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Hypoxia stabilizes SETDB1 to maintain genome stability.

Sungryul Park1, Jin Hwa Cho1, Jong-Hwan Kim2

  • 1Disease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea.

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|October 18, 2023
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Summary

The Von Hippel-Lindau (VHL) tumor suppressor targets SETDB1 for degradation, a process vital for maintaining genome stability. Loss of VHL function under hypoxia leads to SETDB1 accumulation, triggering immune responses and DNA damage.

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • The Von Hippel-Lindau (VHL) protein is a tumor suppressor and a key component of the CRL2VHL E3 ubiquitin ligase complex.
  • While VHL's role in tumor suppression is established, the full spectrum of its substrates and mechanisms remains under investigation.

Purpose of the Study:

  • To identify novel substrates of the CRL2VHL complex and elucidate VHL's tumor suppressive functions, particularly concerning oxygen levels.
  • To investigate the functional consequences of SETDB1 accumulation under hypoxic conditions.

Main Methods:

  • Proteomic analysis to identify VHL-interacting proteins.
  • Biochemical assays to study the oxygen-dependent regulation of SETDB1 by CRL2VHL.
  • Analysis of transposable element activity, immune response, and DNA damage in cells with altered SETDB1 levels under varying oxygen conditions.

Main Results:

  • The histone H3K9 methyltransferase SETDB1 was identified as a novel substrate of the CRL2VHL complex.
  • SETDB1 is hydroxylated in an oxygen-dependent manner, marking it for CRL2VHL-mediated degradation.
  • Hypoxia leads to SETDB1 accumulation, increased transposable element (TE) derepression, heightened immune-inflammatory responses, and DNA damage-induced cell death.

Conclusions:

  • The CRL2VHL E3 complex mediates oxygen-dependent degradation of SETDB1.
  • SETDB1 plays a critical role in maintaining genome stability under hypoxic stress by suppressing transposable element activity.
  • Dysregulation of SETDB1 degradation by VHL contributes to cellular responses under hypoxia, impacting genome integrity and potentially tumorigenesis.