Nucleolar Development in the Interphase of the Cell Cycle

1974 ◽  
Vol 16 (2) ◽  
pp. 333-347
Author(s):  
A. SACRISTÁN-GÁRATE ◽  
M. H. NAVARRETE ◽  
C. DE LA TORRE
Keyword(s):  
Cell Cycle ◽  
Growth Rate ◽  
Structural Changes ◽  
Gene Dosage ◽  
Structural Basis ◽  
Proliferating Cells ◽  
A Cell ◽  
Nucleolar Volume ◽  
Preceding Interval ◽  
S Period

Stereology of nucleoli at 3 different points of the cell cycle, in the middle of the G1, S and G2 of interphase, was accomplished in a naturally synchronous cell population rendered binucleate and thus ‘labelled’ and made identifiable by 1 h caffeine treatment in root meristems of Allium cepa L. Consistent structural changes were found so that nucleolar parameters by themselves can locate a cell at any interphase period. The growth of the nucleolus in the course of interphase takes place exclusively in its granular portion. The growth rate of this last component was found to be greater in the first half of interphase (5.4 µm5 h-1) than in the second (2.9 µm3 h-1), as calculated for a nucleus with only one fused nucleolus. The changes in volume of the nucleolar components during interphase do not parallel the gene dosage. Nucleolar surface at each point seems to be the factor which determines the growth rate in the preceding interval, since these rates are inverted for fused and unfused nucleoli. The nucleolar volume occupied by lacunae is minimal in the S-period and shows an enormous increase by the middle of G2. We think our data may be the structural basis on which a model for nucleolar functioning in proliferating cells could be built.

S-phase-specific expression of the Mad3 gene in proliferating and differentiating cells

2001 ◽  
Vol 359 (2) ◽  
pp. 361-367 ◽  
Author(s):  
Elizabeth J. FOX ◽  
Stephanie C. WRIGHT
Keyword(s):  
Cell Cycle ◽  
Cellular Proliferation ◽  
Cultured Cells ◽  
S Phase ◽  
Proliferating Cells ◽  
Specific Expression ◽  
Related Function ◽  
Erythroleukemia Cells ◽  
A Cell ◽  
Pass Through

The Myc/Max/Mad transcription factor network plays a central role in the control of cellular proliferation, differentiation and apoptosis. In order to elucidate the biological function of Mad3, we have analysed the precise temporal patterns of Mad3 mRNA expression during the cell cycle and differentiation in cultured cells. We show that Mad3 is induced at the G1/S transition in proliferating cells; expression persists throughout S-phase, and then declines as cells pass through G2 and mitosis. The expression pattern of Mad3 is coincident with that of Cdc2 throughout the cell cycle. In contrast, the expression of Mad3 during differentiation of cultured mouse erythroleukemia cells shows two transient peaks of induction. The first of these occurs at the onset of differentiation, and does not correlate with the S-phase of the cell cycle, whereas the second is coincident with the S-phase burst that precedes the terminal stages of differentiation. Our results therefore suggest that Mad3 serves a cell-cycle-related function in both proliferating and differentiating cells, and that it may also have a distinct role at various stages of differentiation.

scholarly journals A KINETIC ANALYSIS OF MYOGENESIS IN VITRO

1972 ◽  
Vol 52 (1) ◽  
pp. 52-65 ◽  
Author(s):  
Michael C. O'Neill ◽  
Frank E. Stockdale
Keyword(s):  
Cell Cycle ◽  
Cell Fusion ◽  
Tritiated Thymidine ◽  
Culture Conditions ◽  
Complete Fusion ◽  
Low Density ◽  
A Cell ◽  
Muscle Cultures ◽  
S Period

