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Knockdown of RMI1 impairs DNA repair under DNA replication stress.

Author information

Affiliations

  • 1. Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China; State Key Laboratory of Medicinal Chemical Biology, NanKai University, Tianjin, China.
      Authors
    • Xu C 1
    (1 author)
  • 2. Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
      Authors
    • Fang L 2
    • Kong Y 2
    • Xiao C 2
    • Yang M 2
    • Du LQ 2
    • Liu Q 2
    (6 authors)

ORCIDs linked to this article

Biochemical and Biophysical Research Communications, 14 Oct 2017, 494(1-2):158-164
https://doi.org/10.1016/j.bbrc.2017.10.062 PMID: 29042194 

Abstract 

RMI1 (RecQ-mediated genome instability protein 1) forms a conserved BTR complex with BLM, Topo IIIα, and RMI2, and its absence causes genome instability. It has been revealed that RMI1 localizes to nuclear foci with BLM and Topo IIIα in response to replication stress, and that RMI1 functions downstream of BLM in promoting replication elongation. However, the precise functions of RMI1 during replication stress are not completely understood. Here we report that RMI1 knockdown cells are hypersensitive to hydroxyurea (HU). Using comet assay, we show that RMI1 knockdown cells exhibit accumulation of broken DNAs after being released from HU treatment. Moreover, we demonstrate that RMI1 facilitates the recovery from activated checkpoint and resuming the cell cycle after replicative stress. Surprisingly, loss of RMI1 results in a failure of RAD51 loading onto DNA damage sites. These findings reveal the importance of RMI1 in response to replication stress, which could explain the molecular basis for its function in maintaining genome integrity.

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Read article at publisher's site: https://doi.org/10.1016/j.bbrc.2017.10.062

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Funding 

Funders who supported this work.

CAMS Innovation Fund for Medical Science (1)

Fundamental Research Funds for CAMS & PUMC (4)

Fundamental Research Funds for the Central Universities (2)

National Natural Science Foundation of China (2)

Natural Science Foundation of Tianjin (1)

PUMC Youth Fund

    Research Funds for the Innovation Team of IRM-CAMS (1)

    State Key Laboratory of Medicinal Chemical Biology