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Updated: Aug 30, 2025

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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The histone methyltransferase SETD2 negatively regulates cell size.

Thom M Molenaar1, Muddassir Malik1, Joana Silva2

  • 1Division of Gene Regulation, Netherlands Cancer Institute, 1066CX Amsterdam, The Netherlands.

Journal of Cell Science
|September 2, 2022
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The tumor suppressor SETD2 negatively regulates cell size and protein synthesis. Disrupting SETD2 function or its histone mark (H3K36 methylation) increases cell size, impacting cancer development.

Keywords:
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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Cell size is crucial for cellular function and tightly regulated.
  • Aberrant cell size is a hallmark of cancer.
  • SETD2, a tumor suppressor, is involved in transcription, RNA processing, and DNA repair.

Purpose of the Study:

  • To investigate the role of SETD2 in cell size regulation.
  • To understand the molecular mechanisms by which SETD2 controls cell size.

Main Methods:

  • Genetic perturbation strategies to alter SETD2 levels.
  • Analysis of global protein synthesis rates.
  • Investigation of histone modifications (H3K36 methylation).
  • Overexpression of related proteins (KDM4A, H3.3K36M) and SETD2 domains.

Main Results:

  • SETD2 acts as a negative regulator of global protein synthesis and cell size.
  • Overexpression of H3K36 demethylase KDM4A or oncohistone H3.3K36M increases cell size.
  • Disruption of SETD2's Set2-Rbp1 interacting (SRI) domain leads to increased cell size.

Conclusions:

  • SETD2 plays a significant role in regulating cellular physiology, specifically cell size.
  • These findings highlight SETD2's function beyond its known roles in transcription and DNA repair.
  • Further research is needed to elucidate SETD2's distinct functions in cancer progression.