[Action of triethylene melamine on segmentation mitosis, epithelial mitosis and ependymal mitosis in frogs].
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Animals↗
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Results for “Mitosis”
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Mitosis-specific phosphorylation of caldesmon: possible molecular mechanism of cell rounding during mitosis.
One of the profound changes in cellular morphology during mitosis is a massive alteration in the organization of microfilament cytoskeleton. It has been recently discovered that nonmuscle caldesmon, an actin and calmodulin binding microfilament-associated protein of relative molecular mass Mr = 83,000, is dissociated from microfilaments during mitosis, apparently as a consequence of mitosis-specific phosphorylation. cdc2 kinase, which is a catalytic subunit of MPF (maturation or mitosis promoting factor), is found to be responsible for the mitosis-specific phosphorylation of caldesmon. Because caldesmon is implicated in the regulation of actin myosin interactions and/or microfilament organization, these results suggest that cdc2 kinase directly affects microfilament re-organization during mitosis.
Actin Cytoskeleton↗
Tradescantia cytogenetic tests (root-tip mitosis, pollen mitosis, pollen mother-cell meiosis). A report of the U.S. Environmental Protection Agency Gene-Tox Program.
3 kinds of cytogenetic tests for screening of environmental mutagens were established for Tradescantia, namely, root-tip mitosis, pollen mitosis, and pollen mother-cell meiosis [commonly referred to as the Tradescantia-micronucleus (Trad-MCN) test]. All these tests are technically simple, inexpensive, and can yield reliable results in a relatively short time (36-72 h). The root-tip mitosis test is suitable only for liquid agents, while pollen mitosis is suitable for both liquid and gaseous agents. Pollen tube mitotic chromosomes are extremely sensitive to mutagens; therefore, they are good materials for detecting very low concentrations of mutagens. Both root-tip mitosis and pollen mitosis tests use chromosome and/or chromatid aberrations as end points for scoring. The Trad-MCN test is suitable for both liquid and gaseous agents. In addition, it is especially suitable for in situ monitoring of water and air pollutants. Of the 12 chemicals tested, 5-fluorouracil and 1,2-dibromoethane indicate that they are very potent mutagens based on the effective dosage used to produce a positive response. Sulfur dioxide, ethyl methanesulfonate, sodium azide, Phosdrin, and Bladex rank next in potency.
Meiosis↗
Dissociation of FAK/p130(CAS)/c-Src complex during mitosis: role of mitosis-specific serine phosphorylation of FAK.
At mitosis, focal adhesions disassemble and the signal transduction from focal adhesions is inactivated. We have found that components of focal adhesions including focal adhesion kinase (FAK), paxillin, and p130(CAS) (CAS) are serine/threonine phosphorylated during mitosis when all three proteins are tyrosine dephosphorylated. Mitosis-specific phosphorylation continues past cytokinesis and is reversed during post-mitotic cell spreading. We have found two significant alterations in FAK-mediated signal transduction during mitosis. First, the association of FAK with CAS or c-Src is greatly inhibited, with levels decreasing to 16 and 13% of the interphase levels, respectively. Second, mitotic FAK shows decreased binding to a peptide mimicking the cytoplasmic domain of beta-integrin when compared with FAK of interphase cells. Mitosis-specific phosphorylation is responsible for the disruption of FAK/CAS binding because dephosphorylation of mitotic FAK in vitro by protein serine/threonine phosphatase 1 restores the ability of FAK to associate with CAS, though not with c-Src. These results suggest that mitosis-specific modification of FAK uncouples signal transduction pathways involving integrin, CAS, and c-Src, and may maintain FAK in an inactive state until post-mitotic spreading.
Amino Acid Sequence↗
Conservation of mechanisms controlling entry into mitosis: budding yeast wee1 delays entry into mitosis and is required for cell size control.
