scholarly journals Proteomics of M-phase entry: ‘Omen’ vs. ‘Omre’, the battle for oocyte quality and beyond

2011 ◽  
Vol 49 (1) ◽  
pp. 1-7
Author(s):  
Jacek Z. Kubiak
Keyword(s):  
Oocyte Quality ◽  
M Phase ◽  
Phase Entry

scholarly journals Control of timing of embryonic M-phase entry and exit is differentially sensitive to CDK1 and PP2A balance

2014 ◽  
Vol 58 (10-11-12) ◽  
pp. 767-774 ◽  
Author(s):  
Mohammed El Dika ◽  
Damian Dudka ◽  
Claude Prigent ◽  
Jean-Pierre Tassan ◽  
Malgorzata Kloc ◽  
...  
Keyword(s):  
Entry And Exit ◽  
M Phase ◽  
Phase Entry

scholarly journals Phosphatase 1 Nuclear Targeting Subunit Is an Essential Regulator of M-phase Entry, Maintenance, and Exit

2014 ◽  
Vol 289 (34) ◽  
pp. 23745-23752 ◽  
Author(s):  
Laura A. Fisher ◽  
Ling Wang ◽  
Lan Wu ◽  
Aimin Peng
Keyword(s):  
Nuclear Targeting ◽  
M Phase ◽  
Phase Entry

scholarly journals Mutant Caldesmon Lacking cdc2 Phosphorylation Sites Delays M-Phase Entry and Inhibits Cytokinesis

2001 ◽  
Vol 12 (1) ◽  
pp. 239-250 ◽  
Author(s):  
Shigeko Yamashiro ◽  
Hueylan Chern ◽  
Yoshihiko Yamakita ◽  
Fumio Matsumura
Keyword(s):  
Cho Cells ◽  
Kinase Activity ◽  
Chinese Hamster ◽  
Phosphorylation Sites ◽  
Wild Type ◽  
Cdc2 Kinase ◽  
Effective Inhibition ◽  
M Phase ◽  
Phase Progression ◽  
Phase Entry

Caldesmon is phosphorylated by cdc2 kinase during mitosis, resulting in the dissociation of caldesmon from microfilaments. To understand the physiological significance of phosphorylation, we generated a caldesmon mutant replacing all seven cdc2 phosphorylation sites with Ala, and examined effects of expression of the caldesmon mutant on M-phase progression. We found that microinjection of mutant caldesmon effectively blocked early cell division ofXenopus embryos. Similar, though less effective, inhibition of cytokinesis was observed with Chinese hamster ovary (CHO) cells microinjected with 7th mutant. When mutant caldesmon was introduced into CHO cells either by protein microinjection or by inducible expression, delay of M-phase entry was observed. Finally, we found that 7th mutant inhibited the disassembly of microfilaments during mitosis. Wild-type caldesmon, on the other hand, was much less potent in producing these three effects. Because mutant caldesmon did not inhibit cyclin B/cdc2 kinase activity, our results suggest that alterations in microfilament assembly caused by caldesmon phosphorylation are important for M-phase progression.

scholarly journals Proteomic screen for potential regulators of M-phase entry and quality of meiotic resumption in Xenopus laevis oocytes

2010 ◽  
Vol 73 (8) ◽  
pp. 1542-1550 ◽  
Author(s):  
Romain D'Inca ◽  
Gaëlle Marteil ◽  
Franck Bazile ◽  
Aude Pascal ◽  
Nathalie Guitton ◽  
...  
Keyword(s):  
Xenopus Laevis ◽  
Xenopus Laevis Oocytes ◽  
Proteomic Screen ◽  
M Phase ◽  
Phase Entry

scholarly journals Cyclin A2/Cdk1 is Essential for the in vivo S Phase Entry by Phosphorylating Top2a

2019 ◽  
Author(s):  
Miaomiao Jin ◽  
Ruikun Hu ◽  
Baijie Xu ◽  
Weilai Huang ◽  
Hong Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cyclin B1 ◽  
S Phase ◽  
Downstream Target ◽  
Early Embryonic Lethality ◽  
M Phase ◽  
Phase Progression ◽  
Cyclin A2 ◽  
Phase Entry

