Topic
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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TL;DR: Four distinct cell populations, representing G1, S, G2, and M, respectively, could be demonstrated in cycling cells on the basis of their PCNA/cyclin and Ki-67 levels, and the cell cycle phase specificity could be verified using metaphase, colcemide, and G2 phase blocking agents, as well as by stainings with a mitosis-specific antibody (MPM-2).
191 citations
TL;DR: The bromodeoxyuridine; sensitivity of 33258 Hoechst fluorescence allows microfluorometric analysis of sister chromatid exchanges in human metaphase chromosomes, which appears to occur predominantly in interband regions, as defined by quinacrine fluorescence, or very near band-interband junctions.
Abstract: The bromodeoxyuridine; sensitivity of 33258 Hoechst fluorescence allows microfluorometric analysis of sister chromatid exchanges in human metaphase chromosomes. The frequency of sister chromatid exchanges among chromosomes correlates with chromosome length. Exchanges appear to occur predominantly in interband regions, as defined by quinacrine fluorescence, or very near band-interband junctions. A few regions are involved unusually frequently.
190 citations
TL;DR: A model to explain cleavage plane geometry in which the length of astral microtubules is limited by interaction with these boundaries, causing length asymmetries is proposed.
190 citations
TL;DR: Cells originating from the thymus of newborn mice were fused with mouse oocytes using polyethylene glycol and the behaviour of thymocyte nuclei was studied in non-activated metaphase II oocytes, and in oocytes activated in vitro with ethanol.
Abstract: Cells originating from the thymus of newborn mice were fused with mouse oocytes using polyethylene glycol. The behaviour of thymocyte nuclei was studied in non-activated metaphase II oocytes, and in oocytes activated in vitro with ethanol. In non-activated oocytes all thymocyte nuclei undergo premature chromosome condensation with individualization of chromosomes; the chromosomes form separate groups in the cytoplasm, or are assembled around the metaphase II spindle, or located on the extra-spindle. In activated oocytes thymocyte nuclei start to develop along a pronucleus-like pathway (decondensation, visualization of nucleoli, swelling) and increase up to 200 times in volume during 24 h culture in vitro, eventually reaching the size of a fully grown pronucleus. Activation/fusion timing seems to be critical for the full remodelling of thymocyte nuclei. Nuclei introduced before (10-30 min) or shortly after (up to 60 min) activation often grow larger than the female pronucleus. Those introduced into oocytes long before activation (greater than 30 min) undergo premature condensation with subsequent reformation of nuclei that are sometimes deficient (as indicated by the presence of micronuclei), or of hybrid character. Nuclei introduced late after activation (greater than 60 min) are mostly doomed to retarded development. The implications of the present observations for nuclear transfer experiments in mammals are discussed.
189 citations
TL;DR: In this article, it was shown that INCENP phosphorylation by cyclin-dependent kinase 1 (Cdk1) is necessary for the recruitment of Plk1 to the kinetochore, and that the complex formation of plk1 and Aurora-B may play crucial roles in the regulation of chromosomal dynamics.
Abstract: Mitotic chromosomal dynamics is regulated by the coordinated activities of many mitotic kinases, such as cyclin-dependent kinase 1 (Cdk1), Aurora-B or Polo-like kinase 1 (Plk1), but the mechanisms of their coordination remain unknown. Here, we report that Cdk1 phosphorylates Thr 59 and Thr 388 on inner centromere protein (INCENP), which regulates the localization and kinase activity of Aurora-B from prophase to metaphase. INCENP depletion disrupts Plk1 localization specifically at the kinetochore. This phenotype is rescued by the exogenous expression of INCENP wild type and INCENP mutated at Thr 59 to Ala (T59A), but not at Thr 388 to Ala (T388A). The replacement of endogenous INCENP with T388A resulted in the delay of progression from metaphase to anaphase. We propose that INCENP phosphorylation by Cdk1 is necessary for the recruitment of Plk1 to the kinetochore, and that the complex formation of Plk1 and Aurora-B on INCENP may play crucial roles in the regulation of chromosomal dynamics.
189 citations