(Alliance, FBgn0004861 )

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. Plays a role in regulating the expression of other pair-rule genes such as eve, ftz, and H.

(UniProt, P39769)

A member of the Polycomb group of genes; seems to be the only one that is strongly required both maternally and zygotically for normal embryonic development. Two mutagenic events are necessary to produce null mutations, suggesting that the locus is complex, and in fact molecular determinations indicate that the locus comprises a direct repeat. Single-event mutations are viable as males and homozygous females; such mutations produce transformations similar to those of known dominant gain-of-function mutants in the ANTC and BXC, i.e., transformation of wings to halteres, second and third legs to first legs, and anterior abdominal segments to more posterior segments (mutants may also show loss of the humerus). Two-event lethal mutations die in mid embryogenesis and completely lack ventral and abdominal epidermal derivatives; they show transformations of most of the segments toward the eighth abdominal segment (Dura et al., 1988). There is an alteration in the pattern of axon pathways in the CNS. The axons fail to form commissures or connectives but instead form large bundles in the middle of each hemi-ganglion (Smouse et al., 1988). Trans heterozygotes between viable and lethal alleles or between viable alleles and a deficiency for ph die in late embryogenesis and exhibit posteriorly directed transformations; i.e. viable alleles are haplo insufficient. Dura et al. (1987) postulate that mutations can occur in either or both of the repeated sequences such that -+/-+ = +-/+- = -+/+- = viable mutant constitutions (--/++ not stated to be mutant); -+/-- = +-/-- = late embryonic lethals; and --/-- = mid-embryonic-stage lethals. The ph+ product is required autonomously in imaginal cells. A total lack of ph+ function prevents viability of the cuticular derivatives of these cells, but amorphic ph clones induced in late third instar survive. ph has a strong maternal effect on segmental identity and epidermal development that cannot be rescued by a single paternally supplied dose of ph+ in the zygote (Dura et al., 1988). The expression of ph is inversely related to dosage of the ANTC and the BXC; the gene interacts with Pc, Pcl, and esc (Dura et al., 1985). At the shortened germ band stage (but not at the blastoderm stage), ph seems to be involved in the regulation, not only of the homeotic genes Scr and Ubx, but also in the regulation of the segmentation genes ftz, eve, and en (Dura and Ingham, 1988).