Polycomb group (PcG) protein. While PcG proteins are generally required to maintain the transcriptionally repressive state of homeotic genes throughout development, this protein is specifically required during the first 6 hours of embryogenesis to establish the repressed state. Component of the Esc/E(z) complex, which methylates 'Lys-9' and 'Lys-27' residues of histone H3, leading to transcriptional repression of the affected target gene. The Esc/E(z) complex is necessary but not sufficient for the repression of homeotic target genes, suggesting that the recruitment of the distinct PRC1 complex is also required. Required for the correct spatial expression of the homeotic genes of the Antennapedia and Bithorax complexes.

(UniProt, Q24459)

Pcl+, like Pc+, may be considered a negative regulator of the BXC and the ANTC. 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 (Duncan, 1982); 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 (Jurgens, 1985). 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 (Duncan, 1982). 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 (Duncan, 1982). 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).