Chromatin remodeller Fun30Fft3 induces nucleosome disassembly to facilitate RNA polymerase II elongation
Previous studies have revealed that nucleosomes impede elongation of RNA polymerase II (RNAPII). Recent observations suggest a role for ATP-dependent chromatin remodellers in modulating this process, but direct in vivo evidence for this is unknown. Here using fission yeast, we identify Fun30 Fft3 as...
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Published in | Nature communications Vol. 8; no. 1; p. 14527 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
20.02.2017
Nature Publishing Group Nature Portfolio |
Subjects | |
Online Access | Get full text |
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Summary: | Previous studies have revealed that nucleosomes impede elongation of RNA polymerase II (RNAPII). Recent observations suggest a role for ATP-dependent chromatin remodellers in modulating this process, but direct
in vivo
evidence for this is unknown. Here using fission yeast, we identify Fun30
Fft3
as a chromatin remodeller, which localizes at transcribing regions to promote RNAPII transcription. Fun30
Fft3
associates with RNAPII and collaborates with the histone chaperone, FACT, which facilitates RNAPII elongation through chromatin, to induce nucleosome disassembly at transcribing regions during RNAPII transcription. Mutants, resulting in reduced nucleosome-barrier, such as deletion mutants of histones H3/H4 themselves and the genes encoding components of histone deacetylase Clr6 complex II suppress the defects in growth and RNAPII occupancy of cells lacking Fun30
Fft3
. These data suggest that RNAPII utilizes the chromatin remodeller, Fun30
Fft3
, to overcome the nucleosome barrier to transcription elongation.
Nucleosomes have been shown to impede the elongation of RNA polymerase II during transcription. Here, the authors provide evidence that in fission yeast chromatin remodeller Fun30
Fft3
localizes to transcribing regions to promote transcription by nucleosome disassembly
in vivo
. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work |
ISSN: | 2041-1723 2041-1723 |
DOI: | 10.1038/ncomms14527 |