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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
13 Mar 1980-Nature
TL;DR: The hypothesis that H1 histone phosphorylation controls the initiation step of mitosis through chromosome condensation is supported.
Abstract: Changes in the structural organisation of chromatin are necessary for the progression of the cell cycle. These changes are thought to be regulated mainly by the modification of chromosomal proteins by reactions such as phosphorylation1–8, acetylation9–12, methylation13,14 and poly(ADP-ribosyl)-ation15,16. Among these modifications, phosphorylation of histones, especially that of the H1 histone, is the most likely candidate for a factor which regulates chromosome condensation1–8. It has been proposed that the phosphorylated form of H1 histone may be involved in the initiation of chromosome condensation1–4 or in the maintenance of the condensed state of chromatin8. The latter possibility is unlikely because zinc chloride, which inhibits phosphatase in vivo and preserves the highly phosphorylated form of H1 histone at metaphase, does not prevent the dispersion of chromosomes at the end of mitosis17. As for the former possibility, Bradbury et al. reported2 that the activity of H1 histone phosphorylation is closely correlated with mitotic triggering in the cell cycle and suggest3,4 that H1 histone phosphokinase is involved in the initiation of mitosis. However, no causal relationship has been established. To analyse the mechanism of the progression of the cell cycle, we have isolated several temperature-sensitive (ts) growth mutants from FM3A, a cell line derived from C3H mouse mammary carcinoma18. We report here on one of these ts mutants, designated the ts85 strain, which shows an abnormal chromosome condensation as well as deficiency in H1 histone phosphorylation at the non-permissive temperature. Our results support the hypothesis that H1 histone phosphorylation controls the initiation step of mitosis through chromosome condensation.

114 citations

Journal ArticleDOI
TL;DR: The results suggest that, throughout this isometric state, an outward force exerted on the spindle poles by MT sliding motors is balanced by flux, and that suppression of flux could tip the balance of forces at the onset of anaphase B, allowing MT sliding and polymerization to push the poles apart.
Abstract: We proposed that spindle morphogenesis in Drosophila embryos involves progression through four transient isometric structures in which a constant spacing of the spindle poles is maintained by a balance of forces generated by multiple microtubule (MT) motors and that tipping this balance drives pole-pole separation. Here we used fluorescent speckle microscopy to evaluate the influence of MT dynamics on the isometric state that persists through metaphase and anaphase A and on pole-pole separation in anaphase B. During metaphase and anaphase A, fluorescent punctae on kinetochore and interpolar MTs flux toward the poles at 0.03 μm/s, too slow to drive chromatid-to-pole motion at 0.11 μm/s, and during anaphase B, fluorescent punctae on interpolar MTs move away from the spindle equator at the same rate as the poles, consistent with MT-MT sliding. Loss of Ncd, a candidate flux motor or brake, did not affect flux in the metaphase/anaphase A isometric state or MT sliding in anaphase B but decreased the duration of the isometric state. Our results suggest that, throughout this isometric state, an outward force exerted on the spindle poles by MT sliding motors is balanced by flux, and that suppression of flux could tip the balance of forces at the onset of anaphase B, allowing MT sliding and polymerization to push the poles apart.

114 citations

Journal ArticleDOI
TL;DR: It is proposed that the loss of this targeting function leads to abnormal endothelial tube formation, thereby explaining the mechanism of formation of cerebral cavernous malformation (CCM) lesions.
Abstract: Mutations in Krev1 interaction trapped gene 1 (KRIT1) cause cerebral cavernous malformation, an autosomal dominant disease featuring malformation of cerebral capillaries resulting in cerebral hemorrhage, strokes, and seizures. The biological functions of KRIT1 are unknown. We have investigated KRIT1 expression in endothelial cells by using specific anti-KRIT1 antibodies. By both microscopy and coimmunoprecipitation, we show that KRIT1 colocalizes with microtubules. In interphase cells, KRIT1 is found along the length of microtubules. During metaphase, KRIT1 is located on spindle pole bodies and the mitotic spindle. During late phases of mitosis, KRIT1 localizes in a pattern indicative of association with microtubule plus ends. In anaphase, the plus ends of the interpolar microtubules show strong KRIT1 staining and, in late telophase, KRIT1 stains the midbody remnant most strongly; this is the site of cytokinesis where plus ends of microtubules from dividing cells overlap. These results establish that KRIT1 is a microtubule-associated protein; its location at plus ends in mitosis suggests a possible role in microtubule targeting. These findings, coupled with evidence of interaction of KRIT1 with Krev1 and integrin cytoplasmic domain-associated protein-1 alpha (ICAP1 α), suggest that KRIT1 may help determine endothelial cell shape and function in response to cell–cell and cell–matrix interactions by guiding cytoskeletal structure. We propose that the loss of this targeting function leads to abnormal endothelial tube formation, thereby explaining the mechanism of formation of cerebral cavernous malformation (CCM) lesions.

