Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo.
EMBO J
; 23(21): 4243-52, 2004 Oct 27.
Article
em En
| MEDLINE
| ID: mdl-15457216
ABSTRACT
The mechanism and kinetics of RNA polymerase II transcription and histone acetylation were studied by chromatin immunoprecipitation in yeast. Our results indicate that a significant fraction of polymerases starting transcription never make it to the end of a long GAL-VPS13 fusion gene. Surprisingly, induction of GAL genes results in substantial loss of histone-DNA contacts not only in the promoter but also in the coding region. The loss of nucleosomes is dependent on active transcript elongation, but apparently occurs independently of histone acetylation. In contrast, histones in genes previously shown to require the histone acetyltransferases GCN5 and ELP3 for normal transcription do not lose DNA contacts, but do become acetylated as a result of transcription. Together, these results suggest the existence of at least two distinct mechanisms to achieve efficient transcript elongation through chromatin a pathway based on loss of histone-DNA contacts, and a histone acetylation-dependent mechanism correlating with little or no net loss of nucleosomes.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Transcrição Gênica
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RNA Polimerase II
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Cromatina
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Regulação da Expressão Gênica
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article