Chromatin remodelling at the PHO8 promoter requires SWI–SNF and SAGA at a step subsequent to activator binding

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Abstract
The SWI–SNF and SAGA complexes possess ATP‐dependent nucleosome remodelling activity and histone acetyltransferase (HAT) activity, respectively. Mutations that eliminate the ATPase activity of the SWI–SNF complex, or the HAT activity of SAGA, abolish proper chromatin remodelling at the PHO8 promoter in vivo . These effects are mechanistically distinct, since the absence of SWI–SNF freezes chromatin in the repressed state, while the absence of Gcn5 permits a localized perturbation of chromatin structure immediately adjacent to the upstream transactivator binding site. However, this remodelling is not propagated to the proximal promoter, and no activation is observed under all conditions. Furthermore, Pho4 is bound to the PHO8 promoter in the absence of Snf2 or Gcn5, confirming a role for SWI–SNF and SAGA in chromatin remodelling independent of activator binding. These data provide new insights into the roles of the SWI–SNF and SAGA complexes in chromatin remodelling in vivo .