AbstractCyclin-dependent kinase 1 (CDK1) plays essential roles in cell cycle regulation. However, due to the early embryonic lethality of mouse Cdk1 mutants, the in vivo role of CDK1 in regulating cell cycle and embryonic development remains unclear. Here, by generating zebrafish cdk1 mutants using CRISPR/Cas9 system, we show that cdk1−/− embryos exhibit severe microphthalmia accompanied with multiple defects in polarized cell division, S phase entry and M phase progression, cell apoptosis and cell differentiation, but not in interkinetic nuclear migration (IKNM). By informatics analysis, we identified Top2a as a potential downstream target, and Cyclin A2 and Cyclin B1 as partners of Cdk1 in cell cycle. Depletion of either Cyclin A2 or Top2a leads to decreased S phase entry and increased DNA damage response in zebrafish retinal cells, and depletion of Cyclin B1 leads to M phase arrest. Immunoprecipitation shows that Cdk1 and Cyclin A2 physically interact in vivo. Moreover, phosphorylation of Top2a on Serine 1213 (S1213) site is almost absent in either cdk1 or ccna2 mutants, but in not ccnb1 mutants. Furthermore, overexpression of TOP2AS1213, the phosphomimetic form of human TOP2A, rescues S phase entry and microphthalmia defects in cdk1−/− and ccna2−/− embryos. Taken together, our data suggests that Cdk1 interacts with Cyclin A2 to regulate S phase entry through phosphorylating Top2a, and with Cyclin B1 to regulate M phase progression in vivo.

scholarly journals Flexibility vs. robustness in cell cycle regulation of timing of M-phase entry in Xenopus laevis embryo cell-free extract

2016 ◽  
Vol 60 (7-8-9) ◽  
pp. 305-314
Author(s):  
Mateusz Debowski ◽  
Mohammed El Dika ◽  
Jacek Malejczyk ◽  
Robert Zdanowski ◽  
Claude Prigent ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Xenopus Laevis ◽  
Cell Cycle Regulation ◽  
Embryo Cell ◽  
Cell Free Extract ◽  
Laevis Embryo ◽  
Xenopus Laevis Embryo ◽  
M Phase ◽  
Cycle Regulation ◽  
Phase Entry

scholarly journals Mutant MyoD Lacking Cdc2 Phosphorylation Sites Delays M-Phase Entry

2004 ◽  
Vol 24 (4) ◽  
pp. 1809-1821 ◽  
Author(s):  
Lionel A. J. Tintignac ◽  
Valentina Sirri ◽  
Marie Pierre Leibovitch ◽  
Yann Lécluse ◽  
Maria Castedo ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Kinase Activity ◽  
Expression Patterns ◽  
Cyclin B ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Cdc2 Kinase ◽  
Specific Expression ◽  
M Phase ◽  
Phase Entry

ABSTRACT The transcription factors MyoD and Myf-5 control myoblast identity and differentiation. MyoD and Myf-5 manifest opposite cell cycle-specific expression patterns. Here, we provide evidence that MyoD plays a pivotal role at the G2/M transition by controlling the expression of p21Waf1/Cip1 (p21), which is believed to regulate cyclin B-Cdc2 kinase activity in G2. In growing myoblasts, MyoD reaccumulates during G2 concomitantly with p21 before entry into mitosis; MyoD is phosphorylated on Ser5 and Ser200 by cyclin B-Cdc2, resulting in a decrease of its stability and down-regulation of both MyoD and p21. Inducible expression of a nonphosphorylable MyoD A5/A200 enhances the MyoD interaction with the coactivator P/CAF, thereby stimulating the transcriptional activation of a luciferase reporter gene placed under the control of the p21 promoter. MyoD A5/A200 causes sustained p21 expression, which inhibits cyclin B-Cdc2 kinase activity in G2 and delays M-phase entry. This G2 arrest is not observed in p21−/− cells. These results show that in cycling cells MyoD functions as a transcriptional activator of p21 and that MyoD phosphorylation is required for G2/M transition.

scholarly journals Higher anti-tumour efficacy of platinum(IV) complex LA-12 is associated with its ability to bypass M-phase entry block induced in oxaliplatin-treated human colon cancer cells

2013 ◽  
Vol 46 (6) ◽  
pp. 665-676 ◽  
Author(s):  
O. Vondálová Blanářová ◽  
I. Jelínková ◽  
A. Hyršlová Vaculová ◽  
P. Sova ◽  
J. Hofmanová ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
M Phase ◽  
Human Colon Cancer Cells ◽  
Phase Entry ◽  
Entry Block
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