The cytoskeleton-dependent localization of cdc2/cyclin B in blastomere cortex duringXenopus embryonic cell cycle

2005 ◽  
Vol 72 (3) ◽  
pp. 336-345 ◽  
Author(s):  
Norihiko Nakamura ◽  
Toshinobu Tokumoto ◽  
Shuichi Ueno ◽  
Yasuhiro Iwao
Keyword(s):  
Cell Cycle ◽  
Embryonic Cell ◽  
Cyclin B ◽  
Embryonic Cell Cycle

Cyclin B mRNA depletion only transiently inhibits the Xenopus embryonic cell cycle

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 1173-1178 ◽  
Author(s):  
D.L. Weeks ◽  
J.A. Walder ◽  
J.M. Dagle
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Antisense Oligonucleotides ◽  
Normal Development ◽  
Embryonic Cell ◽  
Cyclin B ◽  
Xenopus Embryos ◽  
Embryonic Cleavage ◽  
Embryonic Cell Cycle

The control of the cell cycle is dependent on the ability to synthesize and degrade proteins called cyclins. When antisense oligonucleotides are used to deplete Xenopus embryos of mRNA encoding cyclin B protein, embryonic cleavage is inhibited. Surprisingly, after missing several rounds of cleavage, the cell cycle and cell division resumes. These studies indicate that the early embryonic cell cycle can proceed with undetectable levels of cyclin B encoding mRNA. In contrast, other events of normal development, including the activation of embryonic transcription and gastrulation, are inhibited.

Association of cyclin-bound p34cdc2 with subcellular structures in xenopus eggs

1992 ◽  
Vol 102 (2) ◽  
pp. 285-297 ◽  
Author(s):  
D. Leiss ◽  
M.A. Felix ◽  
E. Karsenti
Keyword(s):  
Cell Cycle ◽  
Ribosomal Proteins ◽  
Cell Cycle Progression ◽  
Gradient Centrifugation ◽  
Preliminary Evidence ◽  
Embryonic Cell ◽  
Cytoskeletal Proteins ◽  
Cyclin B ◽  
Post Translational Modifications ◽  
Egg Extracts

Cell cycle progression is controlled by changes in kinase activity of homologs of the fission yeast protein p34cdc2. The p34cdc2 kinase is activated by its association with a cyclin subunit, followed by post-translational modifications. Here, we show that in Xenopus eggs stimulated to enter the early embryonic cell cycle by an electric shock, part of the p34cdc2 becomes associated with subcellular fractions as the eggs progress towards mitosis. This occurs as a result of cyclin accumulation because most of the B-type cyclins and some of the A-type cyclins are found in the particulate fraction. Moreover, as soon as cyclins are degraded, p34cdc2 is released in the soluble fraction. The p34cdc2-cyclin complex can be solubilised by 80 mM beta-glycerophosphate (in the standard MPF extraction buffer) or by high salt concentrations. The post-translational modifications leading to cdc2 kinase activation by cyclin occur in the insoluble form. Following fractionation of egg extracts by sucrose gradient centrifugation, the p34cdc2-cyclin B complex is found in several fractions, but especially in two discrete peaks. We present evidence that in the slow-sedimenting peak the p34cdc2-cyclin B complex is associated with the 60 S subunit of monoribosomes. It could be targeted in this fashion to substrates such as ribosomal proteins and maybe to cytoskeletal proteins, since ribosomes bind to microtubules and are present in the spindle. The p34cdc2-cyclin B complex is also found in a faster-migrating fraction containing various membranous structures, including Golgi stacks. Therefore, as observed by immunofluorescence in other systems, it seems that cyclin subunits target p34cdc2 to specific cellular sites and this is certainly important for its function. In addition, we present preliminary evidence suggesting that some component present in the ribosome-containing fraction is required for activation of the p34cdc2-cyclin B complex.

scholarly journals Accumulation and dynamics of proteins of the MCM family during mouse oogenesis and the first embryonic cell cycle

2007 ◽  
Vol 51 (4) ◽  
pp. 283-295 ◽  
Author(s):  
Lukasz Swiech ◽  
Katarzyna Kisiel ◽  
Renata Czolowska ◽  
Maciej Zientarski ◽  
Ewa Borsuk
Keyword(s):  
Cell Cycle ◽  
Embryonic Cell ◽  
Embryonic Cell Cycle

scholarly journals A Role for Cdk2 Kinase in Negatively Regulating DNA Replication during S Phase of the Cell Cycle

