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Calling RNF168 to action.

Somaira Nowsheen1, Zhenkun Lou2

  • 1Mayo Clinic Medical Scientist Training Program, Mayo Medical School and Mayo Graduate School, Mayo Clinic, Rochester, MN 55905, USA.

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|June 22, 2019
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Summary
This summary is machine-generated.

Researchers identified lethal(3) malignant brain tumor like 2 (L3MBTL2) as a key linker protein in DNA double-strand break (DSB) repair. L3MBTL2 connects ubiquitin ligases RNF8 and RNF168, facilitating the recruitment of repair factors like BRCA1 and 53BP1.

Keywords:
ATMDNA damage responseDNA double strand break repairE3 ligaseL3MBTL2MDC1RNF168RNF8phosphorylationubiquitin

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Genomic stress causes DNA damage, with DNA double-strand breaks (DSBs) being the most critical.
  • Cellular response involves signaling molecules, protein modifications like phosphorylation and ubiquitination.
  • ATM kinase initiates DSB response by phosphorylating substrates like MDC1 and histone H2AX.

Purpose of the Study:

  • To identify the unknown linker protein connecting E3 ubiquitin ligases RNF8 and RNF168 in the DNA damage response pathway.
  • To elucidate the sequential recruitment mechanism of ubiquitin ligases crucial for DSB repair.

Main Methods:

  • Investigated the interaction between RNF8, RNF168, and their substrates.
  • Utilized biochemical assays to confirm protein modifications and interactions.
  • Employed techniques to analyze ubiquitination events and recruitment to DNA lesions.

Main Results:

  • Identified lethal(3) malignant brain tumor like 2 (L3MBTL2) as the substrate of RNF8.
  • Demonstrated ATM-mediated phosphorylation of L3MBTL2, facilitating its interaction with MDC1.
  • Showed RNF8-mediated K63-linked polyubiquitination of L3MBTL2, enabling RNF168 recruitment and subsequent histone ubiquitination.

Conclusions:

  • L3MBTL2 acts as a crucial linker protein, connecting RNF8 and RNF168 in the DSB repair pathway.
  • The sequential action of L3MBTL2, RNF8, and RNF168 amplifies the DNA damage signal and recruits repair proteins like BRCA1 and 53BP1.