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A Biosensor for the Mitotic Kinase MPS1 Reveals Spatiotemporal Activity Dynamics and Regulation. | LitMetric

AI Article Synopsis

  • * Researchers developed a FRET-based biosensor (MPS1sen) to study MPS1 activity, finding that its activation begins in the nucleus 9-12 minutes before the nuclear envelope breaks down (NEB) and peaks at NEB completion.
  • * The study also reveals that MPS1 activity is influenced by regulators like Aurora B and PP2A-B56, and highlights abnormal MPS1 signaling in colorectal cancer cell lines, indicating a link to genomic instability.

Article Abstract

Accurate chromosome segregation during cell division critically depends on error correction of chromosome-spindle interactions and the spindle assembly checkpoint (SAC) [1-3]. The kinase MPS1 is an essential regulator of both processes, ensuring full chromosome biorientation before anaphase onset [3, 4]. To understand when and where MPS1 activation occurs and how MPS1 signaling is modulated during mitosis, we developed MPS1sen, a sensitive and specific FRET-based biosensor for MPS1 activity. By placing MPS1sen at different subcellular locations, we show that MPS1 activity initiates in the nucleus ∼9-12 min prior to nuclear envelope breakdown (NEB) in a kinetochore-dependent manner and reaches the cytoplasm at the start of NEB. Soon after initiation, MPS1 activity increases with switch-like kinetics, peaking at completion of NEB. We further show that timing and extent of pre-NEB MPS1 activity is regulated by Aurora B and PP2A-B56. MPS1sen phosphorylation declines in prometaphase as a result of formation of kinetochore-microtubule attachments, reaching low but still detectable levels at metaphase. Finally, leveraging the sensitivity and dynamic range of MPS1sen, we show deregulated MPS1 signaling dynamics in colorectal cancer cell lines and tumor organoids with diverse genomic instability phenotypes.

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Source
http://dx.doi.org/10.1016/j.cub.2020.07.062DOI Listing

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