EZ, pco, l(3)1902, Su(z)301, polycombeotic
transcription factor - polycomb group with trithorax homology - chromatin associated - catalytic component of the Polycomb Repressive Complex 2 (PRC2) methyltransferase that methylates histone H3 lysine27 -together with PRC1, PRC2 silences developmental genes to determine specific differentiated cell identities
Gene model reviewed during 5.46
Component of the Esc/E(z) complex, composed of Caf1, esc, E(z), Su(z)12, and possibly pho. The Esc/E(z) complex may also associate with Pcl and Rpd3 during early embryogenesis. This complex is distinct from the PRC1 complex, which contains many other PcG proteins like Pc, Ph, Psc, Su(z)2. The two complexes however cooperate and interact together during the first 3 hours of development to establish PcG silencing. Interacts with corto in vitro.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\E(z) using the Feature Mapper tool.
Abundant E(z) protein is observed in male germline stem cells, gonialblasts, spermatogonia, and very early spermatocytes. Protein levels drop abruptly in spermatocytes in early G2 of meiotic prophase.
GBrowse - Visual display of RNA-Seq signalsView Dmel\E(z) in GBrowse 2
Genetic map position contradicts cytological map position.
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 GBrowse 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.
DNA-protein interactions: genome-wide binding profile assayed for E(z) protein in Kc167 cells; see Chromatin_types_NKI collection report. Individual protein-binding experiments listed under "Samples" at GEO_GSE22069 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22069).
E(z) is required for normal neuroblast proliferation in postembryonic central nervous system development.
dsRNA has been made from templates generated with primers directed against this gene. RNAi of E(z) causes an increase in branch number and an expansion of the receptive field of class I neurons. RNAi also causes defects in muscle, defects in dendrite morphogenesis and reproducible defects in da dendrite development.
Evidence of physical interaction between esc and E(z) in vitro and in vivo and coimmunoprecipitation in vivo suggests the proteins are direct partners in Pc-G mediated repression and this relationship has been evolutionarily conserved.
E(z) protein is ubiquitously distributed in embryonic and larval nuclei and binds many of the same polytene chromosome nuclei as other Pc-G proteins. Lack of E(z) protein activity disrupts chromosome binding by trx protein.
Although E(z) has been classified as a member of the Polycomb group of genes, it can also be classified as a member of the trithorax group. The requirement for E(z) activity as either a trithorax group or Polycomb group gene depends on the homeotic selector gene locus as well as on spatial and temporal cues.
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. 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. Duplications of E(z) enhance homeotic phenotypes of esc mutants.
E(z) mutations can express phenotypes characteristic of mutations in the trx-group of genes. Loss of function for E(z) during early development results in homeotic gene expression defects reminiscent of a trx-group mutation, while loss later in development results in gene expression defects characteristic of a Pc-group mutation.
A screen for suppressors of nos mutations identified alleles of E(z). E(z) is a negative transcriptional regulator of kni and gt and is required to maintain their expression domain initiated by the maternal hb gradient. A small region of the kni promoter mediates regulation by E(z) and hb. Imprinting at the chromatin level may underlie the determination of anteroposterior polarity in the early embryo.
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.
Embryos mutant for two or more Pc group genes (Pc, Scm, Pcl, Psc, Asx, E(Pc), E(z), ph-d, pho and esc) show strong ectopic en expression, but only weak derepression occurs if embryo is mutant at only one of the Pc group genes. This effect is independent of the function of en itself, and wg.
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 E(z) product were generated to determine abd-A and Abd-B expression patterns.
Reduction of E(z)+ activity suppresses the z1 eye colour. Maternally and zygotically produced E(z)+ activity is required to correctly regulate the segment identity genes during embryonic and imaginal development.
E(z) locus is involved in the suppression of the z1 eye colour and is also associated with homeotic transformations.
Locus named after original gain-of-function allele E(z)1 (Kalisch and Rasmuson, 1974); subsequently designated polycombeotic (pco) (by Phillips and Shearn, 1980) based on phenotype of lethal homozygotes. Loss of function alleles recovered as (a) recessive lethal mutations (b) reversions of E(z)1 and (c) reversions of the antimorphic allele, E(z)59. Reduction of E(z)+ activity leads to suppression of the z eye color, whereas gain-of-function alleles are dominant enhancers of zeste eye color <up>i.e., z w+/Y; E(z)1/+ males have brownish eyes as do z w+/z+ w+; E(z)1/+ females</up>. E(z)59 an antimorphic allele, is a dominant suppressor of z <up>i.e. z w+; E(z)59/+ females have orange eyes</up>. Hemizygosity for E(z)+ produces a very mild suppression of the z eye color. No effects on eye color in z+ or za backgrounds and effects on eye color not specific to a particular w allele. Reduction of E(z)+ activity also allows ectopic expression of the segment identity genes of the Antennapedia and bithorax gene complexes, resulting in homeotic transformations. This latter effect defines E(z) as a Polycomb-group locus. E(z)61 displays temperature-sensitive suppression of z eye color and homeotic phenotypes. At 22oC, z wis/Y; Hemizygous E(z)61 males have orange eyes and no homeotic transformations. At 29oC, such males have wild-type red eyes and die as pharate adults with strong homeotic transformations of the mesothoracic and metathoracic legs toward the prothoracic state. Embryos produced by E(z)61 homozygous females at 29oC die with homeotic transformations of most segments toward the eighth abdominal segment. Even two copies of paternally contributed E(z)+ does not rescue viability of these embryos. Complete lack of zygotically produced E(z)+ results in early pupal lethality and small imaginal discs. Larval brain squashes from individuals homozygous for an amorphic allele reveal a very low mitotic index; metaphase chromosomes irregularly condensed and fragmented (Gatti and Baker, 1989).