Conditions which yielded reproducible growth kinetics with extensive, relatively synchronous differentiation are described for chick muscle cultures. The effects of cell density and medium changes on the timing of cell fusion were examined. Low-density cultures which received a change of medium at 24 hr after plating show the highest rate of cell fusion, increasing from 15 to 80% fused cells in a 10 hr period. These optimal culture conditions were employed to reexamine two questions from the earlier literature on muscle culture: (a) can cells which normally would fuse at the end of one cell cycle be forced to go through another cell cycle before fusion; and (b) how soon after its final S period can a cell complete fusion? In answer to the first question, it was found that if the medium is changed, many cells which would otherwise fuse can be made to undergo another cell cycle before fusion. In the second case, radioautographs were made from cultures incubated with tritiated thymidine for various times at the beginning of the fusion period. These show labeled nuclei in myotubes as early as 3 hr after the beginning of the incubation period. This indicates that cells can fuse as early as the beginning of the G1 period, and suggests that there is not an obligatory exit from the cell cycle or a prolonged G1 period before cell fusion and differentiation during myogenesis.

scholarly journals Pocket Protein Complexes Are Recruited to Distinct Targets in Quiescent and Proliferating Cells

2005 ◽  
Vol 25 (18) ◽  
pp. 8166-8178 ◽  
Author(s):  
Egle Balciunaite ◽  
Alexander Spektor ◽  
Nathan H. Lents ◽  
Hugh Cam ◽  
Hein te Riele ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Regulatory Networks ◽  
Protein Complexes ◽  
Proliferating Cells ◽  
Quiescent Cells ◽  
Pocket Protein ◽  
Genome Wide ◽  
E2f Transcription Factor ◽  
A Cell ◽  
Cycle Dependent

ABSTRACT Biochemical and genetic studies have determined that retinoblastoma protein (pRB) tumor suppressor family members have overlapping functions. However, these studies have largely failed to distinguish functional differences between the highly related p107 and p130 proteins. Moreover, most studies pertaining to the pRB family and its principal target, the E2F transcription factor, have focused on cells that have reinitiated a cell cycle from quiescence, although recent studies suggest that cycling cells exhibit layers of regulation distinct from mitogenically stimulated cells. Using genome-wide chromatin immunoprecipitation, we show that there are distinct classes of genes directly regulated by unique combinations of E2F4, p107, and p130, including a group of genes specifically regulated in cycling cells. These groups exhibit both distinct histone acetylation signatures and patterns of mammalian Sin3B corepressor recruitment. Our findings suggest that cell cycle-dependent repression results from recruitment of an unexpected array of diverse complexes and reveals specific differences between transcriptional regulation in cycling and quiescent cells. In addition, factor location analyses have, for the first time, allowed the identification of novel and specific targets of the highly related transcriptional regulators p107 and p130, suggesting new and distinct regulatory networks engaged by each protein in continuously cycling cells.

scholarly journals Structural and functional characterization of a cell cycle associated HDAC1/2 complex reveals the structural basis for complex assembly and nucleosome targeting

2015 ◽  
Vol 43 (4) ◽  
pp. 2033-2044 ◽  
Author(s):  
Toshimasa Itoh ◽  
Louise Fairall ◽  
Frederick W. Muskett ◽  
Charles P. Milano ◽  
Peter J. Watson ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Functional Characterization ◽  
Structural Basis ◽  
Complex Assembly ◽  
A Cell

Human monoclonal antibody BT32/A6 and a cell cycle—independent glioma-associated surface antigen

1995 ◽  
Vol 82 (3) ◽  
pp. 475-480 ◽  
Author(s):  
Michael D. Dan ◽  
Elizabeth M. Earley ◽  
Mark C. Griffin ◽  
Pradip K. Maiti ◽  
Ashok K. Prashar ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Monoclonal Antibody ◽  
Flow Cytometry ◽  
Growth Rate ◽  
Cell Growth ◽  
Surface Antigen ◽  
Immunoglobulin M ◽  
Cell Growth Rate ◽  
Culture Viability ◽  
A Cell

