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Resolution: standard / high Figure 3.
Regulation of centrosome number. (a) The canonical centrosome cycle. Procentriole formation begins in S phase orthogonally
to its mother. CDK2 activity may be necessary for speeding up procentriole formation
and elongation, thus coordinating this event with DNA replication. In G2, the daughter
centriole reaches full elongation and maturation with the recruitment of several molecules
to the pericentriolar material (PCM). CDK1 activity increases in G2 regulating a variety
of molecules and processes needed for entry into mitosis, such as changes in microtubule
dynamics. Through the concerted action of molecules such as the kinase Nek2, the two
centrosomes separate. The mitotic spindle segregates the chromosomes equally to the
two daughter cells. When a cell exits mitosis, the centrioles within the centrosome
disengage. That process may allow recruitment or activation of molecules necessary
for duplication. Adapted with kind permission from Springer Science + Business Media:
Cell Mol Life Sci Centrioles: active players or passengers during mitosis? 67 (2010). 2173–2194. Debec A, Sullivan W, and Bettencourt Dias M, figure 4, Copyright
© The Author(s) 2010. (b) Formation of multiple centrioles during ciliogenesis of epithelial cells. Hundreds
of centrioles are formed either around a pre-existing mother centriole (1) or a deuterosome
(2). These centrioles migrate and dock to the cell membrane, where they nucleate cilia.
(c)De novo centriole formation during oogenesis of parthenogenic insect species. Centrioles
disappear during oogenesis in many animal species. Female meiosis is acentriolar.
After egg activation multiple centrioles arise de novo and join the female pronucleus resulting from meiosis. In the absence of fertilization,
those MTOCS set up the first mitotic spindle in the unfertilized egg. The remaining
MTOCs disappear. Adapted with permission from John Wiley and Sons: Cunha-Ferreira
I, Bento I, and Bettencourt Dias M. Traffic. Copyright Journal compilation © 2009
Blackwell Munksgaard.
Bettencourt-Dias BMC Biology 2013 11:28 doi:10.1186/1741-7007-11-28 |