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Microcephalin 1/BRIT1-TRF2 interaction promotes telomere replication and repair, linking telomere dysfunction to primary microcephaly.

Alessandro CicconiRekha RaiXuexue XiongCayla BrotonAmer Al-HiyasatChunyi HuSiying DongWenqi SunJennifer GarbarinoRanjit S BindraCarl SchildkrautYu-Hang ChenSandy Chang
Published in: Nature communications (2020)
Telomeres protect chromosome ends from inappropriately activating the DNA damage and repair responses. Primary microcephaly is a key clinical feature of several human telomere disorder syndromes, but how microcephaly is linked to dysfunctional telomeres is not known. Here, we show that the microcephalin 1/BRCT-repeats inhibitor of hTERT (MCPH1/BRIT1) protein, mutated in primary microcephaly, specifically interacts with the TRFH domain of the telomere binding protein TRF2. The crystal structure of the MCPH1-TRF2 complex reveals that this interaction is mediated by the MCPH1 330YRLSP334 motif. TRF2-dependent recruitment of MCPH1 promotes localization of DNA damage factors and homology directed repair of dysfunctional telomeres lacking POT1-TPP1. Additionally, MCPH1 is involved in the replication stress response, promoting telomere replication fork progression and restart of stalled telomere replication forks. Our work uncovers a previously unrecognized role for MCPH1 in promoting telomere replication, providing evidence that telomere replication defects may contribute to the onset of microcephaly.
Keyphrases
  • zika virus
  • dna damage
  • intellectual disability
  • binding protein
  • oxidative stress
  • endothelial cells
  • autism spectrum disorder
  • signaling pathway
  • deep learning
  • small molecule
  • copy number
  • protein protein
  • wild type