Requirements of Cyclin A for Mitosis Are Independent of Its Subcellular Localization

Dienemann, Axel; Sprenger, Frank

doi:10.1016/j.cub.2004.06.024

Cited by 24 publications

(22 citation statements)

References 31 publications

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“…Rca1 overexpression has been shown to prevent premature Cyclin B degradation and restore mitosis 16 in the epidermis of CycA mutant embryos (Dienemann and Sprenger, 2004). Based on these observations, the failure of mitosis 16 in CycA mutants was proposed to reflect premature Fzr activation (Dienemann and Sprenger, 2004), a suggestion fully confirmed by our work. It is conceivable, therefore, that the Cyclin A-mediated suppression of Fzr psm activity involves Rca1 or other unknown targets.…”

Section: Research Articlesupporting

confidence: 77%

“…The numbers in lower right panel corners represent the cell counts in the regions of the right segments shown in E-X. and Sprenger, 2004). Interestingly, premature disappearance was not observed within the prospective anterior spiracle region of CycA mutant embryos where mitosis 16 is not the terminal mitosis (Fig.…”

Section: Research Articlementioning

confidence: 97%

“…Development 133 (16) control by Cdk phosphorylation, Fzr is inhibited by the Emi1-like Drosophila protein Rca1 (Dienemann and Sprenger, 2004). Rca1 overexpression has been shown to prevent premature Cyclin B degradation and restore mitosis 16 in the epidermis of CycA mutant embryos (Dienemann and Sprenger, 2004).…”

Section: Research Articlementioning

confidence: 99%

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Terminal mitoses require negative regulation of Fzr/Cdh1 by Cyclin A,preventing premature degradation of mitotic cyclins and String/Cdc25

2006

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Cyclin A expression is only required for particular cell divisions during Drosophila embryogenesis. In the epidermis, Cyclin A is 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 E overexpression.

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Section: Research Articlesupporting

confidence: 77%

Section: Research Articlementioning

confidence: 97%

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Terminal mitoses require negative regulation of Fzr/Cdh1 by Cyclin A,preventing premature degradation of mitotic cyclins and String/Cdc25

2006

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“…A-type cyclins have been found to exist in both the cytoplasm and nucleus (Castro et al, 1994;ChaubetGigot, 2000;Dienemann and Sprenger, 2004), and the function of cyclin A in Drosophila mitosis is independent of its subcellular localization (Dienemann and Sprenger, 2004). Sections P and Q in Figure 3 indicate that the GFP signal appeared to be in both the cytoplasm and the nucleus in the tetrad, with a slightly higher level in the nucleolus.…”

Section: Cyca1;2-gfp Is Localized In Both the Cytoplasm And Nucleusmentioning

confidence: 97%

Progression through Meiosis I and Meiosis II in Arabidopsis Anthers Is Regulated by an A-Type Cyclin Predominately Expressed in Prophase I

et al. 2004

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(J.-L.M., S.M.)Meiosis is often described as a special case of cell division since it differs from mitosis in having two nuclear divisions without an intervening S-phase. It will be of great interest to uncover what molecular mechanisms underlie these special features of meiosis. We previously reported that the tardy asynchronous meiosis (tam) mutant of Arabidopsis (Arabidopsis thaliana) is slower in cell cycle progression in male meiosis. Here we report that TAM encodes the A-type cyclin, CYCA1;2. The point mutation in tam replaced a conserved threonine with an isoleucine in the linker region between the a4 and a5 helices of the first cyclin fold. By studying the dynamics of a CYCA1;2-green fluorescent protein fusion protein under the control of the CYCA1;2 promoter, we found that the fusion protein was most abundant at pachytene, but was undetectable from late prophase I until telophase II. Nonetheless, cell cycle progression in tam was delayed in both pachytene and meiosis II. We conclude either that the CYCA1;2 produced in prophase I indirectly regulates meiosis II progression, or that a very low level of CYCA1;2 directly regulates meiosis II progression. Either of these scenarios is a deviation from the typical mode of action of mitotic cyclins in mitosis and meiosis I, in which each nuclear division is coupled with a peak of expression of mitotic cyclins.A hallmark of cell cycle progression in mitosis is that mitotic cyclins oscillate once with each cell cycle; a high level at the G2/M transition or some time into the M-phase is followed by an abrupt decline before exit from M-phase (Nurse, 2002). Meiosis, in contrast to mitosis, consists of two consecutive nuclear divisions without an intervening S-phase for chromosome duplication, defining an M-M phase transition between meiosis I and meiosis II (Kishimoto, 2003). However, at the molecular level, if or how the meiosis I-meiosis II transition differs from the transition between two consecutive mitotic cell cycles remains largely unknown.There are two types of mitotic cyclins: A and B. There is some information about meiotic modulation of the oscillation of B-type cyclins. It has been found that degradation of cyclin B is not required for the meiosis I-meiosis II transition (Taieb et al., 2001). This phenomenon suggests that the meiosis I-meiosis II transition does not likely involve an exit from an earlier M-phase and reentry into a subsequent M-phase, because degradation of mitotic cyclins is required for exit from M-phase in mitosis (Nurse, 2002). In fact, incomplete degradation of cyclin B at the end of meiosis I is essential for preventing the entry into S-phase in meiosis II in animals (Picard et al., 1996;Sakamoto et al., 1998;Iwabuchi et al., 2000;Taieb et al., 2001;Perez et al., 2002). In female meiosis of some animal species that normally undergo an arrest in metaphase II, depletion of cyclin B leads to the absence of the meiosis II spindle, underscoring the importance of new cyclin B synthesis for stabilizing the metaphase II spindle in these sp...