BACKGROUND: In fission yeast, the Wee1 kinase delays entry into mitosis until a critical cell size has been reached; however, a similar role for Wee1-related kinases has not been reported in other organisms. SWE1, the budding yeast homolog of wee1, is thought to function in a morphogenesis checkpoint that delays entry into mitosis in response to defects in bud morphogenesis. RESULTS: In contrast to previous studies, we found that budding yeast swe1 Delta cells undergo premature entry into mitosis, leading to birth of abnormally small cells. Additional experiments suggest that conditions that activate the morphogenesis checkpoint may actually be activating a G2/M cell size checkpoint. For example, actin depolymerization is thought to activate the morphogenesis checkpoint by inhibiting bud morphogenesis. However, actin depolymerization also inhibits bud growth, suggesting that it could activate a cell size checkpoint. Consistent with this possibility, we found that actin depolymerization fails to induce a G2/M delay once daughter buds pass a critical size. Other conditions that activate the morphogenesis checkpoint block bud formation, which could also activate a size checkpoint if cell size at G2/M is monitored in the daughter bud. Previous work reported that Swe1 is degraded during G2, which was proposed to account for failure of large-budded cells to arrest in response to actin depolymerization. However, we found that Swe1 is present throughout G2 and undergoes hyperphosphorylation as cells enter mitosis, as found in other organisms. CONCLUSIONS: Our results suggest that the mechanisms known to coordinate entry into mitosis in other organisms have been conserved in budding yeast.
Blotting, Western↗
The Aspergillus nidulans bimE (blocked-in-mitosis) gene encodes multiple cell cycle functions involved in mitotic checkpoint control and mitosis.
The bimE (blocked-in-mitosis) gene appears to function as a negative mitotic regulator because the recessive bimE7 mutation can override certain interphase-arresting treatments and mutations, causing abnormal induction of mitosis. We have further investigated the role of bimE in cell cycle checkpoint control by: (1) coordinately measuring mitotic induction and DNA content of bimE7 mutant cells; and (2) analyzing epistasis relationships between bimE7 and 16 different nim mutations. A combination of cytological and flow cytometric techniques was used to show that bimE7 cells at restrictive temperature (44 degrees C) undergo a normal, although somewhat slower cell cycle prior to mitotic arrest. Most bimE7 cells were fully reversible from restrictive temperature arrest, indicating that they are able to enter mitosis normally, and therefore require bimE function in order to finish mitosis. Furthermore, epistasis studies between bimE7 and mutations in cdc2 pathway components revealed that the induction of mitosis caused by inactivation of bimE requires functional p34cdc2 kinase, and that mitotic induction by bimE7 depends upon several other nim genes whose functions are not yet known. The involvement of bimE in S phase function and mitotic checkpoint control was suggested by three lines of evidence. First, at restrictive temperature the bimE7 mutation slowed the cell cycle by delaying the onset or execution of S phase. Second, at permissive temperature (30 degrees C) the bimE7 mutation conferred enhanced sensitivity to the DNA synthesis inhibitor hydroxyurea. Finally, the checkpoint linking M phase to the completion of S phase was abolished when bimE7 was combined with two nim mutations that cause arrest in G1 or S phase. A model for bimE function based on these findings is presented.
Aspergillus nidulans↗
Computer simulations of mitosis and interdependencies between mitosis orientation, cell shape and epithelia reshaping.
Finite element-based computer simulations are used to investigate mitosis and how mitosis, cell shape, and epithelium reshaping depend on each other. Frame- and cell-oriented patterns of mitosis with growing and non-growing daughter cells are considered. Previous simulations have shown that applied stresses or strains can reshape cells so that their long axes are aligned in the principal stretch direction. The simulations reported here show that this can produce global alignment of the mitosis cleavage planes. Other simulations reported here show that mitoses with suitably aligned cleavage planes can drive epithelium reshaping. Formulas that quantify these and other dependencies are derived. These formulas provide quantitative relationships against which current hypotheses regarding epithelia reshaping in real biological systems can be evaluated.
Animals↗
Mitosis-specific activation of LIM motif-containing protein kinase and roles of cofilin phosphorylation and dephosphorylation in mitosis.
