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BAHCC1 binds H4K20me1 to facilitate the MCM complex loading and DNA replication.

Dongxu Li1,2, Zhi-Min Zhang3,4, Liu Mei1

  • 1Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.

Nature Communications
|July 1, 2025
PubMed
Summary

The BAHCC1 tandem Tudor domain (TTD) reads histone H4K20me1, facilitating DNA replication origin activation. This interaction recruits the MCM complex, crucial for cell cycle progression and DNA repair.

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Area of Science:

  • Epigenetics and chromatin biology
  • Molecular mechanisms of DNA replication
  • Cell cycle regulation

Background:

  • Histone modifications, such as mono-methylation of histone H4 lysine 20 (H4K20me1), play critical roles in regulating fundamental cellular processes.
  • The precise mechanisms by which H4K20me1 influences DNA replication, cell cycle progression, and DNA damage repair are not fully understood.

Purpose of the Study:

  • To elucidate the role of the BAHCC1 tandem Tudor domain (BAHCC1TTD) in recognizing H4K20me1.
  • To investigate how BAHCC1TTD-mediated H4K20me1 recognition facilitates DNA replication origin activation and overall DNA replication.

Main Methods:

  • Biochemical assays to assess protein-protein interactions and binding specificity.
  • Structural biology to determine the interaction interface between BAHCC1TTD and H4K20me1.
  • Genomic analyses to map recruitment sites and assess genome-wide effects.
  • Cellular experiments to evaluate the impact of BAHCC1 depletion or BAHCC1TTD:H4K20me1 interaction disruption on DNA replication and cell cycle progression.

Main Results:

  • BAHCC1TTD selectively binds to H4K20me1, distinguishing it from other methylation states.
  • BAHCC1TTD facilitates the recruitment of BAHCC1 and the Mini-chromosome Maintenance (MCM) complex to replication origins.
  • The interaction between BAHCC1TTD and H4K20me1, alongside the Origin Recognition Complex (ORC) reading H4K20me2, is essential for MCM loading and replication origin activation.
  • Depletion of BAHCC1 or disruption of the BAHCC1TTD:H4K20me1 interaction impairs MCM loading, leading to replication defects and cell cycle progression issues.

Conclusions:

  • BAHCC1TTD acts as a key effector that translates H4K20me1 signals into the recruitment of the MCM complex.
  • This mechanism is vital for efficient DNA replication origin activation and subsequent cell cycle progression.
  • The study reveals a novel epigenetic regulatory pathway controlling DNA replication initiation through specific histone mark recognition.