114 citations

Journal ArticleDOI
TL;DR: Ect2 and MgcRacGAP regulate the activation and function of Cdc42 in mitosis, and are suggested to be Rho GTPase guanine nucleotide exchange factor and GTP enzyme activating protein.
Abstract: Although Rho regulates cytokinesis, little was known about the functions in mitosis of Cdc42 and Rac. We recently suggested that Cdc42 works in metaphase by regulating bi-orient attachment of spindle microtubules to kinetochores. We now confirm the role of Cdc42 by RNA interference and identify the mechanisms for activation and down-regulation of Cdc42. Using a pull-down assay, we found that the level of GTP-Cdc42 elevates in metaphase, whereas the level of GTP-Rac does not change significantly in mitosis. Overexpression of dominant-negative mutants of Ect2 and MgcRacGAP, a Rho GTPase guanine nucleotide exchange factor and GTPase activating protein, respectively, or depletion of Ect2 by RNA interference suppresses this change of GTP-Cdc42 in mitosis. Depletion of Ect2 also impairs microtubule attachment to kinetochores and causes prometaphase delay and abnormal chromosomal segregation, as does depletion of Cdc42 or expression of the Ect2 and MgcRacGAP mutants. These results suggest that Ect2 and MgcRacGAP regulate the activation and function of Cdc42 in mitosis.

114 citations

Journal ArticleDOI
TL;DR: It is concluded that myocardial cells can no longer be cited in support of the dogma, that differentiated cells do no divide, that there is a temporary competition between the two phenomena at the metaphase-anaphase stages.
Abstract: Ventricular heart cultures were prepared from newborn rats and examined in Rose chambers by high resolution, phase-contrast optics. Details of the procedure are given for obtaining a high yield of myocardial or endothelial cells. Photographic records were obtained of living cells by using photomicrography, cinematography, and high speed filming to document the cytological differences between endothelial and myocardial cells, details of mitosis in the two cell types, and patterns of contractility. Myocardial cells can be distinguished from endothelial cells in the living state by the following criteria; dense cytoplasm; giant and pleomorphic mitochondria or sarcosomes: presence of small, round nuclei; binucleation; one or two round, dense nucleoli; a specialized Golgi apparatus around the nucleus; myofobrils; intercalated discs; myopodia; small, cell size; failure of cell migration; spontaneous contractions; formation of synchronized networks; and flattened appearance with adhesion to other cells during mitosis. Contracting myocardial cells are shown to undergo mitosis. Contractions become weaker at metaphase and then cease at anaphase. Daughter cells may resume contractions. Organized myofibrils are generally not detected during the mitotic periods when contractions are minimal or absent. It is proposed that myofibrils undergo a transient disorganization during mid-mitosis and become reorganized in the daughter cell(s). It is suggested that there is a competition for energy at the time of spindle changes and chromosome movements, so that priority is given to the mitotic process rather than to myofibrillar contractions. Myofibrillogenesis is considered to be a relatively rapid process. The average mitotic time is 2.5 hr fore endothelial cells and 6.1 hr for myocardial cells. Failure of cytokinesis frequently occurs in dividing myocardial cells and results in the formation of binucleated cells. A sequence, is presented of a binucleated myocardial cell which undergoes an abormal multipolar mitosis, leading to polynucleation. Myocardial cells incorporate tritiated thymidine into nuclear DNA. The question of mitosis and differentiation of myocardial cells is reviewed. It is concluded that myocardial cells can no longer be cited in support of the dogma, that differentiated cells do no divide. However, these is a temporary competition between the two phenomena at the metaphase-anaphase stages.

114 citations


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