# Refined mechanism of promoter nucleosome-depleted regions resetting after replication

## TL;DR

This study reveals how chromatin structure resets after DNA replication, focusing on the roles of chromatin remodelers and transcription factors in yeast.

## Contribution

The paper identifies a two-step mechanism involving chromatin remodelers and transcription factors for resetting nucleosome-depleted regions post-replication.

## Key findings

- Chromatin remodelers RSC and INO80 are primarily responsible for repositioning nucleosomes after replication.
- Transcription factors Reb1 and Abf1 are not essential for resetting but are crucial for maintaining nucleosome-depleted regions through H3 acetylation.
- A two-step model is proposed for NDR resetting involving chromatin remodelers followed by a combination with transcription factors.

## 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.

Graphical Abstract