scholarly journals Model of the delayed translation of cyclin B maternal mRNA after sea urchin fertilization

2016 ◽  
Vol 83 (12) ◽  
pp. 1070-1082 ◽  
Author(s):  
Vincent Picard ◽  
Odile Mulner-Lorillon ◽  
Jérémie Bourdon ◽  
Julia Morales ◽  
Patrick Cormier ◽  
...  
Keyword(s):  
Sea Urchin ◽  
Cyclin B ◽  
Maternal Mrna ◽  
Delayed Translation

scholarly journals c-mos and cdc2 Cooperate in the Translational Activation of Fibroblast Growth Factor Receptor-1 duringXenopus Oocyte Maturation

1999 ◽  
Vol 10 (11) ◽  
pp. 3567-3581 ◽  
Author(s):  
Patricia A. Culp ◽  
Thomas J. Musci
Keyword(s):  
Cell Cycle ◽  
Oocyte Maturation ◽  
Growth Factor Receptor ◽  
Cyclin B ◽  
Meiotic Cell ◽  
Fgf Receptor ◽  
Maternal Mrna ◽  
Mapk Activity ◽  
Cellular Events ◽  
Translational Activation

During oocyte maturation in Xenopus, previously quiescent maternal mRNAs are translationally activated at specific times. We hypothesized that the translational recruitment of individual messages is triggered by particular cellular events and investigated the potential for known effectors of the meiotic cell cycle to activate the translation of the FGF receptor-1 (XFGFR) maternal mRNA. We found that both c-mos and cdc2 activate the translation of XFGFR. However, although oocytes matured by injection of recombinant cdc2/cyclin B translate normal levels of XFGFR protein, c-mos depletion reduces the level of XFGFR protein induced by cdc2/cyclin B injection. In oocytes blocked for cdc2 activity, injection of mos RNA induced low levels of XFGFR protein, independent of MAPK activity. Through the use of injected reporter RNAs, we show that the XFGFR 3′ untranslated region inhibitory element is completely derepressed by cdc2 alone. In addition, we identified a new inhibitory element through which both mos and cdc2 activate translation. We found that cdc2 derepresses translation in the absence of polyadenylation, whereas mos requires poly(A) extension to activate XFGFR translation. Our results demonstrate that mos and cdc2, in addition to functioning as key regulators of the meiotic cell cycle, cooperate in the translational activation of a specific maternal mRNA during oocyte maturation.

Activation of maternal mRNA in the absence of poly(A) formation in fertilised sea urchin eggs

Nature ◽  
1974 ◽  
Vol 249 (5453) ◽  
pp. 138-139 ◽  
Author(s):  
ANTHONY MESCHER ◽  
TOM HUMPHREYS
Keyword(s):  
Sea Urchin ◽  
Sea Urchin Eggs ◽  
Maternal Mrna

SEA URCHIN HATCHING PROTEASE: TRANSLATION IN BLASTULA OF MATERNAL mRNA

1978 ◽  
pp. 207-215 ◽  
Author(s):  
D. Barrett ◽  
D.A. Hursh ◽  
J. Landercasper ◽  
M.M. McRorie
Keyword(s):  
Sea Urchin ◽  
Maternal Mrna

MATERNAL mRNA AND PROTEIN SYNTHESIS IN THE EMBRYO

1973 ◽  
Vol 74 (Suppl) ◽  
pp. S244-S262 ◽  
Author(s):  
P. R. Gross ◽  
K. W. Gross ◽  
A. I. Skoultchi ◽  
J. V. Ruderman
Keyword(s):  
Protein Synthesis ◽  
Sea Urchin ◽  
Messenger Rna ◽  
Direct Proof ◽  
Indirect Evidence ◽  
Translation Control ◽  
Histone Mrna ◽  
Translational Machinery ◽  
Maternal Mrna ◽  
Histone Synthesis

