共查询到20条相似文献，搜索用时 15 毫秒
1.
Continuous measurement and imaging of the intracellular free calcium ion concentration ([Ca2+]i) of mitotic and interphase PtK1 cells was accomplished with the new fluorescent Ca2+ indicator fura-2. No statistically significant difference between basal [Ca2+]i of interphase and mitotic cells was detected. However, mitotic cells showed a rapid elevation of [Ca2+]i from basal levels of 130 nM to 500 to 800 nM at the metaphase-anaphase transition. The [Ca2+]i transient was brief, lasting approximately 20 seconds and the elevated [Ca2+]i appeared uniformly distributed over the entire spindle and central region of the cell. The close temporal association of the [Ca2+]i transient with the onset of anaphase suggests that calcium may have a signaling role in this event. 相似文献
2.
The inner centromere-like protein (INCENP) forms a complex with the evolutionarily conserved family of Aurora Bkinases. The INCENP-Aurora complex helps coordinate chromosome segregation, spindle behavior, and cytokinesis during mitosis. INCENP-Aurora associates with kinetochores in metaphase and with spindle microtubules in anaphase, yet the trigger for this abrupt transfer is unknown. Here we show that the conserved phosphatase Cdc14 regulated the yeast INCENP-Aurora complex, Sli15-Ipl1. Cdc14 dephosphorylated Sli15 and thereby directed the complex to spindles. Activation of Cdc14 by separase was sufficient for Sli15 dephosphorylation and relocalization. Cdc14 not only regulates mitotic exit but also modulates spindle midzone assembly through Sli15-Ipl1. 相似文献
3.
Palframan WJ Meehl JB Jaspersen SL Winey M Murray AW 《Science (New York, N.Y.)》2006,313(5787):680-684
The spindle checkpoint delays cell cycle progression until microtubules attach each pair of sister chromosomes to opposite poles of the mitotic spindle. Following sister chromatid separation, however, the checkpoint ignores chromosomes whose kinetochores are attached to only one spindle pole, a state that activates the checkpoint prior to metaphase. We demonstrate that, in budding yeast, mutual inhibition between the anaphase-promoting complex (APC) and Mps1, an essential component of the checkpoint, leads to sustained inactivation of the spindle checkpoint. Mps1 protein abundance decreases in anaphase, and Mps1 is a target of the APC. Furthermore, expression of Mps1 in anaphase, or repression of the APC in anaphase, reactivates the spindle checkpoint. This APC-Mps1 feedback circuit allows cells to irreversibly inactivate the checkpoint during anaphase. 相似文献
4.
Cohesins keep sister chromatids associated from the time of their replication in S phase until the onset of anaphase. In vertebrate cells, two distinct pathways dissociate cohesins, one acts on chromosome arms and the other on centromeres. Here, we describe a third pathway that acts on telomeres. Knockdown of tankyrase 1, a telomeric poly(ADP-ribose) polymerase caused mitotic arrest. Chromosomes aligned normally on the metaphase plate but were unable to segregate. Sister chromatids separated at centromeres and arms but remained associated at telomeres, apparently through proteinaceous bridges. Thus, telomeres may require a unique tankyrase 1-dependent mechanism for sister chromatid resolution before anaphase. 相似文献
5.
Chromosome alignment on the mitotic spindle is monitored by the spindle checkpoint. We identify Sgo1, a protein involved in meiotic chromosome cohesion, as a spindle checkpoint component. Budding yeast cells with mutations in SGO1 respond normally to microtubule depolymerization but not to lack of tension at the kinetochore, and they have difficulty attaching sister chromatids to opposite poles of the spindle. Sgo1 is thus required for sensing tension between sister chromatids during mitosis, and its degradation when they separate may prevent cell cycle arrest and chromosome loss in anaphase, a time when sister chromatids are no longer under tension. 相似文献
6.
Coordination of cytokinesis with chromosome congression and segregation is critical for proper cell division, but the mechanism is unknown. Here, septins, a conserved family of polymerizing guanosine triphosphate-binding proteins, localized to the metaphase plate during mitosis. Septin depletion resulted in chromosome loss from the metaphase plate, lack of chromosome segregation and spindle elongation, and incomplete cytokinesis upon delayed mitotic exit. These defects correlated with loss of the mitotic motor and the checkpoint regulator centromere-associated protein E (CENP-E) from the kinetochores of congressing chromosomes. Mammalian septins may thus form a mitotic scaffold for CENP-E and other effectors to coordinate cytokinesis with chromosome congression and segregation. 相似文献
7.
