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TopBP1 controls BLM protein level to maintain genome stability.

Jiadong Wang1, Junjie Chen1, Zihua Gong1

  • 1Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

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TopBP1 stabilizes Bloom syndrome helicase (BLM) in S phase, preventing genomic instability. This interaction is crucial for DNA repair, as TopBP1 depletion increases sister chromatid exchange (SCE).

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Cycle Regulation

Background:

  • TopBP1 is a key protein in DNA replication checkpoint control.
  • Bloom syndrome helicase (BLM) plays a role in maintaining genomic stability.

Purpose of the Study:

  • To investigate the interaction between TopBP1 and BLM.
  • To elucidate the role of this interaction in cell cycle regulation and DNA repair.

Main Methods:

  • Studied phosphorylation and cell-cycle dependent interactions.
  • Utilized TopBP1 depletion and MIB1 depletion experiments.
  • Analyzed protein levels, sister chromatid exchange (SCE), and radiation sensitivity.

Main Results:

  • TopBP1 depletion decreased BLM levels and increased SCE.
  • MIB1 ubiquitinated and degraded BLM in G1 phase; TopBP1 stabilized BLM in S phase.
  • MIB1 depletion rescued BLM levels and SCE in TopBP1-depleted cells.
  • Undegradable BLM mutant caused radiation sensitivity by inhibiting NHEJ in G1.

Conclusions:

  • BLM is downregulated in G1 to promote NHEJ DNA repair.
  • TopBP1 stabilizes BLM in S phase to suppress SCE and prevent genomic instability.