High-resolution visualization of H3 variants during replication reveals their controlled recycling

Camille Clément, Guillermo A. Orsi, Alberto Gatto, Ekaterina Boyarchuk, Audrey Forest, Bassam Hajj, Judith Miné-Hattab, Mickaël Garnier, Zachary A. Gurard-Levin, Jean-Pierre Quivy and Geneviève Almouzni ()
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Camille Clément: Equipe Labellisée Ligue contre le Cancer
Guillermo A. Orsi: Equipe Labellisée Ligue contre le Cancer
Alberto Gatto: Equipe Labellisée Ligue contre le Cancer
Ekaterina Boyarchuk: Equipe Labellisée Ligue contre le Cancer
Audrey Forest: Equipe Labellisée Ligue contre le Cancer
Bassam Hajj: Laboratoire Physico-Chimie
Judith Miné-Hattab: UMR3664
Mickaël Garnier: UMR3664
Zachary A. Gurard-Levin: Equipe Labellisée Ligue contre le Cancer
Jean-Pierre Quivy: Equipe Labellisée Ligue contre le Cancer
Geneviève Almouzni: Equipe Labellisée Ligue contre le Cancer

Nature Communications, 2018, vol. 9, issue 1, 1-17

Abstract: Abstract DNA replication is a challenge for the faithful transmission of parental information to daughter cells, as both DNA and chromatin organization must be duplicated. Replication stress further complicates the safeguard of epigenome integrity. Here, we investigate the transmission of the histone variants H3.3 and H3.1 during replication. We follow their distribution relative to replication timing, first in the genome and, second, in 3D using super-resolution microscopy. We find that H3.3 and H3.1 mark early- and late-replicating chromatin, respectively. In the nucleus, H3.3 forms domains, which decrease in density throughout replication, while H3.1 domains increase in density. Hydroxyurea impairs local recycling of parental histones at replication sites. Similarly, depleting the histone chaperone ASF1 affects recycling, leading to an impaired histone variant landscape. We discuss how faithful transmission of histone variants involves ASF1 and can be impacted by replication stress, with ensuing consequences for cell fate and tumorigenesis.

Date: 2018
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DOI: 10.1038/s41467-018-05697-1

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