Maintenance of homeotic gene expression during Drosophila development relies on the Polycomb and the trithorax groups of genes. Classically, the Polycomb proteins act as repressors of homeotic gene function, whereas trithorax proteins function as activators. However, recent investigation has indicated that some of these maintenance genes may act both as repressors and activators. One of those is the Drosophila Trithorax-like gene that codes for the GAGA factor. To investigate its dual activator/repressor role, we have studied the function of the Trithorax-like throughout Drosophila development. Embryos lacking both the maternal and the zygotic Trithorax-like function do not develop suggesting that Trithorax-like might be required in oogenesis. Homozygous Trithorax-like null mutant embryos show reduced expression levels of some of the homeotic proteins. Trithorax-like mutant larval clones, however, do not show phenotypes indicative of either activation or repression of homeotic gene function. These results suggest that Trithorax-like is required during embryogenesis but not throughout larval development for the regulation of homeotic gene expression. Moreover, this temporal requirement seems also to regulate MCP-mediated silencing. Finally, lack of Trithorax-like function modulates the gain of function phenotypes caused by over-expression of homeotic genes. To explain Trithorax-like gene function, we propose a model where very early in development, GAGA factor probably establishes a chromatin ground state for transcription. The differential "on/off" transcriptional state of the homeotic genes is then established and propagated by the action of the specific regulatory proteins independently of the GAGA factor. We also suggest that GAGA factor may not have a dual activator/repressor function. Rather, Trithorax-like mutations may produce dual loss of activation and loss of repression effects.