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Metaphase

About: Metaphase is a research topic. Over the lifetime, 6925 publications have been published within this topic receiving 291590 citations. The topic is also known as: GO:0007091 & mitotic metaphase/anaphase transition.


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Journal ArticleDOI
TL;DR: The conclusion has been drawn that the bulk of attachment sites of DNP fibrils to axial chromosomal structures remains unchanged during the cell cycle.
Abstract: The fragments of DNA attached to protein skeleton of interphase nuclei or metaphase chromosomes were obtained Both the method involving restriction endonuclease treatment/1,2/and a novel procedure based on mild staphylococcal nuclease digestion were used In the latter case, DNA fragments remaining bound to nuclei or chromosomes are not enriched in satellite but only in abundant middle repetitive DNA The shorter the fragments of attached DNA, the higher the content of middle repetitive DNA in the fraction It has a slightly higher density in a CsCl gradient comparing to the main DNA The yield of attached DNA, its distribution in a CsCl density gradient, and its renaturation properties are essentially the same for interphase and metaphase chromosomes The average size of DNA loops was found to be equal to approximately 60 kb for both metaphase chromosomes and interphase nuclei The conclusion has been drawn that the bulk of attachment sites of DNP fibrils to axial chromosomal structures remains unchanged during the cell cycle

98 citations

Journal Article
TL;DR: Three permanent human neoplastic cell strains were cultured in a fluid medium and reacted to elevated temperatures at first with increased rate of growth, then with temporary interruption of the mitotic cycle in metaphase, and finally with irreversible heat injury.
Abstract: Summary Three permanent human neoplastic cell strains were cultured in a fluid medium. Their reactions to elevated temperatures were studied. HeLa and J96 showed the same tolerance to heat, while H.Ep. #2 was more resistant. The three strains reacted to elevated temperatures at first with increased rate of growth (maximum at 38° C.), then with temporary interruption of the mitotic cycle in metaphase (39°–40° C.), finally with irreversible heat injury. The lethal exposure times were determined between 42° and 46° C. for single and divided heat application. The thermotolerance increased by culturing the cells at 39° C. previous to the experiment and was decreased by culturing them at 31° C. Cells surviving heat application became considerably more thermoresistant for at least 3 months. Sublines with higher thermotolerance were developed from all three strains. The morphologic changes during and after heat treatment were described.

98 citations

Journal ArticleDOI
TL;DR: The cytotoxic neutral cysteine protease inhibitor Nacetylleucylleu and leucine leucinesucinal (ALLN) inhibits cell-cycle progression in CHO cells, affecting the G1/S and metaphase-anaphase transition points as mentioned in this paper.
Abstract: The cytotoxic neutral cysteine protease inhibitor N-acetylleucylleucylnorleucinal (ALLN) inhibits cell-cycle progression in CHO cells, affecting the G1/S and metaphase-anaphase transition points, as well as S phase. Mitotic arrest induced by ALLN is associated with the inhibition of cyclin B degradation. At mitosis-inhibiting concentrations of ALLN, cells undergo nuclear-envelope breakdown, spindle formation, chromosome condensation, and congression to the metaphase plate. However, normal anaphase events do not occur, and cells arrest in a metaphase configuration for a prolonged period. Steady-state levels of cyclin B increase to greater than normal mitotic levels, and cyclin B is not degraded for an extended period. Histone H1 kinase activity remains elevated during mitotic arrest. Duration of mitotic arrest depends on ALLN concentration; high concentrations (> 50 micrograms/ml) produce a prolonged mitotic arrest, whereas at lower concentrations, cells are transiently delayed through mitosis (up to 4-12 hr), after which they undergo aberrant cell division resulting in randomly sized daughter cells containing variable amounts of DNA. Cyclin B degradation fails to occur, and histone H1 kinase remains activated for the duration of mitotic arrest at all ALLN concentrations.

98 citations

Journal ArticleDOI
TL;DR: It is suggested that the transferred piece of human genetic material is smaller than 20% of the human X chromosome or less than 1% ofThe human genome.
Abstract: We have transferred the human gene for hypoxanthine-guanine phosphoribosyltransferase (HPRT, EC 2.4.2.8; IMP:pyrophosphate phosphoribosyltransferease) via isolated metaphase chromosomes from human HeLa S3 cells into murine A9 cells which lack functional murine HPRT activity, using the technique of McBride and Ozer (Proc, Nat. Acad. Sci. USA 70, 1258-1262, 1973). Three transformed clones were isolated which contained human HPRT activity as determined by electrophoretic and immunochemical assays. Twenty human isozymes other than HPRT whose genes have been assigned to 14 human chromosomes were found to be absent in our transformed clones. Moreover, the human isozymes of hlucose-6-phosphate dehydrogenase (EC 1.1.1.49; D-glucose 6-phosphate:NADP 1-oxidoreductase) and phosphoglycerate kinase (EC 2.7.2.3;ATP:3-phospho-D-glycerate 1-phosphotransferase), whose genes have been linked with the HPRT gene to the long are of the human X chromosome, were also absent. On the basis of the known linkage relationships of the three markers, we thereby suggest that the transferred piece of human genetic material is smaller than 20% of the human X chromosome or less than 1% of the human genome. This estimate assumes a normal syntenic relationship for the long arm of the X chromosome in HeLa S3 cells. In agreement with this conclusion, no human chromosomes could be detected in our transformed clones. When grown under nonselective conditions about 3% of the gene transfer cells lost the human HPRT marker per cell generation. Transformants that had lost human HPRT activity were subjected to hypoxanthine-aminopterin-thymidine selection. The frequency of revertants to the HPRT(+) phenotype was less than 1 x 10(-6), and two revertants that were obtained possessed the mouse electrophoretic phenotype. These results argue against a stable integration of the human donor genetic material into the mouse recipient genome.

98 citations

Journal ArticleDOI
TL;DR: It is shown that the analysis of protein localisation is useful to refine a phenotypic profile and identified C13orf3 (Ska3) as a new component of the Ska complex and show a direct interaction with a regulatory subunit of the protein phosphatase PP2A.
Abstract: Proliferation of mammalian cells requires the coordinated function of many proteins to accurately divide a cell into two daughter cells. Several RNAi screens have identified previously uncharacterised genes that are implicated in mammalian cell division. The molecular function for these genes needs to be investigated to place them into pathways. Phenotypic profiling is a useful method to assign putative functions to uncharacterised genes. Here, we show that the analysis of protein localisation is useful to refine a phenotypic profile. We show the utility of this approach by defining a function of the previously uncharacterised gene C13orf3 during cell division. C13orf3 localises to centrosomes, the mitotic spindle, kinetochores, spindle midzone, and the cleavage furrow during cell division and is specifically phosphorylated during mitosis. Furthermore, C13orf3 is required for centrosome integrity and anaphase onset. Depletion by RNAi leads to mitotic arrest in metaphase with an activation of the spindle assembly checkpoint and loss of sister chromatid cohesion. Proteomic analyses identify C13orf3 (Ska3) as a new component of the Ska complex and show a direct interaction with a regulatory subunit of the protein phosphatase PP2A. All together, these data identify C13orf3 as an important factor for metaphase to anaphase progression and highlight the potential of combined RNAi screening and protein localisation analyses.

98 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202373
2022116
202182
202087
2019113
201888