It is well known that at the beginning of mitosis the nucleolus disassembles but then reassembles at the end of mitosis. However, the mechanisms of these processes are still unclear. In the present work, we show for the first time that selective inhibition of cyclin B-dependent kinase 1 (CDK1) by roscovitine induces premature assembly of the nucleolus in mammalian cells in metaphase. Treatment of metaphase cells with roscovitine induces formation of structures in their cytoplasm that contain major proteins of the mature nucleolus participating in rRNA processing, such as B23/nucleophosmin, C23/nucleolin, fibrillarin, Nop52, as well as partially processed (immature) 46-45S pre-rRNA. This effect is reproducible in cells of various types; this indicates that general mechanisms regulate early stages of the nucleolus reassembly with CDK1 participation in mammalian cells. Based on our and literature data, we suggest that inactivation of the CDK1-cyclin B complex at the end of mitosis results in dephosphorylation of B23/nucleophosmin and C23/nucleolin; this facilitates their interaction with pre-rRNA and leads to formation of insoluble supramolecular complexes--nucleolus-derived foci.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1134/s0006297908040056 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Chromosome alignment and Kif18A action rely on spindle-localized control of Cdk1 activity.
Front Cell Dev Biol
November 2024
Dipartimento di Medicina Molecolare e Biotecnologie Mediche (DMMBM), University of Naples "Federico II", Naples, Italy.
Introduction: During mitosis, chromosome alignment at the mitotic spindle equator grants correct chromosome segregation and proper nuclei formation in daughter cells. The kinesin 8 family member Kif18A plays a crucial role for chromosome alignment by localizing at the kinetochore-microtubule (K-MT) plus ends to dampen MT dynamics and stabilize K-MT attachments. Kif18A action is directly antagonized by the master mitotic kinase cyclin B-dependent kinase 1 (Cdk1) and is promoted by protein phosphatase 1 (PP1).
View Article and Find Full Text PDFFOXG1 as a Potential Therapeutic Target for Alzheimer's Disease with a Particular Focus on Cell Cycle Regulation.
J Alzheimers Dis
April 2022
School of Medicine, Jiangsu University, Zhenjiang, Jiangsu Province, China.
Background: Several recent findings have revealed that targeting of cell cycle reentry and (or) progression may provide an opportunity for the therapeutic intervention of Alzheimer's disease (AD). FOXG1 has been shown to play important roles in pattern formation, cell proliferation, and cell specification. Thus far, the roles of FoxG1 and its involvement in AD are largely unknown.
View Article and Find Full Text PDFMitotic timing is differentially controlled by A- and B-type cyclins and by CDC6 associated with a CDK inhibitor Xic1 in cell-free extract.
Int J Dev Biol
February 2022
Univ Rennes, UMR 6290, CNRS, Institute of Genetics and Development of Rennes - IGDR, Cell Cycle Group, Faculty of Medicine, Rennes, France.
The timing of the M-phase is precisely controlled by a CDC6-dependent mechanism inhibiting the mitotic histone H1 kinase. Here, we describe the differential regulation of the dynamics of this mitotic kinase activity by exogenous cyclin A or cyclin B in the cycling extracts. We show that the experimental increase in cyclin A modifies only the level of histone H1 kinase activity, while the cyclin B increase modifies two parameters: histone H1 kinase activity and the timing of its full activation, which is accelerated.
View Article and Find Full Text PDFN-Methyl-D-Aspartate Receptor Signaling-Protein Kinases Crosstalk in Cerebral Ischemia.
Adv Exp Med Biol
February 2021
Department of Toxicology, Faculty of Pharmacy, Gazi University, Ankara, Turkey.
Although stroke is very often the cause of death worldwide, the burden of ischemic and hemorrhagic stroke varies between regions and over time regarding differences in prognosis, prevalence of risk factors, and treatment strategies. Excitotoxicity, oxidative stress, dysfunction of the blood-brain barrier, neuroinflammation, and lysosomal membrane permeabilization, sequentially lead to the progressive death of neurons. In this process, protein kinases-related checkpoints tightly regulate N-methyl-D-aspartate (NMDA) receptor signaling pathways.
View Article and Find Full Text PDFSpatiotemporal control of mitotic exit during anaphase by an aurora B-Cdk1 crosstalk.
Elife
August 2019
Chromosome Instability & Dynamics Group, i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
According to the prevailing 'clock' model, chromosome decondensation and nuclear envelope reformation when cells exit mitosis are byproducts of Cdk1 inactivation at the metaphase-anaphase transition, controlled by the spindle assembly checkpoint. However, mitotic exit was recently shown to be a function of chromosome separation during anaphase, assisted by a midzone Aurora B phosphorylation gradient - the 'ruler' model. Here we found that Cdk1 remains active during anaphase due to ongoing APC/C- and APC/C-mediated degradation of B-type Cyclins in and human cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!