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.

Cyclin B translation during first meiotic cell cycle of starfish oocytes

1992 ◽  
Vol 76 (2) ◽  
pp. 217-217
Author(s):  
Galas Simon ◽  
Doree Marcel ◽  
Picard André
Keyword(s):  
Cell Cycle ◽  
Cyclin B ◽  
Meiotic Cell

scholarly journals A MAPK cascade couples maternal mRNA translation and degradation to meiotic cell cycle progression in mouse oocytes

Development ◽  
2016 ◽  
Vol 144 (3) ◽  
pp. 452-463 ◽  
Author(s):  
Qian-Qian Sha ◽  
Xing-Xing Dai ◽  
Yujiao Dang ◽  
Fuchou Tang ◽  
Junping Liu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Mrna Translation ◽  
Mapk Cascade ◽  
Meiotic Cell ◽  
Cycle Progression ◽  
Mouse Oocytes ◽  
Maternal Mrna

scholarly journals Definition of conditions that enable antigen-specific activation of the majority of isolated trinitrophenol-binding B cells.

1982 ◽  
Vol 156 (6) ◽  
pp. 1635-1649 ◽  
Author(s):  
J C Cambier ◽  
J G Monroe ◽  
M J Neale
Keyword(s):  
Cell Cycle ◽  
T Cell ◽  
Interleukin 1 ◽  
Isolated Cells ◽  
Cellular Events ◽  
Accessory Cells ◽  
B Cell Growth Factor ◽  
Human Gamma Globulin ◽  
Definition Of ◽  
T Cell Help

In an effort to further elucidate the early cellular events in generation of antibody responses, we have determined the requirements for antigen-specific initiation of the G0 to G1 transition by isolated trinitrophenol (TNP) -binding B lymphocytes. TNP-binding cells were isolated from normal B6D2F1 splenocyte populations using hapten affinity fractionation on disulfide-bonded TNP-gelatin-coated plates. Populations prepared in this way are greater than or equal to 96% immunoglobulin positive and 70-95% antigen binding. Isolated cells were cultured for 48 h in the presence of a variety of TNP conjugates including TNP-Brucella abortus (Ba), TNP-Ficoll, TNP-sheep erythrocytes (SRBC), TNP-human gamma globulin (HGG), or TNP-ovalbumin (OVA) before being harvested and subjected to acridine orange cell cycle analysis. As many as 80% of cells were in cycle by 48 h in response to TNP-Ba, a thymus-independent (TI1 antigen. A smaller proportion (congruent to 40%) were in cycle in response to TNP-Ficoll, a TI2 antigen. Significant activation was not detected in cultures challenged with the thymus-dependent immunogens TNP-SRBC, TNP-HGG, and TNP-OVA. Addition of interleukin 1 (IL-1), IL-2, B cell growth factor, and/or T cell-replacing factor to cultures did not facilitate responses to these immunogens, suggesting a requirement for antigen-specific T cell help for entry into cell cycle induced by thymus dependent antigens. Activation by TNP-Ba was antigen specific and independent of accessory cells, occurring with equal efficiency in bulk and single-cell cultures. Activation by TNP-Ba was inhibitable by anti-Fab and anti-mu antibodies, but not by anti-delta antibodies. Results indicate that activation of TNP-binding cells to enter cell cycle by TNP-Ba is independent of accessory cells and requires interaction of antigen with cell surface IgM. Exposure to thymus-dependent TNP-immunogens plus nonspecific helper factors is insufficient to cause entry of TNP-binding cells into cycle.

Involvement of caveolin-1 in meiotic cell-cycle progression in Caenorhabditis elegans

10.1038/10100 ◽  
1999 ◽  
Vol 1 (2) ◽  
pp. 127-129 ◽  
Author(s):  
Jochen Scheel ◽  
Jagan Srinivasan ◽  
Ulrike Honnert ◽  
Annemarie Henske ◽  
Teymuras V. Kurzchalia
Keyword(s):  
Cell Cycle ◽  
Caenorhabditis Elegans ◽  
Cell Cycle Progression ◽  
Meiotic Cell ◽  
Cycle Progression ◽  
Caveolin 1

Androgen receptors in prostate cancer.

2002 ◽  
pp. 155-170 ◽  
Author(s):  
Z Culig ◽  
H Klocker ◽  
G Bartsch ◽  
A Hobisch
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Point Mutations ◽  
Growth Factor Receptor ◽  
Clinical Situation ◽  
Activation Function ◽  
Flufenamic Acid ◽  
Cell Cycle Regulators ◽  
Industrialized Countries ◽  
Chemopreventive Agents

The androgen receptor (AR), a transcription factor that mediates the action of androgens in target tissues, is expressed in nearly all prostate cancers. Carcinoma of the prostate is the most frequently diagnosed neoplasm in men in industrialized countries. Palliative treatment for non-organ-confined prostate cancer aims to down-regulate the concentration of circulating androgen or to block the transcription activation function of the AR. AR function during endocrine therapy was studied in tumor cells LNCaP subjected to long-term steroid depletion; newly generated sublines could be stimulated by lower concentrations of androgen than parental cells and showed up-regulation of AR expression and activity as well as resistance to apoptosis. Androgenic hormones regulate the expression of key cell cycle regulators, cyclin-dependent kinase 2 and 4, and that of the cell cycle inhibitor p27. Inhibition of AR expression could be achieved by potential chemopreventive agents flufenamic acid, resveratrol, quercetin, polyunsaturated fatty acids and interleukin-1beta, and by the application of AR antisense oligonucleotides. In the clinical situation, AR gene amplification and point mutations were reported in patients with metastatic disease. These mutations generate receptors which could be activated by other steroid hormones and non-steroidal antiandrogens. In the absence of androgen, the AR could be activated by various growth-promoting (growth factors, epidermal growth factor receptor-related oncogene HER-2/neu) and pleiotropic (protein kinase A activators, interleukin-6) compounds as well as by inducers of differentiation (phenylbutyrate). AR function is modulated by a number of coactivators and corepressors. The three coactivators, TIF-2, SRC-1 and RAC3, are up-regulated in relapsed prostate cancer. New experimental therapies for prostate cancer are aimed to down-regulate AR expression and to overcome difficulties which occur because of the acquisition of agonistic properties of commonly used antiandrogens.

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