✓ The purpose of this study was to ascertain how various growth parameters may influence the labeling of SK-MG-1, a human glioma cell line, by BT32/A6, a human immunoglobulin M monoclonal antibody (MAb). By growing SKMG-1 cells at different culture split ratios, significant trends in cell growth rate, culture viability, and cell cycle state were produced. Labeling of SK-MG-1 cells by BT32/A6, however, was shown to be unaffected by culture split ratio (p > 0.05) and is therefore independent of cell growth rate, culture viability, and cell cycle state. Using flow cytometry and fluorescence-activated cell sorting, BT32/A6 was shown to label a cell surface antigen on viable, clonogenic cells of SK-MG-1. Approximately 100% of SK-MG-1 cells were shown by flow cytometry to express the BT32/A6 antigen. The recognition of a glioma-associated, cell cycle-independent surface antigen by MAb BT32/A6 makes it a promising candidate for further studies aimed at elucidating its usefulness as an adjunct in the treatment of human malignant gliomas.

scholarly journals Expression of genes in the16p11.2locus during human fetal cortical neurogenesis

2019 ◽  
Author(s):  
Sarah Morson ◽  
Yifei Yang ◽  
David J. Price ◽  
Thomas Pratt
Keyword(s):  
Cell Cycle ◽  
Cerebral Cortex ◽  
Gene Dosage ◽  
Cell Types ◽  
Autism Spectrum ◽  
Cycle Phase ◽  
Human Cerebral Cortex ◽  
Proliferating Cells ◽  
Protein Coding ◽  
Expression Of Genes

AbstractThe 593 kbp16p11.2copy number variation (CNV) affects the gene dosage of 29 protein coding genes, with heterozygous16p11.2microduplication or microdeletion implicated in about 1% of autism spectrum disorder (ASD) cases. The16p11.2CNV is frequently associated with macrocephaly or microcephaly indicating early defects of neurogenesis may contribute to subsequent ASD symptoms, but it is unknown which16p11.2transcripts are expressed in progenitors and whose levels are likely, therefore, to influence neurogenesis. Analysis of human fetal gene expression data revealed that of all the16p11.2transcripts only two,ALDOAandKIF22, are significantly enriched in progenitors. To investigate the role ofALDOAandKIF22in human cerebral cortex development we used immunohistochemical staining to describe their expression in late first and early second trimester human cerebral cortex. KIF22 protein is restricted to proliferating cells with its levels increasing during the cell cycle and peaking at mitosis. ALDOA protein is expressed in all cell types and does not vary with cell-cycle phase. Our expression analysis suggests the hypothesis that the simultaneous changes in KIF22 and ALDOA dosage in cortical progenitors causes defects in neurogenesis that may contribute to ASD in16p11.2CNV patients.

scholarly journals Cell cycle inhibitor Whi5 records environmental information to coordinate growth and division in yeast

2019 ◽  
Author(s):  
Yimiao Qu ◽  
Jun Jiang ◽  
Xiang Liu ◽  
Ping Wei ◽  
Xiaojing Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Doubling Time ◽  
Optimal Timing ◽  
Proliferating Cells ◽  
Cell Cycle Entry ◽  
Cellular Decision Making ◽  
Need To Evaluate ◽  
A Cell ◽  
Made In

SUMMARYProliferating cells need to evaluate the environment to determine the optimal timing for cell cycle entry, which is essential for coordinating cell division and growth. In the budding yeast Saccharomyces cerevisiae, the commitment to the next round of division is made in G1 at the Start, triggered by the inactivation of the inhibitor Whi5 through multiple mechanisms. However, how a cell reads environmental condition and uses this information to regulate Start is poorly understood. Here, we show that Whi5 is a key environmental indicator and plays a crucial role in coordinating cell growth and division. We found that under a variety of nutrient and stress conditions, the concentration of Whi5 in G1 is proportional to the doubling time in the environment. Thus, under a poorer condition a longer doubling time results in a higher Whi5 concentration, which in turn delays the next cell cycle entry to ensure sufficient cell growth. In addition, the coordination between division and the environment is further fine-tuned in G1 by environmentally dependent G1 cyclin-Cdk1 contribution and Whi5 threshold at Start. Our results show that Whi5 serves as an environmental ‘memory’ and that the cell adopts a simple and elegant mechanism to achieve an adaptive cellular decision making.

