Polycomb Group complexes assemble at polycomb response elements (PREs) in v
ivo and silence genes in the surrounding chromatin, To study the recruitmen
t of silencing complexes, we have targeted various Polycomb Group (PcG) pro
teins by fusing them to the LexA DNA binding domain. When LexA-PC, -PSC, -P
H or -SU(Z)2 are targeted to a reporter gene, they recruit functional PcG-s
ilencing complexes that recapitulate the silencing behavior of a PRE: silen
cing is sensitive to the state of activity of the target chromatin. When th
e target is transcriptionally active, silencing is not established but when
the target is not active at syncytial blastoderm, it becomes silenced. The
repressed state persists through embryonic development but cannot be maint
ained in larval imaginal discs even when the LexA-PcG fusion is constitutiv
ely expressed, suggesting a discontinuity in the mechanism of repression. T
hese proteins also interact with other PC-containing complexes in embryonic
nuclear extracts. In contrast LexA-PHO is neither able to silence nor to i
nteract with PC-containing complexes. Analysis of pho mutant embryos and of
PRE constructs whose PHO-binding sites are mutated suggests that, while PH
O is important for silencing in imaginal discs, it is not necessary for emb
ryonic PcG silencing.