(Alliance, FBgn0003042 )

Polycomb group (PcG) protein. PcG proteins act by forming multiprotein complexes, which are required to maintain the transcriptionally repressive state of homeotic genes throughout development. PcG proteins are not required to initiate repression, but to maintain it during later stages of development. Component of the PcG multiprotein PRC1 complex, a complex that acts via chromatin remodeling and modification of histones; it mediates monoubiquitination of histone H2A 'Lys-118', rendering chromatin heritably changed in its expressibility. Promotes locus-specific chromatin compaction.

(UniProt, P26017)

Pc+ may be considered a negative regulator of the bithorax complex (BXC) and the Antennapedia complex (ANTC), with a decreasing gradient of activity from anterior to posterior. When homozygous or hemizygous, Pc mutants are late embryonic lethals. Embryos with at least one dose of the BXC show incomplete head development and caudad transformations, the thoracic and first seven abdominal segments being partially transformed into the eighth abdominal segment (Lewis, 1978; Denell, 1982; Haynie, 1983, Dev. Biol. 100: 399-411; Denell and Frederick, 1983, Dev. Biol. 97: 34-47). This homeotic effect in homozygotes is enhanced by increasing the dosage of the BXC. Transformations involve brain and ventral nerve cord as well as epidermis (Jimenez and Campos-Ortega, 1981). Pc+ alleles in the mother weaken the homeotic effect (Denell, 1982; Lawrence, Johnson, and Struhl, 1983, Cell 35: 27-34). Pc2/Pc2 or Pc3/Pc3 clones induced in leg and eye-antennal tissue during larval development also show similar posteriorly-directed transformations (Struhl, 1981; Duncan and Lewis, 1982). Pc/+ flies carrying at least one dose of the BXC show caudad transformations, i.e. partial conversion of wings into halteres and of anterior abdominal segments into more posterior ones. Some Pc heterozygotes show phenotypes characteristic of ANTC mutants, i.e. partial conversion of antennae into legs and of second and third legs into first legs (with sex combs in males) (Hannah-Alava, 1958; Duncan, 1982). The frequency of wing transformations varies directly with the BXC dosage, but does not seem to be changed by variation in ANTC dosage (Duncan and Lewis, 1982; Botas et al., 1982). The number of abdominal transformations, however, varies inversely with the doses of the BXC while it increases as the doses of the ANTC are increased (Duncan, 1982; Duncan and Lewis, 1982). Other changes observed in Pc/+ flies include a transformation of ventral to dorsal wing (Tiong; Sato et al., 1983), elevated, divergent, or crinkled wings, terminal gaps in the L4 wing vein, bent humeral or notopleural bristles, and defective sternopleural bristles, all abnormalities being less extreme in males than in females (sometimes absent in males). When doubly heterozygous with AntpYu and AntpB, Pc enhances Antp. The expression of all Pc mutant heterozygotes (including deficiencies for the locus) is enhanced by the second chromosome dominant, E(Pc) (Sato et al., 1983, 1984). Pc3/Pc3/Dp(1;3;4)7 flies (carrying a Pc+ duplication) show stronger leg and wing transformations than E(Pc)/+;Pc3/+ flies (Duncan and Lewis, 1982; Sato et al., 1983).