xenicid, xen
Please see the JBrowse view of Dmel\Asx 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 5.46
7.0 (northern blot)
None of the polypeptides share 100% sequence identity.
1668 (aa); 182 (kD predicted)
Component of the polycomb repressive deubiquitinase (PR-DUB) complex, at least composed of caly/calypso, Asx and sba (MBD5/6 homolog) (PubMed:20436459, PubMed:30258054, PubMed:30639226, PubMed:36180891). Interacts (via DEUBAD domain) with caly/calypso (via ULD domain); the interaction produces a stable heterodimer with a composite binding site for ubiquitin (PubMed:20436459, PubMed:30258054, PubMed:30639226). Two copies of the caly-Asx heterodimer assemble into a bidentate tetramer (PubMed:30258054). Interacts (via PHD domain) with sba (probably via MBD domain); the interaction is important for the stability of the PR-DUB complex (PubMed:36180891). Interacts with tant (PubMed:11397012). Interacts with cyclin CycG (PubMed:25995770).
The DEUBAD domain is involved in modulation of the ubiquitin C-terminal hydrolase activity of caly/calypso (PubMed:30639226). It contains two Leu-Xaa-Xaa-Leu-Leu (LXXLL) motifs involved in the interaction with caly/calypso (PubMed:30639226). It also contains an Asn-Glu-Phe (NEF) motif involved in stabilizing the association of the PR-DUB complex with ubiquitin to promote deubiquitinase activity (PubMed:30258054, PubMed:30639226).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Asx 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).
Asx transcript is present at high levels in 0-1.5 hr embryos. Levels decline at 1.5-3 hours, then rise again. Levels are low in larvae, and increase in pupae and adults. Three transcripts are detected in adult males. Asx transcript is abundant in nurse cells, but absent from stage S10 oocytes. In the blastoderm stage embryo, expression is detected in a broad band in the anterior, and a narrower band in the posterior of the embryo. The transcript is ubiquitous during the rest of embryogenesis, though higher levels are detected in the neurectoderm and later in the central nervous system.
Asx protein is first detected in the cellular blastoderm embryo, in both the nucleus and cytoplasm. The protein may be at slightly higher levels in the anterior of the embryo. Later in embryogenesis, the protein is ubiquitous but non-uniform, with higher levels detected in the neurectoderm, and later in the central nervous system. Asx protein localizes to about 90 sites in polytene chromosomes.
JBrowse - Visual display of RNA-Seq signals
View Dmel\Asx in JBrowse2-71
2-75.6
Located on 2R.
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.
Asx is required for both the activation and repression of homeotic loci.
Identification: Genetic screen for autosomal mutations that produce blisters in somatic wing clones. 1 allele of xen has been isolated.
In an effort to subdivide the Pc-group genes functionally, the phenotypes of adult flies heterozygous for every pairwise combination of Pc-group mutation were examined. Asx, Pc, Pcl, Psc, Scm and Sce have similar functions in some imaginal tissues. Genetic interactions have been demonstrated between esc, Asx, E(Pc), Pcl, E(z) and sxc. Most duplications of Pc-group genes neither exhibit anterior transformations nor suppress the extra sex comb phenotype of Pc-group mutations, suggesting that not all Pc-group genes behave as predicted by the mass action model.
Mosaic and expression pattern analysis reveals that the Pc-group genes do not act only in a common complex or pathway: they must have some independent functions.
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 bithorax complex context. The Pc-group products apparently provide stable memory or imprinting of boundaries which are specified by gap and pair-rule regulators.
Mutations of genes in the Polycomb group (esc, E(z), Pc, ph-p, ph-d, Scm, Pcl, Sce, Asx, Psc, pho and Antp) cause abnormal segmental development due to the ectopic expression of abd-A and Abd-B. Embryos lacking both maternal and zygotic Asx product were generated to determine abd-A and Abd-B expression patterns.
Embryonic and adult phenotypes suggest that Asx is required zygotically for determination of segment number and polarity. A construct carrying an eve promoter fused to a Ecol\lacZ gene was used to demonstrate that 40% of the mutant Asx embryos exhibit some ectopic expression of eve. This suggests Asx is required for the normal expression of eve.
The Pc-group genes are negative regulators of homeotic genes.
Pole cell transplantation techniques demonstrate that Asx is maternally expressed and is required for normal the bithorax complex expression during embryogenesis.
Asx/+ males have extra sex-comb teeth on meso- and metathoracic legs. Homozygote embryonic lethal. Abdominal denticles in head and thoracic segments; abdominal segments 1-7 transformed into more posterior segments. In double mutant combinations with Pcl, Psc, or Scm shows strong posterior transformation of all segments and failure of head involution. The presence of the bithorax complex+ required for expression of phenotype.
Source for identity of: Asx CG8787
