A great deal has been learned in recent years about transcription control in eukaryotes. Genes encoding about 2000 activators and repressors can be recognized in the human genome. We now have a glimpse of how the astronomical number of possible combinations of these transcription factors can generate the complexity of gene control required to produce organisms as remarkable as those we see around us. But very much remains to be understood. While we now have some understanding of what processes turn a gene on and off, we have very little understanding of how the frequency of transcription is controlled in order to provide a cell with the appropriate amounts of its various proteins. In a red blood cell precursor, for example, the globin genes are transcribed at a far greater rate than the genes encoding the enzymes of intermediary metabolism. How are the vast differences in the frequency of transcription initiation at various genes achieved? What happens to the multiple interactions between activation domains, co-activator complexes, general transcription factors, and RNA polymerase II when the polymerase initiates transcription and transcribes away from the promoter region? Do these completely dissociate at promoters that are transcribed infrequently, so that the combination of multiple factors required for transcription must be

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