Cell cycle in the Fucus zygote parallels a somatic cell cycle but displaysa unique translational regulation of cyclin-dependent kinases

Citation
F. Corellou et al., Cell cycle in the Fucus zygote parallels a somatic cell cycle but displaysa unique translational regulation of cyclin-dependent kinases, PL CELL, 13(3), 2001, pp. 585-598
Citations number
61
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT CELL
ISSN journal
10404651 → ACNP
Volume
13
Issue
3
Year of publication
2001
Pages
585 - 598
Database
ISI
SICI code
1040-4651(200103)13:3<585:CCITFZ>2.0.ZU;2-T
Abstract
In eukaryotic cells, the basic machinery of cell cycle control is highly co nserved. In particular, many cellular events during cell cycle progression are controlled by cyclin-dependent kinases (CDKs). The cell cycle in animal early embryos, however, differs substantially from that of somatic cells o r yeasts. For example, cell cycle checkpoints that ensure that the sequence of cell cycle events is correct have been described in somatic cells and y easts but are largely absent in embryonic cells. Furthermore, the regulatio n of CDKs is substantially different in the embryonic and somatic coils. In this study, we address the nature of the first cell cycle in the brown alg a Fucus, which is evolutionarily distant from the model systems classically used for cell cycle studies in embryos. This cycle consists of well-define d G1, S, G2, and Pn phases. The purine derivative olomoucine inhibited CDKs activity in vivo and in vitro and induced different cell cycle arrests, in cluding at the G1/S transition, suggesting that, as in somatic cells, CDKs tightly control cell cycle progression. The cell cycle of Fucus zygotes pre sented the other main features of a somatic cell cycle, such as a functiona l spindle assembly checkpoint that targets CDKs and the regulation of the e arly synthesis of two PSTAIRE CDKs, p32 and p34, and the associated histone H1 kinase activity as well as the regulation of CDKs by tyrosine phosphory lation. Surprisingly, the synthesis after fertilization of p32 and p34 was translationally regulated, a regulation not described previously for CDKs. Finally, our results suggest that the activation of mitotic CDKs relies on an autocatalytic amplification mechanism.