ABSTRACT According to the masked maternal messenger RNA hypothesis, a large part if not all the protein synthesis of early development is directed by mRNA already present in the cytoplasm of unfertilized eggs. This mRNA is supposed to be synthesized during oogenesis and stored in some unavailable form until some later time in development, when it is selectively associated with the translational machinery. To the indirect evidence, which is nevertheless very strong, there can now be added a direct proof of the hypothesis for the case of histone mRNA. The five main histones of sea urchin embryos are synthesized on small polyribosomes, directed in part by newly-synthesized messages that sediment as a group at about 9S. Some histone synthesis survives total transcription block, however, suggesting that maternal histone mRNA exists. In competition-hybridization experiments, the egg RNA is shown to contain sequences characteristic of functional, embryonic histone mRNA. The competing RNA is localized in ribonucleoprotein particles of egg homogenates that sediment at 20–40S. These same particles contain RNA that stimulates a cell-free heterologous system to synthesize sea urchin histones. The application of these facts to some problems of translation control and of development generally is discussed.

Signal transduction pathways that contribute to CDK1/cyclin B activation during the first mitotic division in sea urchin embryos

2004 ◽  
Vol 296 (2) ◽  
pp. 347-357 ◽  
Author(s):  
Patrick Salaün ◽  
Magali Le Breton ◽  
Julia Morales ◽  
Robert Bellé ◽  
Sandrine Boulben ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Sea Urchin ◽  
Mitotic Division ◽  
Cyclin B ◽  
Signal Transduction Pathways ◽  
Sea Urchin Embryos

scholarly journals A Presumptive Developmental Role for a Sea Urchin Cyclin B Splice Variant

1998 ◽  
Vol 140 (2) ◽  
pp. 283-293 ◽  
Author(s):  
Jean-Claude Lozano ◽  
Philippe Schatt ◽  
François Marquès ◽  
Gérard Peaucellier ◽  
Philippe Fort ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Sea Urchin ◽  
Splice Variant ◽  
Budding Yeast ◽  
Initial Step ◽  
Cyclin B ◽  
Abnormal Development ◽  
Oocyte Meiosis ◽  
Developmental Role ◽  
Variant Protein

We show that a splice variant–derived cyclin B is produced in sea urchin oocytes and embryos. This splice variant protein lacks highly conserved sequences in the COOH terminus of the protein. It is found strikingly abundant in growing oocytes and cells committed to differentiation during embryogenesis. Cyclin B splice variant (CBsv) protein associates weakly in the cell with Xenopus cdc2 and with budding yeast CDC28p. In contrast to classical cyclin B, CBsv very poorly complements a triple CLN deletion in budding yeast, and its microinjection prevents an initial step in MPF activation, leading to an important delay in oocyte meiosis reinitiation. CBsv microinjection in fertilized eggs induces cell cycle delay and abnormal development. We assume that CBsv is produced in growing oocytes to keep them in prophase, and during embryogenesis to slow down cell cycle in cells that will be committed to differentiation.

Promoter Binding Factors Regulating Cyclin B Transcription in the Sea Urchin Embryo

1995 ◽  
Vol 14 (10) ◽  
pp. 869-881 ◽  
Author(s):  
JACK D. THATCHER ◽  
BARBARA McBRIDE ◽  
KAREN S. KATULA
Keyword(s):  
Sea Urchin ◽  
Cyclin B ◽  
Sea Urchin Embryo

scholarly journals Mutations in the Drosophila melanogaster gene three rows permit aspects of mitosis to continue in the absence of chromatid segregation

1993 ◽  
Vol 106 (1) ◽  
pp. 87-98 ◽  
Author(s):  
A.V. Philp ◽  
J.M. Axton ◽  
R.D. Saunders ◽  
D.M. Glover
Keyword(s):  
Drosophila Melanogaster ◽  
Metaphase Plate ◽  
Mitotic Division ◽  
Cyclin B ◽  
P Element ◽  
Mitotic Progression ◽  
Chromosome Microdissection ◽  
Maternal Mrna ◽  
Chromatid Segregation ◽  
Blastoderm Stage

