Cyclins and Cyclin-Dependent Kinases: Theme and Variations

https://doi.org/10.1016/S0065-230X(08)60254-7Get rights and content

Publisher Summary

This chapter introduces cyclins and their partner—cyclin dependent kinases (CDKs)—and the ways in which CDK complexes can be regulated. Cyclins are intimately concerned with regulating and coordinating deoxyribonucleic acid (DNA) replication and cell division. As more and more diverse cyclins and their partner CDKs are identified, more and more cellular processes are likely to be found to be regulated by these highly flexible protein kinase complexes. The cell cycle describes the series of steps by which a cell coordinates the processes of DNA duplication and cell division and is generally divided into four phases: cell division (M phase), the first gap phase (G1), DNA replication (S phase), and the second gap phase (G2). The cell cycle proceeds via a number of “control points.” These are points at which cells monitor the correct completion of a process—such as DNA replication—and whether conditions are favorable to go on to the next stage. To be activated fully, the CDK component of the cyclin–CDK complex needs to be phosphorylated on a conserved threonine in the T loop. There are a variety of inhibitor proteins that bind specifically to the CDKs and inhibit them in a stoichiometric fashion. Start, which is the major cell-cycle control point in most somatic cells, is described in the chapter. At start, there is a clear interaction between the cyclin–CDK complexes. In mammalian cells, the approximate equivalent to start is the restriction point (R), and the D-type cyclins are most likely to be involved in its regulation.

References (214)

  • A. Amon et al.

    Cell

    (1994)
  • A. Amon et al.

    Cell

    (1993)
  • M. Caligiuri et al.

    Cell

    (1993)
  • F. Chang et al.

    Cell

    (1990)
  • Y.-H. Chou et al.

    Cell

    (1990)
  • T.R. Coleman et al.

    Cell

    (1993)
  • F.R. Cross et al.

    Cell

    (1991)
  • J.A. DeCaprio et al.

    Cell

    (1989)
  • S.F. Dowdy et al.

    Cell

    (1993)
  • G. Draetta

    Trends Cell. Biol.

    (1993)
  • V. Duli'c et al.

    Cell

    (1994)
  • W.G. Dunphy et al.

    Cell

    (1991)
  • W.S. El-Deiry et al.

    Cell

    (1993)
  • T. Enoch et al.

    Cell

    (1990)
  • T. Evans et al.

    Cell

    (1983)
  • M.E. Ewen et al.

    Cell

    (1993)
  • R.P. Fisher et al.

    Cell

    (1994)
  • K. Galaktionov et al.

    Cell

    (1991)
  • J. Gautier et al.

    Cell

    (1991)
  • J. Hayles et al.

    Cell

    (1994)
  • R. Heald et al.

    Cell

    (1993)
  • K. Helin et al.

    Cell

    (1992)
  • A. Hershko et al.

    J. Biol. Chem.

    (1994)
  • S.L. Holloway et al.

    Cell

    (1993)
  • T. Hunter

    Cell

    (1991)
  • T. Hunter

    Cell

    (1993)
  • W.G. Kaelin et al.

    Cell

    (1992)
  • J.A. Knoblich et al.

    Cell

    (1994)
  • C. Koch et al.

    Curr. Opinion Cell Biol.

    (1994)
  • W. Krek et al.

    Cell

    (1994)
  • C.E. Alfa et al.

    Nature

    (1990)
  • A. Amon et al.

    Nature

    (1992)
  • F.S. Atherton et al.

    Mol. Cell. Biol.

    (1993)
  • S.J. Aves et al.

    EMBO J.

    (1985)
  • E. Bailly et al.

    J. Cell Sci.

    (1992)
  • L.R. Bandara et al.

    EMBO J.

    (1993)
  • S. Bates et al.

    Oncogene

    (1994)
  • S. Bodrug et al.

    EMBO J.

    (1994)
  • R. Booher et al.

    EMBO J.

    (1988)
  • R.N. Booher et al.

    EMBO J.

    (1993)
  • D. Broek et al.

    Nature

    (1991)
  • D. Broek et al.

    Nature

    (1991)
  • K. Brown et al.

    J. Cell Biol.

    (1994)
  • A. Bueno et al.

    Mol. Cell. Biol.

    (1993)
  • F. Chang et al.

    Mol. Biol. Cell.

    (1992)
  • T. Connolly et al.

    Mol. Cell. Biol.

    (1994)
  • F. Cross et al.

    Mol. Cell. Biol.

    (1994)
  • H.L. De Bondt et al.

    Nature

    (1993)
  • J.A. DeCaprio et al.

    Proc. Natl. Acad. Sci. USA

    (1992)
  • L. Dirick et al.

    Nature (London)

    (1991)
  • Cited by (168)

    • The garlic allelochemical DADS influences cucumber root growth involved in regulating hormone levels and modulating cell cycling

      2018, Journal of Plant Physiology
      Citation Excerpt :

      Certain mitosis-related genes are therefore of importance to understand the proliferation and expansion in the cell structures. Cyclins are the best-known positive regulators of cell proliferation and division, improving root elongation (Pines, 1995). Further, cyclins can influence the cell cycle by regulating CDK activity and, in turn, cyclins are necessary for CDK activation (Inze and De Veylder, 2006).

    • The tomato B-type cyclin gene, SlCycB2, plays key roles in reproductive organ development, trichome initiation, terpenoids biosynthesis and Prodenia litura defense

      2017, Plant Science
      Citation Excerpt :

      Cyclins, which determine the transition between the phases of the cell cycle in eukaryotes, function in many development processes [1].

    View all citing articles on Scopus
    View full text