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New histone supply regulates replication fork speed and PCNA unloading.

Jakob Mejlvang1, Yunpeng Feng, Constance Alabert

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DNA replication speed depends on histone supply for chromatin assembly. Delayed histone production slows replication forks and PCNA unloading, maintaining genome stability during histone shortages.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Epigenetics

Background:

  • DNA replication and chromatin assembly are crucial for genome stability.
  • The coordination between DNA synthesis and histone provision for new chromatin is not fully understood.

Purpose of the Study:

  • To investigate the relationship between histone supply, DNA replication fork speed, and nucleosome assembly.
  • To understand the role of PCNA (proliferating cell nuclear antigen) in response to histone deficiency.

Main Methods:

  • Inhibition of canonical histone biosynthesis.
  • Analysis of replication fork progression and nucleosome occupancy.
  • Investigating PCNA accumulation and unloading dynamics.
  • In vitro and in vivo assays.

Main Results:

  • Histone biosynthesis inhibition slowed replication fork progression and reduced nucleosome occupancy.
  • Replication forks remained stable initially but prolonged histone deficiency caused DNA damage.
  • PCNA accumulated on newly synthesized DNA, and its unloading was delayed without nucleosome assembly.

Conclusions:

  • Replication fork speed is coupled to new histone supply and nucleosome assembly.
  • Delayed PCNA unloading in histone-deficient cells suggests a mechanism to facilitate chromatin assembly.
  • This coupling ensures DNA replication and chromatin integrity during transient histone shortages.