Actin filament dynamics play a critical role in mitosis and cytokinesis. LIM motif-containing protein kinase 1 (LIMK1) regulates actin reorganization by phosphorylating and inactivating cofilin, an actin-depolymerizing and -severing protein. To examine the role of LIMK1 and cofilin during the cell cycle, we measured cell cycle-associated changes in the kinase activity of LIMK1 and in the level of cofilin phosphorylation. Using synchronized HeLa cells, we found that LIMK1 became hyperphosphorylated and activated in prometaphase and metaphase, then gradually returned to the basal level as cells entered into telophase and cytokinesis. Although Rho-associated kinase and p21-activated protein kinase phosphorylate and activate LIMK1, they are not likely to be involved in mitosis-specific activation and phosphorylation of LIMK1. Immunoblot and immunofluorescence analyses using an anti-phosphocofilin-specific antibody revealed that the level of cofilin phosphorylation, similar to levels of LIMK1 activity, increased during prometaphase and metaphase then gradually declined in telophase and cytokinesis. Ectopic expression of LIMK1 increased the level of cofilin phosphorylation throughout the cell cycle and induced the formation of multinucleate cells. These results suggest that LIMK1 is involved principally in control of mitosis-specific cofilin phosphorylation and that dephosphorylation and reactivation of cofilin at later stages of mitosis play a critical role in cytokinesis of mammalian cells.
Actin Depolymerizing Factors↗
The control of mitosis in Physarum polycephalum: the effect of delaying mitosis and evidence for the operation of the control mechanism in the absence of growth.
Possible mechanisms coordinating the control of mitosis and DNA synthesis with growth were experimentally tested in Physarum polycephalum by the response of plasmodia to 2 different kinds of perturbation of the DNA:mass ratio. Mitosis and DNA synthesis were delayed without stopping growth either by the use of fluorodeoxyuridine (FUdR) or puromycin, in both cases the delayed mitosis was followed by a single shortened intermitotic period, as predicted by all the mechanisms considered and substantiating a basic assumption made that the time of mitosis is homeostatically controlled to maintain a constant DNA:mass ratio. When more than 50% of the DNA was destroyed by ultraviolet irradiation 2 consecutive mitoses could occur even when growth was completely stopped by starvation. This result can only be accounted for by 2 of the 5 models considered, a finding which agrees with the results of previous experiments which were also consistent with only these 2 mechanisms.
DNA↗
Mitosis and checkpoints that control progression through mitosis in vertebrate somatic cells.
During mitosis in vertebrates the sister kinetochores on each replicated chromosome interact with two separating arrays of astral microtubules to form a bipolar spindle that produces and/or directs the forces for chromosome motion. In order to ensure faithful chromosome segregation cells have evolved mechanisms that delay progress into and out of mitosis until certain events are completed. At least two of these mitotic "checkpoint controls" can be identified in vertebrates. The first prevents nuclear envelope breakdown, and thus spindle formation, when the integrity of some nuclear component(s) is compromised. The second prevents chromosome disjunction and exit from mitosis until all of the kinetochores are attached to the spindle.
Animals↗
p21Waf1/Cip1/Sdi1-induced growth arrest is associated with depletion of mitosis-control proteins and leads to abnormal mitosis and endoreduplication in recovering cells.
Induction of a cyclin-dependent kinase inhibitor p21Waf1/ Cip1/Sdi1 is an integral part of cell growth arrest associated with senescence and damage response. p21 overexpression from an inducible promoter resulted in senescence-like growth arrest in a human fibrosarcoma cell line. After release from p21-induced growth arrest, cells re-entered the cell cycle but displayed growth retardation, cell death and decreased clonogenicity. The failure to form colonies was associated with abnormal mitosis and endoreduplication in the recovering cells and was correlated with the induced level of p21 and the duration of p21 induction. p21 induction was found to inhibit the expression of multiple proteins involved in the execution and control of mitosis. p21-induced depletion of the cellular pools of mitosis-control proteins was followed by asynchronous resynthesis of such proteins after release from p21, which explains the observed mitotic abnormalities. Genetic destabilization in cells recovering from p21-induced growth arrest may conceivably play a role in carcinogenesis and tumor progression.
Autoantigens↗
Long duration of mitosis and consequences for the cell cycle concept, as seen in the isthmal cells of the mouse pyloric antrum. I. Identification of early and late steps of mitosis.
