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Most of the genome of the African trypanosome Trypanosoma brucei is organized in long constitutively transcribed polycistronic units, whose transcription by RNA polymerase II does not appear to be regulated. Variant surface glycoprotein (VSG) expression sites (ESs) are an exception: the active VSG is transcribed by RNA polymerase I in a monoallelic fashion from 1 of about 15 telomeric ES transcription units. It is unclear how the “counting mechanism” behind ES control operates. The chromatin of active and silent ESs was previously thought to have a similar nucleosome distribution. Because of the possible importance of chromatin structure in regulating ES transcription, this issue has been reinvestigated with methods that were not available at the time of the original studies. Figueiredo and Cross (p. 148) and Stanne and Rudenko (p. 136) now demonstrate that the active ESs have a very different chromatin structure compared with the silent ESs. Using various chromatin analysis techniques, including immunoprecipitation with antihistone antibodies (ChIP), formaldehyde-assisted isolation of regulatory elements (FAIRE), and analysis of micrococcal-nuclease-digested chromatin by quantitative PCR or Southern blotting, they show that the active ES is greatly depleted of nucleosomes. This difference in chromatin structure could provide a level of epigenetic regulation underlying the heritability of active and/or silent transcriptional states.