ATP-dependent chromatin remodeling complexes play a critical role in chromatin 
dynamics. A large number of in vitro studies have pointed towards nucleosome 
sliding as the principal remodeling outcome of SWI/SNF action, whereas few have 
described histone octamer transfer as the principal outcome. In contrast, recent 
in vivo studies have linked the activity of SWI/SNF to histone eviction in trans 
from gene promoters. In this study, we have found that the chimeric 
transcription factor Gal4-VP16 can enhance SWI/SNF histone octamer transfer 
activity, resulting in targeted histone eviction from a nucleosome probe. This 
effect is dependent on the presence of the activation domain. We observed that 
under conditions mimicking the in vivo relative abundance of SWI/SNF with 
respect to the total number of nucleosomes in a cell nucleus, the accessibility 
of the transcription factor binding site is the first determinant in the 
sequence of events leading to nucleosome remodeling. We propose a model 
mechanism for this transcription factor-mediated enhancement of SWI/SNF octamer 
transfer activity.