D E Comings 《Science (New York, N.Y.)》1966,154(755):1463-1464
Cultures of human fibroblasts were labeled briefly with tritiated thymidine and fixed; autoradiographs were made and exposed for 3(1/2) months. No labeling was noted over the centromere of metaphase or anaphase chromosomes. The technique was sensitive to replication at the centromere of a DNA helix only 2.5 microns long, considerably shorter than the estimated length of a replicon in humans. This suggests that chromatid separation during mitosis is not associated with delayed replication of a short segment of chromosomal DNA. 相似文献
8.
N末端乙酰转移酶Naa50在调控拟南芥生长发育方面至关重要。为探究Naa50是否通过调控细胞有丝分裂来影响植物生长发育,将naa50-1突变体与H2B-YFP株系杂交,利用H2B-YFP标示细胞分裂过程中染色体的分离行为。结果表明,与野生型相比,拟南芥naa50-1突变体根尖分生区细胞有丝分裂指数下降,染色体畸变率明显增加,微核率上升,且处在分裂中期的细胞比例增加。将naa50-1突变体与CYCB1-CUS株系杂交,检测根细胞中CYCB1蛋白表达,发现naa50-1突变体中CYCB1蛋白表达量明显增加。PI染色分析表明,naa50-1突变体根部存在部分死细胞。以上结果表明,在细胞有丝分裂过程中,Naa50促进遗传物质平均分配到两个子细胞中,促进细胞从分裂中期向后期转换;Naa50通过调控细胞分裂进而参与植物生长发育的调控。 相似文献
9.
Phosphorylation by cyclin B-Cdk underlies release of mitotic exit activator Cdc14 from the nucleolus
Azzam R Chen SL Shou W Mah AS Alexandru G Nasmyth K Annan RS Carr SA Deshaies RJ 《Science (New York, N.Y.)》2004,305(5683):516-519
Budding yeast protein phosphatase Cdc14 is sequestered in the nucleolus in an inactive state during interphase by the anchor protein Net1. Upon entry into anaphase, the Cdc14 early anaphase release (FEAR) network initiates dispersal of active Cdc14 throughout the cell. We report that the FEARnetwork promotes phosphorylation of Net1 by cyclin-dependent kinase (Cdk) complexed with cyclin B1 or cyclin B2. These phosphorylations appear to be required for FEAR and sustain the proper timing of late mitotic events. Thus, a regulatory circuit exists to ensure that the arbiter of the mitotic state, Cdk, sets in motion events that culminate in exit from mitosis. 相似文献
10.
The spindle checkpoint was characterized in meiosis of budding yeast. In the absence of the checkpoint, the frequency of meiosis I missegregation increased with increasing chromosome length, reaching 19% for the longest chromosome. Meiosis I nondisjunction in spindle checkpoint mutants could be prevented by delaying the onset of anaphase. In a recombination-defective mutant (spo11Delta), the checkpoint delays the biochemical events of anaphase I, suggesting that chromosomes that are attached to microtubules but are not under tension can activate the spindle checkpoint. Spindle checkpoint mutants reduce the accuracy of chromosome segregation in meiosis I much more than that in meiosis II, suggesting that checkpoint defects may contribute to Down syndrome. 相似文献
11.
Neurohr G Naegeli A Titos I Theler D Greber B Díez J Gabaldón T Mendoza M Barral Y 《Science (New York, N.Y.)》2011,332(6028):465-468
Partitioning of chromatids during mitosis requires that chromosome compaction and spindle length scale appropriately with each other. However, it is not clear whether chromosome condensation and spindle elongation are linked. Here, we find that yeast cells could cope with a 45% increase in the length of their longest chromosome arm by increasing its condensation. The spindle midzone, aurora/Ipl1 activity, and Ser10 of histone H3 mediated this response. Thus, the anaphase spindle may function as a ruler to adapt the condensation of chromatids, promoting their segregation regardless of chromosome or spindle length. 相似文献
12.
New details of mitotic spindle structures in the endosperm of Haemanthus katherinae (Bak) have been demonstrated by differential interference microscopy. Spindle fibers are clearly seen in the living spindle extending from the kinetochores to the polar region. Individual spindle fibers consist of a bundle of smaller filaments which diverge slightly from the kinetochore and intermingle with filaments from other spindle fibers as they approach the polar region. The degree of intermingling increases during metaphase and anaphase. The chromosomes stop moving when the spindle fibers are still 5 to 10microns long; then the fibers disappear. These observations explain some aspects of spindle movements which were difficult to reconcile with earlier concepts of spindle organization. 相似文献
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14.
[目的]探讨丙酯草醚的除草机理。[方法]以洋葱根尖为试材,探讨不同时间和不同浓度丙酯草醚对根尖分生细胞有丝分裂的影响。[结果]随着丙酯草醚处理浓度的增加,洋葱根尖有丝分裂指数逐渐下降;在同一浓度下,随着处理时间的延长,有丝分裂指数也呈下降趋势。对不同处理下的洋葱根尖细胞形态观察发现,在低浓度(0.012 5%)丙酯草醚短时间(2 h)处理下,洋葱根尖分生区中仍可见中、后、末期3种分裂状态的细胞。但在超过8 h的高浓度(0.100 0%)丙酯草醚处理下,分裂态细胞明显减少,分生区有明显较多分裂中期的细胞。[结论]丙酯草醚对根尖细胞的分裂有明显抑制作用,并使根尖细胞停滞于有丝分裂中期。 相似文献
15.
