Terminal mitoses require negative regulation of Fzr/Cdh1 by Cyclin A,preventing premature degradation of mitotic cyclins and String/Cdc25
Autor: | Henning W. Jacobs, Christian F. Lehner, Achim Reber |
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Rok vydání: | 2006 |
Předmět: |
Embryo
Nonmammalian Cyclin E Cyclin D Cyclin A Cyclin B Down-Regulation Embryonic Development Mitosis Cell Cycle Proteins Cdh1 Proteins Cyclins Animals Drosophila Proteins Molecular Biology Cyclin-dependent kinase 1 biology G1/S transition Cell cycle Cell biology Mutation biology.protein Cancer research Drosophila Epidermis Protein Tyrosine Phosphatases Cyclin A2 Developmental Biology |
Zdroj: | Development. 133:3201-3211 |
ISSN: | 1477-9129 0950-1991 |
Popis: | Cyclin A expression is only required for particular cell divisions during Drosophila embryogenesis. In the epidermis, Cyclin Ais strictly required for progression through mitosis 16 in cells that become post-mitotic after this division. By contrast, Cyclin A is not absolutely required in epidermal cells that are developmentally programmed for continuation of cell cycle progression after mitosis 16. Our analyses suggest the following explanation for the special Cyclin A requirement during terminal division cycles. Cyclin E is known to be downregulated during terminal division cycles to allow a timely cell cycle exit after the final mitosis. Cyclin E is therefore no longer available before terminal mitoses to prevent premature Fizzy-related/Cdh1 activation. As a consequence,Cyclin A, which can also function as a negative regulator of Fizzy-related/Cdh1, becomes essential to provide this inhibition before terminal mitoses. In the absence of Cyclin A, premature Fizzy-related/Cdh1 activity results in the premature degradation of the Cdk1 activators Cyclin B and Cyclin B3, and apparently of String/Cdc25 phosphatase as well. Without these activators, entry into terminal mitoses is not possible. However, entry into terminal mitoses can be restored by the simultaneous expression of versions of Cyclin B and Cyclin B3 without destruction boxes, along with a Cdk1 mutant that escapes inhibitory phosphorylation on T14 and Y15. Moreover,terminal mitoses are also restored in Cyclin A mutants by either the elimination of Fizzy-related/Cdh1 function or Cyclin Eoverexpression. |
Databáze: | OpenAIRE |
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