In this series of two articles, the duration of mitosis and that of the cell cycle were examined in a group of proliferating cells located in the mouse pyloric antrum and known as isthmal cells. However, before measuring the duration of mitosis, as described in the second article, it is necessary to identify the early and late steps of the mitotic process. This is attempted in the present article, in which the four phases of mitosis and the interphase are described in semithin (0.5 micron thick) Epon serial sections stained with hemalun. The frequency of these phases is then estimated. The beginning of prophase is indicated by the appearance in the nucleus of numerous 0.2-0.3 micron thick basophilic threads. The threads gradually increase in thickness to become the typical chromosomes (about 0.7-micron thick) observed at the end of prophase. Metaphase and anaphase show no remarkable features. At telophase, chromosomes separate from one another, gradually acquire pale segments along their length eventually to look like rows of alternating dark and light patches, and finally vanish. When prophases and telophases are defined in this manner, the enumeration of isthmal cells yields a high proportion of prophases (28%) and telophases (31%), but a low proportion of metaphases (1%) and anaphases (0.3%). Forty per cent of the cells are in interphase.
Anaphase↗
Symmetric pollen mitosis I and suppression of pollen mitosis II prevent pollen development in Brachiaria jubata (Gramineae).
Microsporogenesis and pollen development were analyzed in a tetraploid (2n = 4x = 36) accession of the forage grass Brachiaria jubata (BRA 007820) from the Embrapa Beef Cattle Brachiaria collection that showed partial male sterility. Microsporocytes and pollen grains were prepared by squashing and staining with 0.5% propionic carmine. The meiotic process was typical of polyploids, with precocious chromosome migration to the poles and laggards in both meiosis I and II, resulting in tetrads with micronuclei in some microspores. After callose dissolution, microspores were released into the anther locule and appeared to be normal. Although each microspore initiated its differentiation into a pollen grain, in 11.1% of them nucleus polarization was not observed, i.e., pollen mitosis I was symmetric and the typical hemispherical cell plate was not detected. After a central cytokinesis, two equal-sized cells showing equal chromatin condensation and the same nuclear shape and size were formed. Generative cells and vegetative cells could not be distinguished. These cells did not undergo the second pollen mitosis and after completion of pollen wall synthesis each gave rise to a sterile and uninucleate pollen grain. The frequency of abnormal pollen mitosis varied among flowers and also among inflorescences. All plants were equally affected. The absence of fertile sperm cells in a considerable amount of pollen grains in this accession of B. jubata may compromise its use in breeding and could explain, at least in part, why seed production is low when compared with the amount of flowers per raceme.
Brachiaria↗
Differentiation by colchicine and vincristine sulphate of regenerative hepatocellular mitosis and tumour-associated hepatocellular mitosis.
Colchicine and vincristine sulphate differentiate sharply between hepatocyte mitosis associated with the Ehrlich ascites tumour, and regenerative (post-CCl4 necrosis) hepatocyte mitosis. In the former case there is a gross depression of prophase index and a marked lowering of the overall mitotic index. In the latter, although a degree of prophase depression is evident, this is insufficient to prevent an overall substantial elevation of mitotic index due to accumulation at metaphase. Very low doses of colchicine claimed to be effective in stathmokinesis of hepatocytes under influence of hepatomitogenic tumour brei and tumour extracts, produced no discernible effect on the mitotic pattern of hepatocytes in Ehrlich ascites tumour-bearing mice nor in post-CCl4 regenerating livers. The results are discussed in the context of known features of tumour-associated hepatocellular mitosis.
Animals↗
Effect of aluminum chloride on mitogenesis, mitosis, and cell cycle in human short-term whole blood cultures: lower concentrations enhance mitosis.
