Figure 1. Role of polycomb group (PcG) mutations and polycomb group-response elements (PREs). All figures show Drosophila embryos mounted with anterior to the left, and dorsal up. The line and the arrow mark the normal anterior boundary of ultrabithorax expression. Below each embryo are diagrams indicating whether endogenous gene or reporter construct is transcribed (dashed line) or repressed (box with cross), whether the parasegment-specific enhancer (E) is activating the promoter (presence or absence of bent arrow), and whether the PcG complex is repressing (oval labelled PcG) or inactive (PcG obliterated). (a) Wild-type late embryo, showing ultrabithorax expression obeying anterior boundary. The PcG complex represses in the anterior, but not the posterior part of the embryo. (b) PcG mutant embryo, showing that ultrabithorax is now expressed throughout the embryo. The PcG complex is inactive throughout the embryo. (c) Earlier embryo, showing a lacZ reporter gene under the regulation of an enhancer and a PRE. Reporter expression obeys the anterior boundary. (d) Earlier embryo showing expression of a lacZ reporter gene in either a PcG mutant (top line of diagram) or in the absence of a PRE (bottom line of diagram). The reporter is expressed anterior to the boundary because there is no PRE, or because there is no functional PcG complex.

Figure 2. Models of polycomb group (PcG) function. (a) Heterochromatic model. Heterochromatin spreads from the PcG-response element (PRE), rendering the enhancer (E) and promoter (P) of the ultrabithorax (Ubx) gene inaccessible to transcription factors. (b) Compartmentalization model. The hypothesis is that PcG proteins can restrict target loci to a compartment(s) that are not permissive for transcription. On the left, the Ubx locus is in a nuclear compartment that is permissive for transcription, and the PcG complex is not functional (oval with PcG obliterated). On the right, the Ubx locus is in a nuclear compartment that is not permissive for transcription. The PcG complex is functional (oval with PcG legible), and the Ubx locus is not transcribed (box enclosing a cross). (c) Inhibition of transcription initiation. The PcG complex prevents activity or binding of the RNA polymerase II holoenzyme, or of factors necessary for its activity. (d) Looping model. Interactions between PcG complexes at multiple PcG-binding sites cause DNA to be looped out, preventing interaction between the enhancer (E) and the promoter (P).

Figure 3. Models of polycomb group/trithorax group (PcG/trxG) interaction. (a) Binding site competition model. Binding of PcG proteins prevent binding of trxG proteins, so ultrabithorax (Ubx) gene is inactivated (box enclosing cross). (b) Competition at the regulatory DNA model. Both PcG and trxG proteins can occupy regulatory DNA, but only one complex is active, either because PcG proteins inactivate trxG (oval with trxG obliterated) or because there is competition for a limiting factor. (c) Cooperative model. PcG and trxG proteins are needed for activation and repression.