Tsai MY Wang S Heidinger JM Shumaker DK Adam SA Goldman RD Zheng Y 《Science (New York, N.Y.)》2006,311(5769):1887-1893
Mitotic spindle morphogenesis is a series of highly coordinated movements that lead to chromosome segregation and cytokinesis. We report that the intermediate filament protein lamin B, a component of the interphase nuclear lamina, functions in spindle assembly. Lamin B assembled into a matrix-like network in mitosis through a process that depended on the presence of the guanosine triphosphate-bound form of the small guanosine triphosphatase Ran. Depletion of lamin B resulted in defects in spindle assembly. Dominant negative mutant lamin B proteins that disrupt lamin B assembly in interphase nuclei also disrupted spindle assembly in mitosis. Furthermore, lamin B was essential for the formation of the mitotic matrix that tethers a number of spindle assembly factors. We propose that lamin B is a structural component of the long-sought-after spindle matrix that promotes microtubule assembly and organization in mitosis. 相似文献
16.
The product of the abnormal spindle (asp) gene was found to be an asymmetrically localized component of the centrosome during mitosis, required to focus the poles of the mitotic spindle in vivo. Removing Asp protein function from Drosophila melanogaster embryo extracts, either by mutation or immunodepletion, resulted in loss of their ability to restore microtubule-organizing center activity to salt-stripped centrosome preparations. This was corrected by addition of purified Asp protein. Thus, Asp appears to hold together the microtubule-nucleating gamma-tubulin ring complexes that organize the mitotic centrosome. 相似文献
17.
(亚洲棉×司笃克氏棉)不同倍性杂种一代的育性和花粉母细胞减数分裂行为的研究 总被引：1，自引：0，他引：1
亚洲棉与司笃克氏棉杂交,获得了125粒杂种种子,用0.05%秋水仙素水溶液处理,获得7株加倍的四倍体F_1植株。1984-1987年的研究结果表明,二倍体F_1花粉母细胞减数分裂不正常,中期Ⅰ染色体构型是20.53Ⅰ+2.45Ⅱ+0.19Ⅲ,二价体交叉频率为1.07;后期Ⅰ和后期Ⅱ染色体分向两级不均衡,产生各种类型的异常四分孢子,由此发育的花粉无生活力,用亚洲棉回交或自然授粉均未结铃。四倍体F_1减数分裂较正常,中期Ⅰ染色体构型为0.1Ⅰ+25.9Ⅱ,二价体交叉频率为1.96,后期Ⅰ和后期Ⅱ染色体走向两极较均衡,产生的花粉部分可育,授陆地棉花粉或自然授粉能结少数种子。 相似文献
18.
19.
水稻小孢子发生过程中微管骨架的初步研究 总被引：1，自引：0，他引：1
以正常水稻品种IR36和光温敏核雄性不育系培矮64S为材料,采用间接免疫荧光标记技术,观察了小孢子发生过程中微管构型的变化。两份材料均形成了前期的核周微管、中期的纺锤体微管和末期的成膜体微管等类型。但减数分裂前期不育系培矮64S的部分小孢子母细胞微管构型表现出一些细微变化,微管排列紊乱,粘成柬状。推测这些变化可能与部分小孢子的败育有关． 相似文献
20.
Keck JM Jones MH Wong CC Binkley J Chen D Jaspersen SL Holinger EP Xu T Niepel M Rout MP Vogel J Sidow A Yates JR Winey M 《Science (New York, N.Y.)》2011,332(6037):1557-1561
Centrosomes organize the bipolar mitotic spindle, and centrosomal defects cause chromosome instability. Protein phosphorylation modulates centrosome function, and we provide a comprehensive map of phosphorylation on intact yeast centrosomes (18 proteins). Mass spectrometry was used to identify 297 phosphorylation sites on centrosomes from different cell cycle stages. We observed different modes of phosphoregulation via specific protein kinases, phosphorylation site clustering, and conserved phosphorylated residues. Mutating all eight cyclin-dependent kinase (Cdk)-directed sites within the core component, Spc42, resulted in lethality and reduced centrosomal assembly. Alternatively, mutation of one conserved Cdk site within γ-tubulin (Tub4-S360D) caused mitotic delay and aberrant anaphase spindle elongation. Our work establishes the extent and complexity of this prominent posttranslational modification in centrosome biology and provides specific examples of phosphorylation control in centrosome function. 相似文献