a member of a distinct chromatin complex - functions downstream of Pleiohomeotic in the assembly of a repressive complex that generates high levels of H3-K27 trimethylation in Polycomb target genes
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 5.44
Gene model reviewed during 5.50
Component of a form of the Esc/E(z) complex present specifically during early embryogenesis which is composed of Caf1-55, esc, E(z), Su(z)12, Pcl and HDAC1/Rpd3. 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\Pcl using the Feature Mapper tool.
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
GBrowse - Visual display of RNA-Seq signalsView Dmel\Pcl in GBrowse 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 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.
Source for merge of: Pcl l(2)s1859
Haploinsufficient locus (not associated with strong haplolethality or haplosterility).
DNA-protein interactions: genome-wide binding profile assayed for Pcl 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).
Abd-B MCP725 element is a silencer that functions throughout proliferation of the imaginal discs. MCP725-mediated silencing requires the Pc and Pcl proteins (it is likely that other members of the PcG also interact with the MCP725 silencer).
Silencing activity of the iab-7PRE in the bithorax complex is dependent upon proteins from the Polycomb group.
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.
Strong Pcl mutant alleles (Pcl1, Pcl2) are homozygous lethal, hemizygous lethal and lethal with each other, the embryos having partial posteriorly-directed transformations of the abdominal segments (segment 1 into segment 2 and segments 2-7 into more posterior segments). These mutants are strong enhancers of Pc3, showing Pc-like transformations in embryos and are indistinguishable from Pcl deficiencies in complementation behavior. Extreme posteriorly-directed segmental transformations are found in Pcl1/Df(2R)Pcl11B; Pc3/Pc3 lethal embryos (FBrf0038059); these embryos are considerably more abnormal than the Pc3 homozygotes that are Pcl+. Pcl/Pcl embryos that are also homozygous for Asx, Psc, or Scm show strong posteriorly-directed transformations of the entire body pattern; the triple mutant Psc, Asx, Pcl has a tandem array of posterior abdominal segments including four abdominal denticle bands in the head region (FBrf0043317). Pcl1/Pcl1 clones in the second through the sixth abdominal tergites also show caudal transformations; similar clones in the wing often appear to be partially transformed into haltere tissue. Weak Pcl alleles (Pcl3, Pcl4) survive, at least through eclosion, either as homozygotes or as heterozygotes with strong or weak Pcl alleles (FBrf0038059). Pcl1/Pcl3 and Pcl1/Pcl4 show segmental transformations characteristic of Pc/+ flies, i.e. antenna to leg, second and third leg to first leg, wing to haltere, and posteriorly-directed abdominal transformations (the most frequent abnormality). Increasing the dosage of the BXC in Pcl1/Pcl4 heterozygotes suppresses the posteriorly-directed transformations, but enhances the transformations from leg2 and leg3 to leg1; increasing the dosage of the ANTC enhances both types of transformations (FBrf0038059). Pcl1/Pcl3 females, which die before or soon after eclosion, show a conversion of parovaria to spermathecae. Both strong and weak Pcl alleles are viable as heterozygotes (Pcl/+) and may show partial abdominal and leg transformations, the abnormalities increasing in Pcl/+;Pc/+ flies or when Pcl/+ is combined with E(Pc).
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 Pcl product were generated to determine abd-A and Abd-B expression patterns.
Mutations in Pcl derepress homeotic genes in the BXC and ANTC.
The Pc group genes are negative regulators of homeotic genes.
Pcl is one of the 18 loci identified in a screen for dominant modifiers of Pc and/or Antp phenotypes. Alleles of Pc, Pcl, Scm, Dll, brm, kto, Scr and trx show clear dominant enhancement or suppression of AntpScx, whereas alleles of vtd, Vha55, Su(Pc)37D, urd, mor, skd and osa do not.
Mutants of Pcl exhibit a reduction in sex comb teeth on the second and third legs.
Pole cell transplantation techniques demonstrate that Pcl is maternally expressed and is required for normal BXC expression during embryogenesis.