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“…The best characterized inhibitor of the APC/C-Fzr complex is Rca1, the Drosophila ortholog of the vertebrate Emi1 proteins (Grosskortenhaus and Sprenger 2002). In addition, it has been demonstrated that CycA-Cdk1 and CycE-Cdk2 complexes also contribute to APC/C-Fzr inhibition during Drosophila embryogenesis (Sigrist and Lehner 1997;Grosskortenhaus and Sprenger 2002;Dienemann and Sprenger 2004;Reber et al 2006). However, expression profiling showed that CycA, Cdk1, and Rca1 are only weakly expressed in larval salivary glands, indicating that these genes are presumably not involved in APC/C-Fzr regulation during endoreplication.…”

Section: Cyce-cdk2 Regulates Apc/c-fzr Activity In Salivary Glandsmentioning

confidence: 99%

The anaphase-promoting complex/cyclosome (APC/C) is required for rereplication control in endoreplication cycles

Zielke¹,

Querings²,

Rottig

et al. 2008

Genes Dev.

Self Cite

111

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Endoreplicating cells undergo multiple rounds of DNA replication leading to polyploidy or polyteny. Oscillation of Cyclin E (CycE)-dependent kinase activity is the main driving force in Drosophila endocycles. High levels of CycE-Cdk2 activity trigger S phase, while down-regulation of CycE-Cdk2 activity is crucial to allow licensing of replication origins. In mitotic cells relicensing in S phase is prevented by Geminin. Here we show that Geminin protein oscillates in endoreplicating salivary glands of Drosophila. Geminin levels are high in S phase, but drop once DNA replication has been completed. DNA licensing is coupled to mitosis through the action of the anaphase-promoting complex/cyclosome (APC/C). We demonstrate that, even though endoreplicating cells never enter mitosis, APC/C activity is required in endoreplicating cells to mediate Geminin oscillation. Down-regulation of APC/C activity results in stabilization of Geminin protein and blocks endocycle progression. Geminin is only abundant in cells with high CycE-Cdk2 activity, suggesting that APC/C-Fzr activity is periodically inhibited by CycE-Cdk2, to prevent relicensing in S-phase cells.[Keywords: Anaphase-promoting complex; cell cycle; DNA licensing; Drosophila; endoreplication] Supplemental material is available at http://www.genesdev.org. The precise duplication of the genome is crucial for the survival of any organism. In multicellular organisms genome instability potentially gives rise to cancer and thus compromises the life of the whole organism. To maintain the integrity of the genome, DNA replication, and mitosis must be coordinated during cell division cycles so that DNA replication occurs only once per cycle and mitosis only after complete duplication of the genome. To avoid rereplication events, a network of proteins ensures that cells acquire the license for DNA replication only in a specific phase of the cell cycle. DNA licensing involves the formation of prereplication complexes (pre-RC), which can only assemble during late mitosis and G1 (for review, see Bell and Dutta 2002;Blow and Dutta 2005). Pre-RC assembly on replication origins involves a variety of conserved components including the ORC1-6 complex, Cdc6, Cdt1/Double-parked, and the MCM2-7 helicase. Once MCM2-7 proteins are loaded onto the DNA, licensing is completed and the replication origins are ready for firing (for review, see Bell and Dutta 2002;Blow and Dutta 2005).Several mechanisms ensure that replication origins are fired only once during a cell cycle (for review, see Machida et al. 2005). Of particular importance is the temporal separation of pre-RC formation and origin firing. Pre-RC assembly occurs only in G1 because it depends on low Cdk activity while high Cdk activity is required for origin firing. The increase in Cdk activity at the G1-S transition does not only trigger origin firing, but at the same time also results in phosphorylation of several pre-RC components (ORC, Cdc6, Cdt1,. These modifications are thought to prevent reassembly of these components into pre-R...

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Requirements of Cyclin A for Mitosis Are Independent of Its Subcellular Localization

Cited by 24 publications

References 31 publications

Terminal mitoses require negative regulation of Fzr/Cdh1 by Cyclin A,preventing premature degradation of mitotic cyclins and String/Cdc25

Terminal mitoses require negative regulation of Fzr/Cdh1 by Cyclin A,preventing premature degradation of mitotic cyclins and String/Cdc25

Progression through Meiosis I and Meiosis II in Arabidopsis Anthers Is Regulated by an A-Type Cyclin Predominately Expressed in Prophase I

The anaphase-promoting complex/cyclosome (APC/C) is required for rereplication control in endoreplication cycles

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