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Molecular and Cellular Biology, September 2002, p. 6406-6416, Vol. 22, No. 18
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.18.6406-6416.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Targeted Histone Acetylation at the Yeast CUP1 Promoter Requires the Transcriptional Activator, the TATA Boxes, and the Putative Histone Acetylase Encoded by SPT10

Chang-Hui Shen, Benoit P. Leblanc,,{dagger} Carolyn Neal,,{ddagger} Ramin Akhavan, and David J. Clark*

Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-8028

Received 30 April 2002/ Returned for modification 5 June 2002/ Accepted 18 June 2002

The relationship between chromatin remodeling and histone acetylation at the yeast CUP1 gene was addressed. CUP1 encodes a metallothionein required for cell growth at high copper concentrations. Induction of CUP1 with copper resulted in targeted acetylation of both H3 and H4 at the CUP1 promoter. Nucleosomes containing upstream activating sequences and sequences farther upstream were the targets for H3 acetylation. Targeted acetylation of H3 and H4 required the transcriptional activator (Ace1p) and the TATA boxes, suggesting that targeted acetylation occurs when TATA-binding protein binds to the TATA box or at a later stage in initiation. We have shown previously that induction results in nucleosome repositioning over the entire CUP1 gene, which requires Ace1p but not the TATA boxes. Therefore, the movement of nucleosomes occurring on CUP1 induction is independent of targeted acetylation. Targeted acetylation of both H3 and H4 also required the product of the SPT10 gene, which encodes a putative histone acetylase implicated in regulation at core promoters. Disruption of SPT10 was lethal at high copper concentrations and correlated with slower induction and reduced maximum levels of CUP1 mRNA. These observations constitute evidence for a novel mechanism of chromatin activation at CUP1, with a major role for the TATA box.

* Corresponding author. Mailing address: Laboratory of Cellular and Developmental Biology (NIDDK), National Institutes of Health, Bldg. 50, Rm. 3148, 50 South Dr., Bethesda, MD 20892-8028. Phone: (301) 496-6966. Fax: (301) 496-5239. E-mail: djclark{at}helix.nih.gov.

{dagger} Present address: Geneka Biotechnology, Montréal, QC, Canada H2H 2S5.

{ddagger} Present address: Russell Labs, Madison WI 53706.

Molecular and Cellular Biology, September 2002, p. 6406-6416, Vol. 22, No. 18
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.18.6406-6416.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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