How do the different yeast HAT complexes
(ADA, SAGA, NuA3 and NuA4) regulate transcription from specific
promoters in the context of cellular chromatin? We have shown that,
under competitive in vitro conditions, the activator-mediated
targeting of the histone acetyl transferase activity of SAGA and NuA4
to specific chromatin templates is required for their ability to
stimulate transcription. Interestingly, 'scanning' ChIP assays reveal
a different pattern of acetylation by SAGA and NuA4 upon recruitment:
while acetylation by SAGA is highest at nucleosomes flanking the
activator binding sites, and thereafter sharply decreases in each
direction, NuA4 acetylation is less localized and spreads over a
larger chromatin domain. We are currently investigating whether this
difference is due to potentially different mechanistic properties of
the two HAT complexes, and how it relates to their ability to
stimulate transcription from chromatin templates.
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