ArticleNucleic acids research2025
Refined mechanism of promoter nucleosome-depleted regions resetting after replication.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Nonlinearities and Switch-Like Behavior in Gene Expression: From Genetics to Biochemistry and Back.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Newly synthesized histones: passive or active players in the regulation of epigenetic inheritance?Nucleic acids research · 2026Review
- Epigenetic regulation of metabolism in Saccharomyces cerevisiae: mechanisms, metabolic crosstalk, and engineering applications.Molecular biology reports · 2026Review
- Article
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4 authors.
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Abstract
Replication disrupts chromatin organization. Thus, the rapid resetting of nucleosome positioning is essential to maintain faithful gene expression. The initial step of this reconfiguration occurs at nucleosome-depleted regions (NDRs). While studies have elucidated the role of transcription factors (TFs) and chromatin remodelers (CRs) in vitro or in maintaining NDRs in vivo, none has addressed their in vivo function shortly after replication. Through purification of nascent chromatin in yeast, we dissected the choreography of events governing the proper positioning of the -1/+1 nucleosomes flanking promoter NDRs. Our findings reveal that CRs are the primary contributors of -1/+1 repositioning post-replication, with RSC (Remodeling the Structure of Chromatin) acting upstream of INO80. Surprisingly, while Reb1 and Abf1 TFs are not essential for NDR resetting, they are required for NDR maintenance via the promotion of H3 acetylations. Altogether, we propose a two-step model for NDR resetting in Saccharomyces cerevisiae: first, CRs alone reset promoter NDRs after replication, while a combination of TFs and CRs is required for subsequent maintenance.
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