Cell cycle-dependent chromatin motion: a role for DNA content doubling over cohesion.
- 1University of Toulouse, CNRS, Centre de Biologie Intégrative (CBI), 165 Rue Marianne Grunberg Manago, 31400 Toulouse, France.
- 2University of Toulouse, CNRS, Laboratoire de Physique Théorique, Bât. 3R1B4, 118 route de Narbonne, 31062 Toulouse Cedex 04, France.
Abstract
The spatiotemporal organization of chromatin in the eukaryotic nucleus is fundamental for genome regulation. Chromatin undergoes rapid remodelling and rearrangements within minutes, altering its diffusion properties. Considering the tight coupling between genome function and nuclear architecture, a key question is how chromatin dynamics adapt to or promote nuclear processes. To elucidate the underlying physical principles, we employed high-resolution diffusion mapping (Hi-D) to track chromatin motion throughout interphase in live human cells. Our analysis, that considers both diffusive motion and drift generated by active forces, revealed that chromatin dynamics are heterogeneous, with distinct behaviours in different subnuclear zones. Notably, both diffusive and processive contributions to chromatin motion progressively decrease from G1 to G2 phase, with this reduction occurring uniformly across all subzones. This suggests a global mechanism driving the observed decrease in chromatin mobility during cell cycle progression. By combining genetic knockout experiments and polymer modelling, we demonstrate that the doubling of DNA content, rather than cohesin-mediated sister chromatid entrapment, is responsible for the gradual decrease in chromatin motion during the cell cycle in human nuclei. These findings provide new insights into the physical and functional organization of chromatin and its regulation during cellular proliferation.
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BibTeX
@article{reymillet2026cell,
title = {{Cell cycle-dependent chromatin motion: a role for DNA content doubling over cohesion.}},
author = {Martin Rey-Millet and Léa Costes and Erwan Le Floch and Habib Ayoub and Quentin Saccomani and Manoel Manghi and Kerstin Bystricky},
journal = {Nucleic acids research},
year = {2026},
month = sep,
doi = {10.1093/nar/gkag951},
url = {https://europepmc.org/article/MED/42847246},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Cell cycle-dependent chromatin motion: a role for DNA content doubling over cohesion.
AU - Martin Rey-Millet
AU - Léa Costes
AU - Erwan Le Floch
AU - Habib Ayoub
AU - Quentin Saccomani
AU - Manoel Manghi
AU - Kerstin Bystricky
PY - 2026
DA - 2026/09/01
JO - Nucleic acids research
DO - 10.1093/nar/gkag951
UR - https://europepmc.org/article/MED/42847246
AB - The spatiotemporal organization of chromatin in the eukaryotic nucleus is fundamental for genome regulation. Chromatin undergoes rapid remodelling and rearrangements within minutes, altering its diffusion properties. Considering the tight coupling between genome function and nuclear architecture, a key question is how chromatin dynamics adapt to or promote nuclear processes. To elucidate the underlying physical principles, we employed high-resolution diffusion mapping (Hi-D) to track chromatin motion throughout interphase in live human cells. Our analysis, that considers both diffusive motion and drift generated by active forces, revealed that chromatin dynamics are heterogeneous, with distinct behaviours in different subnuclear zones. Notably, both diffusive and processive contributions to chromatin motion progressively decrease from G1 to G2 phase, with this reduction occurring uniformly across all subzones. This suggests a global mechanism driving the observed decrease in chromatin mobility during cell cycle progression. By combining genetic knockout experiments and polymer modelling, we demonstrate that the doubling of DNA content, rather than cohesin-mediated sister chromatid entrapment, is responsible for the gradual decrease in chromatin motion during the cell cycle in human nuclei. These findings provide new insights into the physical and functional organization of chromatin and its regulation during cellular proliferation.
SN - 0305-1048
SN - 1362-4962
ER -