Nucleosome occupancy within chromatin can affect transcription in a number of ways, from regulating access to transcription factors to posing a barrier to RNA-polymerase elongation. Spt6 is one of multiple histone chaperones involved in the intricate balance between nucleosome deposition and eviction that occurs during transcription. Previous studies have shown that loss of Spt6 results in preferential reduction of nucleosome occupancy on highly transcribed genes, and that the resultant loss of histones can also derepress certain promoters. In a recent study, Bentley and colleagues investigated how Spt6 affects histones and RNA polymerase II (Pol II) occupancy genome wide in the budding yeast Saccharomyces cerevisiae, using a rapidly inactivated Spt6-degron mutant. The key finding is the observation that, upon spt6 inactivation, histone loss—particularly toward the 5′ end of genes—was greater at genes with closed promoters than at those with open promoters, within a subset of genes exhibiting similar Pol II occupancy. Promoter-swap experiments confirmed that histone occupancy within the bodies of genes was determined by the promoters themselves; thus, promoters could confer occupancy levels associated with their respective endogenous genes to unrelated downstream sequences. The precise mechanism by which promoters dictate the level of downstream histone occupancy remains to be determined but probably involves factors such as polymerase density and rates of initiation and/or elongation. Indeed, the authors suggest that closed promoters, which contain TATA boxes and are associated with transcriptional bursting and noisy expression, might be more effective at evicting nucleosomes. Regardless of the ultimate mechanism, the study by Bentley and colleagues uncovered an interesting new element of chromatin biology, which should stimulate further investigations of gene-specific nucleosome dynamics. (EMBO J. doi:10.1038/emboj.2013.194, 6 September 2013)