Updated project metadata. Chromatin organization must be maintained during cell proliferation to preserve cellular identity and genome integrity. However, DNA replication results in transient displacement of DNA bound proteins, and it is unclear how they regain access to newly replicated DNA. Using quantitative MS-based proteomics coupled to Nascent Chromatin Capture, we provide time resolved binding kinetics for thousands of proteins behind replisomes of mid-S replicated regions. This shows that most proteins regain access within the first 15 minutes after the passage of the fork. In contrast, 25% of the identified proteins do not, and this delay cannot be inferred from their known function, physicochemical properties, or nuclear abundance. A sample treated with nocodazole to block the cell cycle progression. The comparison between a normal cell cycle progression and a nocodazole treated sample shows that the reassociation onto chromatin of proteins with a delayed restoration can be regulated by the cell cycle progression and/or the post-replication time. In addition, we provide evidence that DNA replication not only disrupts but also promotes recruitment of transcription factors and chromatin remodellers, providing a significant advance in understanding how DNA replication could contribute to programmed changes of cell memory. Data available in this entry are related with the supplementary table 5 from our manuscript.