β-TrCP- and Casein Kinase II-Mediated Degradation of Cyclin F Controls Timely Mitotic Progression

Cell Rep. 2018 Sep 25;24(13):3404-3412. doi: 10.1016/j.celrep.2018.08.076.

Abstract

Orderly progressions of events in the cell division cycle are necessary to ensure the replication of DNA and cell division. Checkpoint systems allow the accurate execution of each cell-cycle phase. The precise regulation of the levels of cyclin proteins is fundamental to coordinate cell division with checkpoints, avoiding genome instability. Cyclin F has important functions in regulating the cell cycle during the G2 checkpoint; however, the mechanisms underlying the regulation of cyclin F are poorly understood. Here, we observe that cyclin F is regulated by proteolysis through β-TrCP. β-TrCP recognizes cyclin F through a non-canonical degron site (TSGXXS) after its phosphorylation by casein kinase II. The degradation of cyclin F mediated by β-TrCP occurs at the G2/M transition. This event is required to promote mitotic progression and favors the activation of a transcriptional program required for mitosis.

Keywords: CKII; CRLs; F-box protein; SCF; cell cycle; cyclin F; mitosis; ubiquitin; β-TrCP.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Casein Kinase II / metabolism*
  • Cyclins / chemistry
  • Cyclins / metabolism*
  • HEK293 Cells
  • HeLa Cells
  • Humans
  • Mitosis*
  • Proteolysis*
  • beta-Transducin Repeat-Containing Proteins / metabolism*

Substances

  • CCNF protein, human
  • Cyclins
  • beta-Transducin Repeat-Containing Proteins
  • Casein Kinase II