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Plk1 relieves centriole block to reduplication by promoting daughter centriole maturation

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Listed:
  • Anil Shukla

    (Laboratory of Protein Dynamics and Signaling)

  • Dong Kong

    (Laboratory of Protein Dynamics and Signaling)

  • Meena Sharma

    (Laboratory of Protein Dynamics and Signaling)

  • Valentin Magidson

    (Optical Microscopy and Analysis Laboratory, Leidos Biomedical Res Inc., Frederick National Laboratory for Cancer Research)

  • Jadranka Loncarek

    (Laboratory of Protein Dynamics and Signaling)

Abstract

Centrosome overduplication promotes mitotic abnormalities, invasion and tumorigenesis. Cells regulate the number of centrosomes by limiting centriole duplication to once per cell cycle. The orthogonal orientation between a mother and a daughter centriole, established at the time of centriole duplication, is thought to block further duplication of the mother centriole. Loss of orthogonal orientation (disengagement) between two centrioles during anaphase is considered a licensing event for the next round of centriole duplication. Disengagement requires the activity of Polo-like kinase 1 (Plk1), but how Plk1 drives this process is not clear. Here we employ correlative live/electron microscopy and demonstrate that Plk1 induces maturation and distancing of the daughter centriole, allowing reduplication of the mother centriole even if the original daughter centriole is still orthogonal to it. We find that mother centrioles can undergo reduplication when original daughter centrioles are only ∼80 nm apart, which is the distance centrioles normally reach during prophase.

Suggested Citation

  • Anil Shukla & Dong Kong & Meena Sharma & Valentin Magidson & Jadranka Loncarek, 2015. "Plk1 relieves centriole block to reduplication by promoting daughter centriole maturation," Nature Communications, Nature, vol. 6(1), pages 1-13, November.
  • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9077
    DOI: 10.1038/ncomms9077
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    Cited by:

    1. Devashish Dwivedi & Daniela Harry & Patrick Meraldi, 2023. "Mild replication stress causes premature centriole disengagement via a sub-critical Plk1 activity under the control of ATR-Chk1," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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