1997 ◽  
Vol 137 (1) ◽  
pp. 183-192 ◽  
Author(s):  
Xuequn Helen Hua ◽  
Hong Yan ◽  
John Newport
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Cyclin E ◽  
Embryonic Cell ◽  
S Phase ◽  
Negative Regulation ◽  
Sperm Chromatin ◽  
High Concentration ◽  
Low Concentrations ◽  
Embryonic Cell Cycle

Using cell-free extracts made from Xenopus eggs, we show that cdk2-cyclin E and A kinases play an important role in negatively regulating DNA replication. Specifically, we demonstrate that the cdk2 kinase concentration surrounding chromatin in extracts increases 200-fold once the chromatin is assembled into nuclei. Further, we find that if the cdk2–cyclin E or A concentration in egg cytosol is increased 16-fold before the addition of sperm chromatin, the chromatin fails to initiate DNA replication once assembled into nuclei. This demonstrates that cdk2–cyclin E or A can negatively regulate DNA replication. With respect to how this negative regulation occurs, we show that high levels of cdk2–cyclin E do not block the association of the protein complex ORC with sperm chromatin but do prevent association of MCM3, a protein essential for replication. Importantly, we find that MCM3 that is prebound to chromatin does not dissociate when cdk2– cyclin E levels are increased. Taken together our results strongly suggest that during the embryonic cell cycle, the low concentrations of cdk2–cyclin E present in the cytosol after mitosis and before nuclear formation allow proteins essential for potentiating DNA replication to bind to chromatin, and that the high concentration of cdk2–cyclin E within nuclei prevents MCM from reassociating with chromatin after replication. This situation could serve, in part, to limit DNA replication to a single round per cell cycle.

scholarly journals The Design Space of the Embryonic Cell Cycle Oscillator

2017 ◽  
Vol 113 (3) ◽  
pp. 743-752 ◽  
Author(s):  
Henry H. Mattingly ◽  
Moshe Sheintuch ◽  
Stanislav Y. Shvartsman
Keyword(s):  
Cell Cycle ◽  
Design Space ◽  
Embryonic Cell ◽  
Embryonic Cell Cycle

scholarly journals Post-translational modifications in embryonic cell cycle

Cell Cycle ◽  
2014 ◽  
Vol 13 (9) ◽  
pp. 1364-1365
Author(s):  
Siem Van der Laan ◽  
Domenico Maiorano
Keyword(s):  
Cell Cycle ◽  
Embryonic Cell ◽  
Post Translational Modifications ◽  
Embryonic Cell Cycle

scholarly journals Translational Control of the Embryonic Cell Cycle

Cell ◽  
2002 ◽  
Vol 109 (4) ◽  
pp. 473-483 ◽  
Author(s):  
Irina Groisman ◽  
Mi-Young Jung ◽  
Madathia Sarkissian ◽  
Quiping Cao ◽  
Joel D Richter
Keyword(s):  
Cell Cycle ◽  
Translational Control ◽  
Embryonic Cell ◽  
Embryonic Cell Cycle

scholarly journals Chromosome Association of Minichromosome Maintenance Proteins in Drosophila Mitotic Cycles

1997 ◽  
Vol 139 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Tin Tin Su ◽  
Patrick H. O'Farrell
Keyword(s):  
Cell Cycle ◽  
Cyclin E ◽  
Embryonic Cell ◽  
Cyclin B ◽  
Chromatin Interaction ◽  
G1 Phase ◽  
Minichromosome Maintenance ◽  
Cell Cycles ◽  
Mcm Proteins ◽  
Replication Factors

Minichromosome maintenance (MCM) proteins are essential DNA replication factors conserved among eukaryotes. MCMs cycle between chromatin bound and dissociated states during each cell cycle. Their absence on chromatin is thought to contribute to the inability of a G2 nucleus to replicate DNA. Passage through mitosis restores the ability of MCMs to bind chromatin and the ability to replicate DNA. In Drosophila early embryonic cell cycles, which lack a G1 phase, MCMs reassociate with condensed chromosomes toward the end of mitosis. To explore the coupling between mitosis and MCM–chromatin interaction, we tested whether this reassociation requires mitotic degradation of cyclins. Arrest of mitosis by induced expression of nondegradable forms of cyclins A and/or B showed that reassociation of MCMs to chromatin requires cyclin A destruction but not cyclin B destruction. In contrast to the earlier mitoses, mitosis 16 (M16) is followed by G1, and MCMs do not reassociate with chromatin at the end of M16. dacapo mutant embryos lack an inhibitor of cyclin E, do not enter G1 quiescence after M16, and show mitotic reassociation of MCM proteins. We propose that cyclin E, inhibited by Dacapo in M16, promotes chromosome binding of MCMs. We suggest that cyclins have both positive and negative roles in controlling MCM–chromatin association.

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