We have cloned the three rows (thr) gene, by a combination of chromosome microdissection and P element tagging. We describe phenotypes of embryos homozygous for mutations at the thr locus. Maternal mRNA and protein appear to be sufficient to allow 14 rounds of mitosis in embryos homozygous for thr mutations. However, a small percentage of cells in syncytial blastoderm stage thr embryos sink into the interior of the embryo as if they have failed to divide properly. Following cellularisation all cells complete mitosis 14 normally. All cells become delayed at mitosis 15 with their chromosomes remaining aligned on the spindle in a metaphase-like configuration, even though both cyclins A and B have both been degraded. As cyclin B degradation occurs at the metaphase-anaphase transition, subsequent to the microtubule integrity checkpoint, the delay induced by mutations at the thr locus defines a later point in mitotic progression. Chromosomes in the cells of thr embryos do not undertake anaphase separation, but remain at the metaphase plate. Subsequently they decondense. A subset of nuclei go on to replicate their DNA but there is no further mitotic division.

Activation of protein kinase C alters p34cdc2 phosphorylation state and kinase activity in early sea urchin embryos by abolishing intracellular Ca2+ transients

2000 ◽  
Vol 349 (2) ◽  
pp. 489-499 ◽  
Author(s):  
Frank A. SUPRYNOWICZ ◽  
Laurence GROIGNO ◽  
Michael WHITAKER ◽  
Frederick J. MILLER ◽  
Greenfield SLUDER ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Sea Urchin ◽  
Kinase Activity ◽  
Physiological Role ◽  
Cyclin B ◽  
Phosphorylation State ◽  
Permeabilized Cells ◽  
Sea Urchin Embryos ◽  
Kinase C

The p34cdc2 protein kinase, a universal regulator of mitosis, is controlled positively and negatively by phosphorylation, and by association with B-type mitotic cyclins. In addition, activation and inactivation of p34cdc2 are induced by Ca2+ and prevented by Ca2+ chelators in permeabilized cells and cell-free systems. This suggests that intracellular Ca2+ transients may play an important physiological role in the control of p34cdc2 kinase activity. We have found that activators of protein kinase C can be used to block cell cycle-related alterations in intracellular Ca2+ concentration ([Ca2+]i) in early sea urchin embryos without altering the normal resting level of Ca2+. We have used this finding to investigate whether [Ca2+]i transients control p34cdc2 kinase activity in living cells via a mechanism that involves cyclin B or the phosphorylation state of p34cdc2. In the present study we show that the elimination of [Ca2+]i transients during interphase blocks p34cdc2 activation and entry into mitosis, while the elimination of mitotic [Ca2+]i transients prevents p34cdc2 inactivation and exit from mitosis. Moreover, we find that [Ca2+]i transients are not required for the synthesis of cyclin B, its binding to p34cdc2 or its destruction during anaphase. However, in the absence of interphase [Ca2+]i transients p34cdc2 does not undergo the tyrosine dephosphorylation that is required for activation, and in the absence of mitotic [Ca2+]i transients p34cdc2 does not undergo threonine dephosphorylation that is normally associated with inactivation. These results provide evidence that intracellular [Ca2+]i transients trigger the dephosphorylation of p34cdc2 at key regulatory sites, thereby controlling the timing of mitosis entry and exit.

Sea urchin maternal mRNA classes with distinct developmental regulation

1993 ◽  
Vol 14 (5) ◽  
pp. 397-406 ◽  
Author(s):  
Leslie Kelso-Winemiller ◽  
Joonwon Yoon ◽  
Margaret T. Peeler ◽  
Matthew M. Winkler
Keyword(s):  
Sea Urchin ◽  
Developmental Regulation ◽  
Maternal Mrna
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