Chromatin remodeller Fun30Fft3 induces nucleosome disassembly to facilitate RNA polymerase II elongation

Junwoo Lee, Eun Shik Choi, Hogyu David Seo, Keunsoo Kang, Joshua M. Gilmore, Laurence Florens, Michael P. Washburn, Joonho Choe, Jerry L. Workman and Daeyoup Lee ()
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Junwoo Lee: Korea Advanced Institute of Science and Technology
Eun Shik Choi: Korea Advanced Institute of Science and Technology
Hogyu David Seo: Korea Advanced Institute of Science and Technology
Keunsoo Kang: Dankook University
Joshua M. Gilmore: Stowers Institute for Medical Research, Kansas City
Laurence Florens: Stowers Institute for Medical Research, Kansas City
Michael P. Washburn: Stowers Institute for Medical Research, Kansas City
Joonho Choe: Korea Advanced Institute of Science and Technology
Jerry L. Workman: Stowers Institute for Medical Research, Kansas City
Daeyoup Lee: Korea Advanced Institute of Science and Technology

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract 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 Fun30Fft3 as a chromatin remodeller, which localizes at transcribing regions to promote RNAPII transcription. Fun30Fft3 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 Fun30Fft3. These data suggest that RNAPII utilizes the chromatin remodeller, Fun30Fft3, to overcome the nucleosome barrier to transcription elongation.

Date: 2017
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DOI: 10.1038/ncomms14527

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