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Centrosome duplication proceeds during mimosine‐induced G 1 cell cycle arrest
Author(s) -
Durcan Thomas M.,
Halpin Elizabeth S.,
Casaletti Luciana,
Vaughan Kevin T.,
Pierson Maggie R.,
Woods Shane,
Hinchcliffe Edward H.
Publication year - 2008
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21298
Subject(s) - centrosome , centrosome cycle , microbiology and biotechnology , biology , gene duplication , cell cycle , mitosis , centriole , mimosine , cell , genetics , gene , botany , leucaena leucocephala
Centrosome duplication must remain coordinated with cell cycle progression to ensure the formation of a strictly bipolar mitotic spindle, but the mechanisms that regulate this coordination are poorly understood. Previous work has shown that prolonged S‐phase is permissive for centrosome duplication, but prolonging either G 2 or M‐phase cannot support duplication. To examine whether G 1 is permissive for centrosome duplication, we release serum‐starved G 0 cells into mimosine, which delays the cell cycle in G 1 . We find that in mimosine, centrosome duplication does occur, albeit slowly compared with cells that progress into S‐phase; centrosome duplication in mimosine‐treated cells also proceeds in the absence of a rise in Cdk2 kinase activity normally associated with the G 1 /S transition. CHO cells arrested with mimosine can also assemble more than four centrioles (termed “centrosome amplification”), but the extent of centrosome amplification during prolonged G 1 is decreased compared to cells that enter S‐phase and activate the Cdk2‐cyclin complex. Together, our results suggest a model, which predicts that entry into S‐phase and the rise in Cdk2 activity associated with this transition are not absolutely required to initiate centrosome duplication, but rather, serve to entrain the centrosome reproduction cycle with cell cycle progression. J. Cell. Physiol. 215: 182–191, 2008. © 2007 Wiley‐Liss, Inc.