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.

Sections of the Scr regulatory region may be important for regulation of Scr by Polycomb- and trithorax-group genes.

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.

Duplication of ph-d suppress homeotic transformations of Pc and Pcl, this data supports the conclusion that ph-d is at equilibrium with a multimeric complex containing Pc group genes.

Alleles of trx lighten the eye colour of some pairing sensitive allele of w, whereas alleles of Pcl darken their eye colour.

Pcl product is found on larval salivary chromosomes at about 100 specific loci, in the same positions as the products of Pc, ph-d and ph-p genes.

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).

Pcl⁺, like Pc⁺, may be considered a negative regulator of the BXC and the ANTC.

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 Antp^Scx, 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.