# DNA replication recruits a friend to overcome a challenging break-up

**Authors:** James M Dewar

PMC · DOI: 10.1038/s44318-024-00204-3 · 2024-08-21

## TL;DR

This paper explains how leftover DNA replication complexes can block new replication and how cells use specific proteins to resolve this issue.

## Contribution

The study reveals the biochemical mechanisms by which leftover replisomes are removed to allow new DNA replication.

## Key findings

- Leftover replisomes hinder the next round of DNA replication.
- Specific helicases help overcome the problem caused by leftover replisomes.

## Abstract

Replication complexes, or replisomes, are removed from DNA upon completion of DNA synthesis, but the importance of replisome removal, as well as how cells might respond to defects in this process, has remained elusive. New work by Polo Rivera et al (2024) and Olson et al (2024) reveals that leftover replisomes are an obstacle to replication and provides a first glimpse into the biochemical mechanisms that solve this problem.

Two recent articles reveal that leftover replisome impede the next round of replication, and how specific helicases can help to overcome this problem.

## Full-text entities

- **Genes:** DIA2 (DNA-binding SCF ubiquitin ligase subunit DIA2) [NCBI Gene 854247] {aka YOR29-31}, RRM3 (DNA helicase) [NCBI Gene 856426] {aka RTT104}, MCM7 (DNA replication licensing factor MCM7) [NCBI Gene 852501] {aka CDC47}, PIF1 (DNA helicase PIF1) [NCBI Gene 854941] {aka TST1}
- **Species:** Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932], Homo sapiens (human, species) [taxon 9606], Xenopus laevis (African clawed frog, species) [taxon 8355]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11405838/full.md

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Source: https://tomesphere.com/paper/PMC11405838