A chromatin-based mechanism for limiting divergent noncoding transcription
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A chromatin-based mechanism for limiting divergent noncoding transcription. / Marquardt, Sebastian; Escalante-Chong, Renan; Pho, Nam; Wang, Jue; Churchman, L Stirling; Springer, Michael; Buratowski, Stephen.
In: Cell, Vol. 157, No. 7, 2014, p. 1712-23.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - A chromatin-based mechanism for limiting divergent noncoding transcription
AU - Marquardt, Sebastian
AU - Escalante-Chong, Renan
AU - Pho, Nam
AU - Wang, Jue
AU - Churchman, L Stirling
AU - Springer, Michael
AU - Buratowski, Stephen
N1 - Copyright © 2014 Elsevier Inc. All rights reserved.
PY - 2014
Y1 - 2014
N2 - In addition to their annotated transcript, many eukaryotic mRNA promoters produce divergent noncoding transcripts. To define determinants of divergent promoter directionality, we used genomic replacement experiments. Sequences within noncoding transcripts specified their degradation pathways, and functional protein-coding transcripts could be produced in the divergent direction. To screen for mutants affecting the ratio of transcription in each direction, a bidirectional fluorescent protein reporter construct was introduced into the yeast nonessential gene deletion collection. We identified chromatin assembly as an important regulator of divergent transcription. Mutations in the CAF-I complex caused genome-wide derepression of nascent divergent noncoding transcription. In opposition to the CAF-I chromatin assembly pathway, H3K56 hyperacetylation, together with the nucleosome remodeler SWI/SNF, facilitated divergent transcription by promoting rapid nucleosome turnover. We propose that these chromatin-mediated effects control divergent transcription initiation, complementing downstream pathways linked to early termination and degradation of the noncoding RNAs.
AB - In addition to their annotated transcript, many eukaryotic mRNA promoters produce divergent noncoding transcripts. To define determinants of divergent promoter directionality, we used genomic replacement experiments. Sequences within noncoding transcripts specified their degradation pathways, and functional protein-coding transcripts could be produced in the divergent direction. To screen for mutants affecting the ratio of transcription in each direction, a bidirectional fluorescent protein reporter construct was introduced into the yeast nonessential gene deletion collection. We identified chromatin assembly as an important regulator of divergent transcription. Mutations in the CAF-I complex caused genome-wide derepression of nascent divergent noncoding transcription. In opposition to the CAF-I chromatin assembly pathway, H3K56 hyperacetylation, together with the nucleosome remodeler SWI/SNF, facilitated divergent transcription by promoting rapid nucleosome turnover. We propose that these chromatin-mediated effects control divergent transcription initiation, complementing downstream pathways linked to early termination and degradation of the noncoding RNAs.
KW - Chromatin
KW - Chromatin Assembly Factor-1
KW - Chromatin Assembly and Disassembly
KW - Gene Expression Regulation, Fungal
KW - Nucleosomes
KW - Promoter Regions, Genetic
KW - RNA Stability
KW - RNA, Fungal
KW - RNA, Untranslated
KW - Saccharomyces cerevisiae
KW - Saccharomyces cerevisiae Proteins
KW - Transcription Termination, Genetic
KW - Transcription, Genetic
KW - Journal Article
KW - Research Support, N.I.H., Extramural
KW - Research Support, Non-U.S. Gov't
U2 - 10.1016/j.cell.2014.04.036
DO - 10.1016/j.cell.2014.04.036
M3 - Journal article
C2 - 24949978
VL - 157
SP - 1712
EP - 1723
JO - Cell
JF - Cell
SN - 0092-8674
IS - 7
ER -
ID: 183164791