Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo

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Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo. / Kristjuhan, Arnold; Svejstrup, Jesper Q.

In: EMBO Journal, Vol. 23, No. 21, 27.10.2004, p. 4243-4252.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Kristjuhan, A & Svejstrup, JQ 2004, 'Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo', EMBO Journal, vol. 23, no. 21, pp. 4243-4252. https://doi.org/10.1038/sj.emboj.7600433

APA

Kristjuhan, A., & Svejstrup, J. Q. (2004). Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo. EMBO Journal, 23(21), 4243-4252. https://doi.org/10.1038/sj.emboj.7600433

Vancouver

Kristjuhan A, Svejstrup JQ. Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo. EMBO Journal. 2004 Oct 27;23(21):4243-4252. https://doi.org/10.1038/sj.emboj.7600433

Author

Kristjuhan, Arnold ; Svejstrup, Jesper Q. / Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo. In: EMBO Journal. 2004 ; Vol. 23, No. 21. pp. 4243-4252.

Bibtex

@article{c407fef9a5084c95aaff5d7c2164bfac,
title = "Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo",
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.",
keywords = "ELP3, GAL1, GCN5, Histone acetylation, Transcript elongation",
author = "Arnold Kristjuhan and Svejstrup, {Jesper Q.}",
year = "2004",
month = oct,
day = "27",
doi = "10.1038/sj.emboj.7600433",
language = "English",
volume = "23",
pages = "4243--4252",
journal = "E M B O Journal",
issn = "0261-4189",
publisher = "Wiley-Blackwell",
number = "21",

}

RIS

TY - JOUR

T1 - Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo

AU - Kristjuhan, Arnold

AU - Svejstrup, Jesper Q.

PY - 2004/10/27

Y1 - 2004/10/27

N2 - 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.

AB - 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.

KW - ELP3

KW - GAL1

KW - GCN5

KW - Histone acetylation

KW - Transcript elongation

U2 - 10.1038/sj.emboj.7600433

DO - 10.1038/sj.emboj.7600433

M3 - Journal article

C2 - 15457216

AN - SCOPUS:9144274420

VL - 23

SP - 4243

EP - 4252

JO - E M B O Journal

JF - E M B O Journal

SN - 0261-4189

IS - 21

ER -

ID: 331040576