Chromatin remodeling and transcriptional activation: the cast (in order of appearance)

FD Urnov, AP Wolffe - Oncogene, 2001 - nature.com
FD Urnov, AP Wolffe
Oncogene, 2001nature.com
The number of chromatin modifying and remodeling complexes implicated in genome
control is growing faster than our understanding of the functional roles they play. We discuss
recent in vitro experiments with biochemically defined chromatin templates that illuminate
new aspects of action by histone acetyltransferases and ATP-dependent chromatin
remodeling engines in facilitating transcription. We review a number of studies that present
an 'ordered recruitment'view of transcriptional activation, according to which various …
Abstract
The number of chromatin modifying and remodeling complexes implicated in genome control is growing faster than our understanding of the functional roles they play. We discuss recent in vitro experiments with biochemically defined chromatin templates that illuminate new aspects of action by histone acetyltransferases and ATP-dependent chromatin remodeling engines in facilitating transcription. We review a number of studies that present an ‘ordered recruitment’view of transcriptional activation, according to which various complexes enter and exit their target promoter in a set sequence, and at specific times, such that action by one complex sets the stage for the arrival of the next one. A consensus emerging from all these experiments is that the joint action by several types of chromatin remodeling machines can lead to a more profound alteration of the infrastructure of chromatin over a target promoter than could be obtained by these enzymes acting independently. In addition, it appears that in specific cases one type of chromatin structure alteration (eg, histone hyperacetylation) is contingent upon prior alterations of a different sort (ie, ATP-dependent remodeling of histone-DNA contacts). The striking differences between the precise sequence of action by various cofactors observed in these studies may be–at least in part–due to differences between the specific promoters studied, and distinct requirements exhibited by specific loci for chromatin remodeling based on their pre-existing nucleoprotein architecture.
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