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Raptor is phosphorylated by cdc2 during mitosis.

Dana M Gwinn1, John M Asara, Reuben J Shaw

  • 1Molecular and Cell Biology Laboratory, Dulbecco Center for Cancer Research, La Jolla, California, United States of America.

Plos One
|February 20, 2010
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AMP-activated protein kinase (AMPK) regulates cell division by inhibiting mTOR signaling. This study shows raptor, an mTOR binding partner, is phosphorylated by cdc2 during mitosis, directly impacting mTORC1 activity and cell cycle control.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cell cycle control is essential for accurate cell division, involving signaling pathways and checkpoints.
  • AMP-activated protein kinase (AMPK) regulates the G2/M phase by suppressing mammalian target of rapamycin (mTOR) signaling.
  • AMPK phosphorylates raptor, a key mTOR binding partner, inhibiting mTORC1.

Purpose of the Study:

  • To investigate the role of raptor in mitotic control.
  • To determine how raptor contributes to cell cycle progression during mitosis.

Main Methods:

  • Utilized tandem mass spectrometry to identify novel phosphorylation sites on raptor.
  • Generated phospho-specific antibodies to detect mitotic phosphorylation.
  • Employed site-directed mutagenesis and co-immunoprecipitation assays.

Main Results:

  • Raptor is highly phosphorylated during mitosis, specifically at Serine 696 and Threonine 706.
  • Mitotic cyclin-dependent kinase cdc2/CDK1 phosphorylates these sites.
  • Cyclin B co-immunoprecipitates with raptor in mitotic cells.

Conclusions:

  • Raptor is directly phosphorylated by cdc2 during mitosis.
  • This phosphorylation directly modulates the mTORC1 complex during mitosis.
  • Highlights a novel mechanism for mTOR regulation during cell division.