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.

Wolbachia-induced delay of paternal chromatin condensation does not prevent maternal chromosomes from entering anaphase in incompatible crosses of Drosophila simulans

Abstract: The behavior of parental chromosomes during the first mitosis of Drosophila simulans zygotes obtained from unidirectional incompatible crosses is described and it is demonstrated that the condensation of parental chromatin complements was asynchronous. The timing of paternal chromatin condensation appeared to be delayed in these embryos, so that condensed maternal chromosomes and entangled prophase-like paternal fibers congressed in the equatorial plane of the first metaphase spindle. At anaphase the maternal chromosomes migrated to opposite poles of the spindle, whereas the paternal chromatin lagged in the midzone of the spindle. This resulted in dramatic errors in paternal chromatin inheritance leading to the formation of embryos with aneuploid or haploid nuclei. These observations suggest that the anaphase onset of maternal chromosomes is unaffected by the improper alignment of the paternal complement. Since the first metaphase spindle of the Drosophila zygote consists of twin bundles of microtubules each holding one parental complement, we suspect that each half spindle regulates the timing of anaphase onset of its own chromosome set. In normal developing embryos, the fidelity of chromosome transmission is presumably ensured by the relative timing required to prepare parental complements for the orderly segregation that occurs during the metaphase-anaphase transition.

Active involvement of Ca2+ in mitotic progression of Swiss 3T3 fibroblasts.

Abstract: Global Ca2+ transients have been observed to precede nuclear envelope breakdown and the onset of anaphase in Swiss 3T3 fibroblasts in 8% (vol/vol) FBS. The occurrence of these Ca2+ transients was dependent on intracellular stores. These Ca2+ transients could be (a) abolished by serum removal without halting mitosis, and (b) eliminated by increasing intracellular Ca2+ buffering capacity through loading the cells with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) buffer, via the tetra(acetoxymethyl) ester, without hindering the transition into anaphase. Microinjection of sufficient concentrations of BAPTA buffer could block nuclear envelope breakdown. Pulses of Ca2+ generated by flash photolysis of intracellularly trapped nitr-5, a "caged" Ca2+, could precipitate precocious nuclear envelope breakdown in prophase cells. In metaphase cells, photochemically generated Ca2+ pulses could cause changes in the appearance of the chromosomes, but the length of time required for cells to make the transition from metaphase to anaphase remained essentially unchanged regardless of whether a Ca2+ pulse was photoreleased during metaphase. The results from these photorelease experiments were not dependent on the presence of serum in the medium. Discharging intracellular Ca2+ stores with ionomycin in the presence of 1.8 mM extracellular Ca2+ doubled the time for cells to pass from late metaphase into anaphase, whereas severe Ca2+ deprivation by treatment with ionomycin in EGTA-containing medium halted mitosis. Our results collectively indicate that Ca2+ is actively involved in nuclear envelope breakdown, but Ca2+ signals are likely unnecessary for the metaphase-anaphase transition in Swiss 3T3 fibroblasts. Additional studies of intracellular Ca2+ concentrations in mitotic REF52 and PtK1 cells revealed that Ca2+ transients are not observed at all mitotic stages in all cells. The absence of observable global Ca2+ transients, where calcium buffers can block and pulses of Ca2+ can advance mitotic stages, may imply that the relevant Ca2+ movements are too local to be detected.

p93dis1, which is required for sister chromatid separation, is a novel microtubule and spindle pole body-associating protein phosphorylated at the Cdc2 target sites.

Abstract: Fission yeast cold-sensitive (cs) disl mutants are defective in sister chromatid separation. The dis1 + gene was isolated by chromosome walking. The null mutant showed the same phenotype as that of cs mutants. The d/s/+ gene product was identified as a novel 93-kD protein, and its localization was determined by use of anti-disl antibodies and green fluorescent protein (GFP) tagged to the carboxyl end of p93 dis1. The tagged p93 dlsl in living cells localizes along cytoplasmic microtubule arrays in interphase and the elongating anaphase spindle in mitosis, but association with the short metaphase spindle microtubules is strikingly reduced. In the spindle, the tagged p93 ais~ is enriched at the spindle pole bodies (SPBs). Time-lapse video images of single cells support the localization shift of p93 dis~ to the SPBs in metaphase and spindle microtubules in anaphase. The carboxy-terminal fragment, which is essential for Disl function, accumulates around the mitotic SPB. We propose that these localization shifts of p93 dis~ in mitosis facilitates sister chromatid separation by affecting SPB and anaphase spindle function.