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Chromatin Targeting Signals, Nucleosome Positioning Mechanism and Non-Coding RNA-Mediated Regulation of the Chromatin Remodeling Complex NoRC


Tumour cells overexpress ribosomal RNA (rRNA), which is required for ribosome assembly and cell growth. rRNA gene repression is mediated by the chromatin remodeling complex (NoRC) and a non-coding RNA that binds to this enzyme. This study addresses the mechanism of nucleosome positioning by NoRC and the functional role of the non-coding RNA, which is termed pRNA because it corresponds to the promoter sequence. NoRC recognises the promoter nucleosome in a chromatin array with high affinity and uses a release mechanism to position the nucleosome over the transcription initiation site. The pRNA binds specifically to NoRC and inhibits its ATPase activity. We suggest that the RNA retains NoRC at the gene promoter after remodeling, linking its chromatin modification and scaffolding activity to inactive rDNA copies.


Vyšlo v časopise: Chromatin Targeting Signals, Nucleosome Positioning Mechanism and Non-Coding RNA-Mediated Regulation of the Chromatin Remodeling Complex NoRC. PLoS Genet 10(3): e32767. doi:10.1371/journal.pgen.1004157
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.pgen.1004157

Souhrn

Tumour cells overexpress ribosomal RNA (rRNA), which is required for ribosome assembly and cell growth. rRNA gene repression is mediated by the chromatin remodeling complex (NoRC) and a non-coding RNA that binds to this enzyme. This study addresses the mechanism of nucleosome positioning by NoRC and the functional role of the non-coding RNA, which is termed pRNA because it corresponds to the promoter sequence. NoRC recognises the promoter nucleosome in a chromatin array with high affinity and uses a release mechanism to position the nucleosome over the transcription initiation site. The pRNA binds specifically to NoRC and inhibits its ATPase activity. We suggest that the RNA retains NoRC at the gene promoter after remodeling, linking its chromatin modification and scaffolding activity to inactive rDNA copies.


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