Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
Standard
Evidence for distinct mechanisms facilitating transcript elongation through chromatin in vivo. / Kristjuhan, Arnold; Svejstrup, Jesper Q.
I: EMBO Journal, Bind 23, Nr. 21, 27.10.2004, s. 4243-4252.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
Harvard
APA
Vancouver
Author
Bibtex
}
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