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PubMed1983

Structural organization of the meiotic prophase chromatin in the rat testis.

Pachytene nuclei were isolated from rat testes by the unit gravity sedimentation technique and contained histone variants H1a, H1t, TH2A, TH2B, and X2 in addition to the somatic histones H1bde, H1c, H2A, H2B, H3, and H4. The basic organization of the pachytene chromatin namely the nucleosome repeat length and the accessibility to micrococcal nuclease, was similar to that of rat liver interphase chromatin. However, when digested by DNase I, the susceptibility of pachytene chromatin was 25% more than liver chromatin under identical conditions. Nucleosome core particles were isolated from both liver and pachytene nuclei and were characterized for their DNA length and integrity of the nucleoprotein on low ionic strength nucleoprotein gels. While liver core particles contained all the somatic histones H2A, H2B, H3, and H4, in the pachytene core particles, histone variants TH2A, X2, and TH2B had replaced nearly 60% of the respective somatic histones. A comparison of the circular dichroism spectra obtained for pachytene and liver core particles indicated that the pachytene core particles were less compact than the liver core particles. Studies on the thermal denaturation properties of the two types of core particles revealed that the fraction of the pachytene core DNA melting at the premelting temperature region of 55-60 degrees C was significantly higher than that of the liver core DNA.

Animals↗
PubMed1988

Visualization of chromosome assembly during the S and G2 stages of the cycle and chromosome disassembly during the G1 stage in semithin sections of mouse duodenal crypt cells and other cells.

Previous examination of dividing cells in the isthmus of the mouse pyloric antrum by using semithin (0.5-micron-thick) Epon sections revealed that the prophasic condensation of chromosomes began early in the DNA-synthesizing (S) stage. In order to examine whether the same observation could be made in other proliferating cell types, the crypt base columnar cells in mouse duodenum and the hepatocytes of the rat 48 hr after partial hepatectomy were investigated by morphologic and radioautographic techniques. When crypt base columnar cells were studied in semithin Epon sections, the four phases of mitosis showed the characteristic features described by classical cytologists. Moreover, the proportion of cells in prophase and telophase was high. To relate the mitotic phases to the stages of the cell cycle, the "frequency of labeled mitoses method" provided the duration of the cell cycle, 12.3 hr, and of the S stage, 7.3 hr. From the frequency of the occurrence of mitotic phases, it was estimated that metaphase lasted 0.3 hr and anaphase 0.11 hr, in line with previous estimates. However, the durations of prophase and telophase were long, 5.9 and 1.9 hr, respectively. The whole mitotic process took over 8 hr. From the duration of prophase and cycle stages, it was calculated that 67% of the S stage was occupied by prophasic cells. In fair agreement with this estimate, 68% of the labeled cells 10 min after a 3H-thymidine injection were found to be in prophase. In regenerating hepatocytes, the morphological features and frequency of prophase and telophase cells were similar to those observed in duodenal crypt cells. While the cycle time was not measured and, therefore, the duration of cycle stages and mitotic phases could not be estimated, it is likely that their duration would be of the same order of magnitude. In conclusion, the mitotic process in duodenal crypt cells takes over 8 hr. Moreover, the crypt cells, like antral isthmal cells, show features of early prophase soon after they enter the S stage of the cycle.

Animals↗
PubMed1981

Effect of hypothermia (20-25 degrees C) on mitosis in PtK1 cells.

PtK1 cells enter prophase and complete mitosis at 24-25 degrees C but are inhibited from entering prophase at 20-21 degrees C. Cells which have progressed up to midprophase at 24-37 degrees C return to interphase when cooled to 20-21 degrees C, but those in late prophase complete a normal, although prolonged mitosis. If prophase cells which have reverted to interphase at 20-21 degrees C are incubated at 24-37 degrees C they reenter prophase and complete mitosis. This temperature-induced prophase-interphase-prophase transition can be repeated several times on the same cell. At 24-25 degrees C the process of spindle formation (i.e. prometaphase to the initiation of anaphase) encompasses approximately 75% of the total mitotic interval, with a duration of 8-12 h, compared to about 50% of the mitotic interval and a duration of 0.5 to 1.0 h at 37 degrees C.

Anaphase↗
PubMed2004

Visualization of early chromosome condensation: a hierarchical folding, axial glue model of chromosome structure.