Aluminum, the third most common element in the earth's crust (second to oxygen and silicon) and recently suspected by some investigators to be implicated in Alzheimer disease etiology, has been studied in relation to its effect on mitogenesis, mitosis, and cell cycle. We have observed that 2-4 mM concentrations of AlCl3 have decreased the number of cells that undergo mitogenesis (PHA-induced blast transformation) and mitosis in human short term whole blood cultures. We have also shown that the rate of the cell cycle was slowed down, i.e., cell cycle time was increased in the presence of AlCl3. Also, we have demonstrated a reversible effect on aluminum-induced reduced mitotic index in long-term EBV-transformed lymphoblastoid cultures. Although safeguards such as limiting aluminum serum concentrations have been recommended to protect individuals undergoing dialysis, it should be realized that concentration accumulations of aluminum may increase over chronic exposures. Accordingly, if the number of cells stimulated by PHA is reduced in the presence of AlCl3, there may be a reduction of immune competence, since the degree of PHA stimulation has been used as an indicator of immune response. Similar reductions in mitotic index could affect every tissue involved with cell division. Although it may not be the same for higher concentrations, from our results, we have also shown that decreased mitotic rates were reversible in long-term EBV-transformed lymphoblastoid cultures. Increased numbers of mitoses were observed in human short-term whole blood cultures that were exposed to 2 microM concentrations of aluminum chloride.(ABSTRACT TRUNCATED AT 250 WORDS)
Aluminum Chloride↗
CA++ in fertilization and mitosis: the phosphatidylinositol cycle in sea urchin gametes and zygotes is involved in control of fertilization and mitosis.
We determined that the phosphatidylinositol (PI) cycles in both sea urchin sperm and eggs are necessary for normal fertilization, and that the PI cycle in sea urchin zygotes is involved in control of mitosis. The PI cycle is involved in Ca++ homeostasis so our data are direct evidence that Ca++ is involved with control of mitosis and fertilization. We implicated the PI cycle by adding Li+ to sea urchin eggs, sperm, or zygotes: those effects of Li+ due to effects on the PI cycle were overcome by myo-inositol but not by its optical isomer, scyllitol, and not by mannitol.
Animals↗
Effects of TPA on mitosis of V79 Chinese hamster cells. Reduced precision of chromosome distribution and modification of entrance into and exit out of mitosis.
Protein kinase C (PKC) was activated in V79 Chinese hamster cells with 10 nM 12-O-tetradecanoylphorbol-13-acetate (TPA). Within 30 min soluble activity decreased concomitant with a 10-fold increase of particulate activity. The latter was still elevated after 3 h but was back to control levels after 24 h of treatment; by then soluble activity was lost. The frequency of mitotic cells with signs of abnormal spindle function increased within 15 min and reached a plateau after 45-60 min which lasted throughout the 4 h treatment. The c-mitotic effect was delayed and significantly lower when 10 nM TPA was combined with 50 microM of the protein kinase inhibitor H7. The frequency of disturbed mitotic cells decreased after 24 h of treatment but remained significantly higher than in non-treated cells. Change of medium and addition of new TPA caused a slight but significant further increase. It is suggested that PKC takes part in eliciting the c-mitotic effect of TPA. However, the sustained effect coincident with down-regulation points to significant alterations of the level or the activity of an as yet unidentified ultimate elicitor. TPA also caused a transient block in the G2 phase which was ameliorated by H7 and which could not be detected at all in TPA-pretreated cells (24 h) given new TPA. This suggests that PKC takes part in eliciting the G2/M block as well but the mechanism is different from the one(s) behind the c-mitotic effect. V79 cells were found to exit from mitosis in the presence of 0.2 microgram/ml of colcemid but TPA-pretreated cells showed a decreased exit rate. There was no sign of hampered exit among cells going into mitosis soon after the G2 block was reversed, which implies that the spontaneous reversal of the block does not involve rapid down-regulation of PKC.
Animals↗
Prolonged mitosis versus tetraploid checkpoint: how p53 measures the duration of mitosis.
Degradation of p53 requires transcription, and therefore inhibitors of transcription cause p53 accumulation. When transcription resumes, the p53 that accumulated in turn induces p21. During mitosis, chromosomes are condensed, the nuclear envelope is dissolved and transcription is absent. If a cell stays in mitosis too long, (e.g. mitotic arrest caused by Taxol or nocodazole), then p53 accumulates. This explains how p53 can measure mitotic time and perhaps represents the most fundamental function of p53.
Antineoplastic Agents↗