellido, 1981; Ingham, 1981; Ingham, 1983; Ingham, 1985b).
Source for merge of: trx l(3)j14A6
Source for merge of: trx l(3)s5452
Source for identity of: trx CG8651