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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
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Mitotic bookmarking by SWI/SNF subunits.

Zhexin Zhu1, Xiaolong Chen2, Ao Guo3

  • 1Division of Molecular Oncology, Department of Oncology, St Jude Children's Research Hospital, Memphis, TN, USA. zhexin.zhu@stjude.org.

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|May 24, 2023
PubMed
Summary
This summary is machine-generated.

Cell identity relies on a mitotic memory. Mammalian SWI/SNF complexes, specifically SMARCE1, act as crucial mitotic bookmarks, ensuring correct gene expression and cell fate during cell division.

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Area of Science:

  • Epigenetics
  • Cell Biology
  • Molecular Biology

Background:

  • Cellular differentiation requires transmitting state information through mitosis.
  • Mammalian SWI/SNF complexes regulate cell identity via chromatin remodeling.
  • The role of SWI/SNF in cell fate memory during mitosis was previously unclear.

Purpose of the Study:

  • To investigate the role of SWI/SNF complexes in maintaining cell identity during cell division.
  • To determine if SWI/SNF subunits function as mitotic bookmarks.
  • To elucidate the mechanism by which SWI/SNF safeguards cell fate during mitosis.

Main Methods:

  • Analysis of SWI/SNF subunit localization (SMARCE1, SMARCB1) during mitosis.
  • Gene expression analysis following SMARCE1 ablation in mouse embryonic stem cells.
  • Assessment of established bookmark occupancy and neural differentiation.

Main Results:

  • SWI/SNF core subunits SMARCE1 and SMARCB1 bind to promoters during mitosis, not enhancers.
  • This promoter binding is essential for gene reactivation after mitosis.
  • SMARCE1 ablation during mitosis disrupts gene expression and leads to aberrant neural differentiation.

Conclusions:

  • SWI/SNF subunit SMARCE1 functions as a mitotic bookmark.
  • SMARCE1 is critical for maintaining heritable epigenetic fidelity during cell division.
  • This mechanism ensures accurate cell fate determination and transcriptional reprogramming.