Current models of mitotic chromosome structure are based largely on the examination of maximally condensed metaphase chromosomes. Here, we test these models by correlating the distribution of two scaffold components with the appearance of prophase chromosome folding intermediates. We confirm an axial distribution of topoisomerase IIalpha and the condensin subunit, structural maintenance of chromosomes 2 (SMC2), in unextracted metaphase chromosomes, with SMC2 localizing to a 150-200-nm-diameter central core. In contrast to predictions of radial loop/scaffold models, this axial distribution does not appear until late prophase, after formation of uniformly condensed middle prophase chromosomes. Instead, SMC2 associates throughout early and middle prophase chromatids, frequently forming foci over the chromosome exterior. Early prophase condensation occurs through folding of large-scale chromatin fibers into condensed masses. These resolve into linear, 200-300-nm-diameter middle prophase chromatids that double in diameter by late prophase. We propose a unified model of chromosome structure in which hierarchical levels of chromatin folding are stabilized late in mitosis by an axial "glue."

Adenosine Triphosphatases↗
PubMed2000

Microtubule disassembly delays the G2-M transition in vertebrates.

When cell cultures in growth are treated with drugs that cause microtubules to disassemble, the mitotic index (MI) progressively increases as the cells accumulate in a C-mitosis. For many cell types, however, including rat kangaroo kidney PtK(1) cells, the MI does not increase during the first several hours of treatment [1-3] (Figure 1). This 'lag' implies either that cells are entering mitosis but rapidly escaping the block, or that they are delayed from entering division. To differentiate between these possibilities, we fixed PtK(1) cultures 0, 90 and 270 minutes after treatment with nocodazole, colcemid, lumi-colcemid, taxol or cytochalasin D. After 90 minutes, we found that the numbers of prophase cells in cultures treated with nocodazole or colcemid were reduced by approximately 80% relative to cultures treated with lumi-colcemid, cytochalasin D or taxol. Thus, destroying microtubules delays late G(2 )cells from entering prophase and, as the MI does not increase during this time, existing prophase cells do not enter prometaphase. When mid-prophase cells were treated with nocodazole, the majority (70%) decondensed their chromosomes and returned to G(2) before re-entering and completing prophase 3-10 hours later. Thus, a pathway exists in vertebrates that delays the G(2)-M transition when microtubules are disassembled during the terminal stages of G(2). As this pathway induces mid-prophase cells to transiently decondense their chromosomes, it is likely that it downregulates the cyclin A-cyclin-dependent kinase 2 (CDK2) complex, which is required in vertebrates for the early stages of prophase [4].

Animals↗
PubMed2000

Role of dihydropyridine-sensitive calcium channels in meiosis and fertilization in the bivalve molluscs Ruditapes philippinarum and Crassostrea gigas.

Prophase-arrested oocytes of Ruditapes philippinarum can not be fertilized or stimulated by a depolarizing agent such as an excess of KCl, in contrast to the situation found in Crassostrea gigas. We have performed a comparative study between the two situations found in these species. In vitro, both of these oocytes can be triggered to reinitiate meiosis following a treatment by serotonin which promotes an intracellular calcium surge. Ruditapes and Crassostrea oocytes further arrest in metaphase I, at which stage they can be either activated by sperm or by excess KCl. These treatments trigger an intracellular calcium increase. This suggests that functional voltage-operated Ca2+ channels are expressed in Ruditapes during the course of maturation between prophase and metaphase I. Results obtained using pharmacological tools and direct binding of specific dihydropyridines, strongly suggest that these channels are dihydropyridine-sensitive calcium channels. In Ruditapes they become functional after 5-HT stimulation, their number increasing before GVBD. In Crassostrea the dihydropyridine-sensitive Ca2+ channels are already present at prophase stage and their density is constant from prophase to metaphase I. Moreover, we have shown for Ruditapes and Crassostrea that: 1) the addition of 10 microM of S(-)BayK8644, an agonist of dihydropyridine-sensitive calcium channels to metaphase-arrested oocytes releases them from metaphase block; and 2) incubating these oocytes with nicardipine, a potent blocker of dihydropyridine-sensitive Ca2+ channels, inhibits both their activation by excess KCl or fertilization. Taken together these data suggest that the absence of dihydropyridine-sensitive Ca2+ channels in the membrane of prophase-arrested oocytes of Ruditapes may account for their inability to be fertilized at this stage, while the presence of dihydropyridine-sensitive Ca2+ channels in prophase-arrested oocytes of Crassostrea may explain their fertilizability at this stage.

Animals↗