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.
Highlights
Previous studies have revealed that nucleosomes impede elongation of RNA polymerase II (RNAPII)
RNAPII is differentially phosphorylated at its C-terminal repeat domain (CTD) during different stages of transcription: it is phosphorylated at Ser[5] (CTDS5P) during transcription initiation[30], but becomes phosphorylated at Ser[2] (CTDS2P) on the transition to elongation[31]
The nucleosome landscape of a typical eukaryotic gene includes a nucleosome-depleted region (NDR) or unstable nucleosomes at the promoter followed by well-positioned nucleosomes over the transcribing regions that are aligned with the transcription start site
Summary
Previous studies have revealed that nucleosomes impede elongation of RNA polymerase II (RNAPII). Mutants, resulting in reduced nucleosome-barrier, such as deletion mutants of histones H3/H4 themselves and the genes encoding components of histone deacetylase Clr[6] complex II suppress the defects in growth and RNAPII occupancy of cells lacking Fun30Fft[3] These data suggest that RNAPII utilizes the chromatin remodeller, Fun30Fft[3], to overcome the nucleosome barrier to transcription elongation. We show that a histone gene knockdown rescues the defects of RNAPII occupancy at transcribing regions in cells lacking Fun30Fft[3] These results suggest that Fun30Fft[3] plays a major role in nucleosome disassembly during RNAPII elongation, which facilitates the efficient passage of RNAPII through chromatin templates during transcription elongation
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