CMMs may be thought of as switchable elements able to induce and heritably propagate both silenced and open chromatin conformations. The respective chromatin status determined by a regulatory cascade of transcription factors during early embryogenesis might be the primary switch. In the embryo, the zygotic genome has to develop different spatial patterns of homeotic gene expression. Therefore, the developing embryo must be able to erase the epigenetic information of its parental gametes in order to allow differentiation of a variety of cell lineages. As such, in the early zygote the occupation of all CMMs by PcG proteins would be retained, perpetuating silencing as the default state.
Recent evidence speaks in favor of such a mechanism.
In somatic cells, differential transcription induced by patterning factors would switch CMMs into the active mode, which would then be heritably maintained in subsequent cell generations. In the particular transgene combination used in this study, the strong GAL4 induction might have completely removed the PcG-silencing tag from this PRE, which subsequently remains in the active state through several rounds of mitotic and meiotic divisions until it becomes reinactivated by stochastic processes. The Drosophila Polycomb and trithorax group proteins act through chromosomal elements such as Fab-7 to maintain repressed or active gene expression, respectively. A Fab-7 element is switched from a silenced to a mitotically heritable active state by an embryonic pulse of transcription. Here, histone H4 hyperacetylation has been found to be associated with Fab-7 after activation, suggesting that H4 hyperacetylation may be a heritable epigenetic tag of the activated element.