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Histone acetylation and chromatin remodeling: which comes first?

https://doi.org/10.1016/S1096-7192(02)00014-8Get rights and content

Introduction

The packaging of DNA into chromatin prevents access of the transcription machinery necessary to regulate gene expression. To overcome this repressive barrier, the cell contains numerous, multi-subunit chromatin-remodeling enzymes, which work to loosen and open up chromatin structure. The SWI/SNF complex is a multi-subunit, ATP-dependent chromatin-remodeling machine. It is able to use the energy of ATP hydrolysis to alter histone–DNA contacts, and in many cases, leads to movement of the histone octamer along DNA or to transfer of the octamer to another chromosome (for reviews, see [1], [2]). The SAGA complex represents a second class of chromatin-remodeling complexes, histone acetyltransferases (HATs), which covalently modify the amino terminal tails of the histone proteins, possibly leading to alteration of histone–DNA or histone–histone interactions. The multi-subunit SAGA complex contains the yeast Gcn5 protein that possesses its catalytic activity, and has many components that were previously described as being involved in transcription regulation, including Ada, Spt, and Taf proteins (for review, see [3]).

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Evidence for functional interplay between SWI/SNF and SAGA

Over the last few years, evidence for a functional interaction between SWI/SNF and HAT complexes, and in particular the SAGA complex, has accumulated. Many inducible genes whose expression is dependent on the yeast SWI/SNF complex also have been found to be dependent on Gcn5. These genes include INO1, HO, SUC2, HIS3, and Ty elements [4], [5], [6], [7], [8]. Moreover, GCN5 and genes encoding SWI/SNF components exhibit similar genetic interactions with chromatin components. Mutations in the SIN1

Histone acetylation precedes chromatin remodeling

A recent study in support of acetylation before remodeling indicated that acetylation acts as a signal for ATP-dependent remodeling complexes at the PHO8 promoter [24]. Using in vivo chromatin immunoprecipitation, it was shown that when chromatin remodeling was blocked at the PHO8 promoter by inactivation or deletion of Swi2/Snf2, there was a peak of hyperacetylation (both H3 and H4) at the promoter. If remodeling was allowed to go to completion (i.e., in a wild-type yeast strain), the

Chromatin remodeling precedes histone acetylation

It is possible that ATP-dependent remodeling occurs prior to acetylation at some promoters. Some recent studies have found that this seems to be the case at the yeast HO promoter [30], [31]. Furthermore, many genes that are expressed in mitosis were shown to require remodeling before recruitment of HAT activity and efficient expression of the genes [15]. In studies of the HO promoter, in vivo chromatin immunoprecipitation assays demonstrated that the binding of the Swi5 activator to its site in

Conclusions

It seems likely that the recruitment and action of SWI/SNF and HAT complexes at promoters will turn out to be promoter specific, possibly depending on when the gene is most highly expressed during the cell division cycle. Future studies that focus on other genes that are both SWI/SNF-dependent and HAT-dependent will give us a better understanding of the interplay between these chromatin-modifying complexes at target promoters.

Acknowledgments

The work was supported by NIGMS Grant R37 GM47867 to J.L.W. J.L.W. is an Associate Investigator of the Howard Hughes Medical Institute.

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    Present address: Department of Cell Biology and Physiology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, USA.

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