Abstract
Changes in histone acetylation at promoters correlate with transcriptional activation and repression, but whether acetylation of histones in the coding region of genes is important for transcription is less clear. Here, we show that cells lacking the histone acetyltransferases Gcn5 and Elp3 have widespread and severe histone H3 hypoacetylation in chromatin. Surprisingly, severe hypoacetylation in the promoter does not invariably affect the ability of TBP to bind the TATA element, or transcription of the gene. By contrast, similar hypoacetylation of the coding region correlates with inhibition of transcription, and inhibition correlates better with the overall charge of the histone H3 tail than with hypoacetylation of specific lysine residues. These data provide insights into the effects of histone H3 hypoacetylation in vivo and underscore the importance of the overall charge of the histone tail for transcription.
| Original language | English |
|---|---|
| Journal | Molecular Cell |
| Volume | 10 |
| Issue number | 4 |
| Pages (from-to) | 925-933 |
| Number of pages | 9 |
| ISSN | 1097-2765 |
| DOIs | |
| Publication status | Published - 1 Oct 2002 |
| Externally published | Yes |
Bibliographical note
Funding Information:This work was supported by grants from Cancer Research UK and the EU (HPRN-CT-2000-00087) to J.Q.S., by Public Health Service Grant of the National Institutes of Health (NIH) GM23674 to M.G., and by Public Health Service Grant of the NIH GM60415 and support of core facilities by NIH (CA24014) to B.R.C. We thank Kevin Struhl and Alain Verreault for gifts of yeast strains and antibody, respectively. Tomas Lindahl and Alain Verreault are thanked for comments on the manuscript. Cancer Research UK London Research Institute comprises the Lincoln's Inn Fields and Clare Hall Laboratories of the former Imperial Cancer Research Fund following the merger of the ICRF with the Cancer Research Campaign in February 2002.
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