Tubulin polyglutamylase: isozymic variants and regulation during the cell cycle in HeLa cells

1999 ◽  
Vol 112 (23) ◽  
pp. 4281-4289 ◽  
Author(s):  
C. Regnard ◽  
E. Desbruyeres ◽  
P. Denoulet ◽  
B. Edde
Keyword(s):  
Cell Cycle ◽  
Hela Cells ◽  
Molecular Motors ◽  
Dependent Manner ◽  
Proliferating Cells ◽  
Beta Tubulin ◽  
Microtubule Associated Proteins ◽  
Associated Proteins ◽  
A Cell ◽  
Cycle Dependent

Polyglutamylation is a posttranslational modification of tubulin that is very common in neurons and ciliated or flagellated cells. It was proposed to regulate the binding of microtubule associated proteins (MAPs) and molecular motors as a function of the length of the polyglutamyl side-chain. Though much less common, this modification of tubulin also occurs in proliferating cells like HeLa cells where it is associated with centrioles and with the mitotic spindle. Recently, we partially purified tubulin polyglutamylase from mouse brain and described its enzymatic properties. In this work, we focused on tubulin polyglutamylase activity from HeLa cells. Our results support the existence of a tubulin polyglutamylase family composed of several isozymic variants specific for alpha- or beta-tubulin subunits. In the latter case, the specificity probably also concerns the different beta-tubulin isotypes. Interestingly, we found that tubulin polyglutamylase activity is regulated in a cell cycle dependent manner and peaks in G(2)-phase while the level of glutamylated tubulin peaks in mitosis. Consistent results were obtained by treating the cells with hydroxyurea, nocodazole or taxotere. In particular, in mitotic cells, tubulin polyglutamylase activity was always low while glutamylation level was high. Finally, tubulin polyglutamylase activity and the level of glutamylated tubulin appeared to be inversely related. This paradox suggests a complex regulation of both tubulin polyglutamylase and the reverse deglutamylase activity.

scholarly journals Aneuploid yeast strains exhibit defects in cell growth and passage through START

2013 ◽  
Vol 24 (9) ◽  
pp. 1274-1289 ◽  
Author(s):  
Rebecca R. Thorburn ◽  
Christian Gonzalez ◽  
Gloria A. Brar ◽  
Stefan Christen ◽  
Thomas M. Carlile ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Rate ◽  
Cell Proliferation ◽  
Growth Defect ◽  
Cell Cycle Entry ◽  
Yeast Strains ◽  
Additional Chromosome ◽  
A Cell ◽  
Cellular Stresses ◽  
Haploid Karyotype

Aneuploidy, a chromosome content that is not a multiple of the haploid karyotype, is associated with reduced fitness in all organisms analyzed to date. In budding yeast aneuploidy causes cell proliferation defects, with many different aneuploid strains exhibiting a delay in G1, a cell cycle stage governed by extracellular cues, growth rate, and cell cycle events. Here we characterize this G1 delay. We show that 10 of 14 aneuploid yeast strains exhibit a growth defect during G1. Furthermore, 10 of 14 aneuploid strains display a cell cycle entry delay that correlates with the size of the additional chromosome. This cell cycle entry delay is due to a delayed accumulation of G1 cyclins that can be suppressed by supplying cells with high levels of a G1 cyclin. Our results indicate that aneuploidy frequently interferes with the ability of cells to grow and, as with many other cellular stresses, entry into the cell cycle.

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