ライフサイエンスコーパス: metaphase

1 eric and pericentromeric regions during (pro)metaphase.

2 vesiculation is required for progression to metaphase.

3 es fully attached to spindle microtubules at metaphase.

4 by the orientation of its mitotic spindle at metaphase.

5 roximately 1-2 piconewtons (pNs) of force at metaphase.

6 polar attachment of replicated chromatids in metaphase.

7 e, culminating in a peak in MTOC function in metaphase.

8 hase with almost no cells progressing beyond metaphase.

9 ile MDCK cells progress from prometaphase to metaphase.

10 ccumulates at the mother spindle pole during metaphase.

11 hromatin that bridges sister kinetochores in metaphase.

12 ere it is constrained to the spindle axis in metaphase.

13 quired for directed spindle movements during metaphase.

14 symmetrical cortical LGN distribution during metaphase.

15 netochore relative to the mitotic spindle in metaphase.

16 display coordinated motion and stretching in metaphase.

17 condense and to resolve sister chromatids at metaphase.

18 ell cycle is the alignment of chromosomes in metaphase.

19 osomes as cells transit from prometaphase to metaphase.

20 and increase spindle steady-state length at metaphase.

21 1 is required for normal progression through metaphase.

22 omosomes oscillate to align precisely during metaphase.

23 d the centrosomes must be dissolved to reach metaphase.

24 ite2 functions in spindle positioning during metaphase.

25 pacts when spindle forces are maximal during metaphase.

26 kemia (APL), with t(15;17)(q23;q21.1) in all metaphases.

27 hia chromosome translocation in 17 out of 20 metaphases.

28 e, Asap relocalized to the nuclear region at metaphase, a shift that coincided with subtle Golgi reor

29 configuration, which exists from G1 through metaphase, allows for correction of misattachments.

30 duplicated polytene chromosomes persist into metaphase, an anaphase delay prevents tissue malformatio

31 , a kinesin-6, has critical roles during the metaphase-anaphase transition and cytokinesis.

32 ster chromatids together from S phase to the metaphase-anaphase transition and ensures accurate segre

33 -subunit ubiquitin ligase that initiates the metaphase-anaphase transition and mitotic exit by target

34 of the cell cycle and is degraded during the metaphase-anaphase transition by the anaphase-promoting

35 ct group of cargoes was inhibited before the metaphase-anaphase transition in the budding yeast Sacch

36 evenly distributed to daughter cells at the metaphase-anaphase transition.

37 ynamics of chromatin-bound RCC1 pools at the metaphase-anaphase transition.

38 aracteristics such as cell shape, cell size, metaphase/anaphase delays, and mitotic abnormalities inc

39 ntains the spindle at the cell center during metaphase and anaphase in one- and two-cell Caenorhabdit

40 vicinity of overlapping microtubules, during metaphase and anaphase of mitosis.

41 We find that metaphase and anaphase spindles elongate at the same rat

42 oth the cell equator and cell poles, in both metaphase and anaphase.

43 uired for regulating spindle organization in metaphase and cell shape transformation after anaphase o

44 lizes to the nuclear side of the SPBs during metaphase and early anaphase and to the cytoplasmic surf

45 s required for chromosome congression during metaphase and generation of stable kinetochore microtubu

46 Fixed human metaphase and interphase chromosomes were labeled with t

47 was documented in both intact and enucleated metaphase and interphase zygotes and two-cell embryos.

48 of the chromosome pairs formed bivalents at metaphase and many univalents were observed, leading to

49 n also results in chromosome misalignment at metaphase and SAC activation; inactivation of the SAC re

50 their position at the spindle equator during metaphase and segregated properly during anaphase when o

51 associated with kinetochore microtubules in metaphase and then with anaphase spindle midzone.

52 t the spindle poles and inner centromeres in metaphase and translocated to the midbody at telophase.

53 s, whereas cell volume increased slightly in metaphase and was relatively constant during cytokinesis

54 by the inappropriate presence of cyclin A at metaphase, and an increase in the number of cells that f

55 tes at centrosomes during prophase, peaks at metaphase, and decreases through telophase.

56 e angles vary widely during prometaphase and metaphase, and therefore do not reliably predict divisio

57 Furthermore, the metaphase APC co-activator, Cdc20, is specifically recru

58 s of neighboring sister-kinetochore pairs in metaphase are correlated in a distance-dependent manner.

59 Human sister chromatids at metaphase are primarily linked by centromeric cohesion,

60 ressed Kv2.1 is significantly increased upon metaphase arrest in COS-1 and CHO cells, and in a pancre

61 are transient alignment defects followed by metaphase arrest that ultimately results in cohesion fat

62 mplex mitotic phenotype, including prolonged metaphase arrest, anaphase bridges, and multipolar segre

63 ed configuration and became trapped there at metaphase arrest.

64 owed decreased lamin A/C phosphorylation and metaphase arrest.

65 e former leads to cataract and the latter to metaphase arrest.

66 geneity in single cells, or requires FISH in metaphase arrested cells, posing technical challenges.

67 o measure chromosome malorientation rates in metaphase-arrested oocytes, shows that these two rates a

68 position of the center of the spindle during metaphase, as measured by the standard deviation, was on

69 Finally, inactivation of H2A.Z in metaphase-blocked cells led immediately to cohesion defe

70 n-associated SUMO conjugates increase during metaphase but decrease rapidly during anaphase.

71 kinase Ipl1/Aurora B to inner centromeres in metaphase but is not required in interphase.

72 oocyte reprogramming factors present in the metaphase but not in the interphase cytoplasm are 'trapp

73 embryos impaired spindle orientation during metaphase, but chromosome segregation remained robust.

74 d securin once all the chromosomes attach in metaphase, but is rapidly inhibited should kinetochore a

75 egulated-it is inhibited during prophase and metaphase by cyclin-dependent kinase 1 (CDK1)-mediated p

76 ), whereas centromeric cohesin is cleaved in metaphase by the protease separase.

77 des the basis for an approach that (provided metaphases can be generated) could be applied to any ani

78 sts that zygotic cytoplasm, if maintained at metaphase, can also support derivation of embryonic stem

79 However, the relevant metaphase Cdk1 targets were not known.

80 In addition, metaphase cells lacking PTEN exhibit defects of spindle

81 We previously observed that metaphase cells preferentially promote actin cable assem

82 e closely juxtaposed with the KMN network in metaphase cells when their dissociation is blocked and t

83 eward, giving rise to the robust K-fibers of metaphase cells.

84 e cells are considerably less stable than in metaphase cells.

85 regulates key cellular processes, including metaphase chromatid cohesion and centromere organization

86 /4 function redundantly to clear the ER from metaphase chromatin, thereby ensuring correct progressio

87 ule inhibition of MRN using mirin results in metaphase chromosome alignment defects in Xenopus egg ex

88 ion, allowing proper spindle orientation and metaphase chromosome alignment, as well as spindle elong

89 veloped a new quantitative model to describe metaphase chromosome dynamics via kinetochore-microtubul

90 ailure in AURKC-CPC function that results in metaphase chromosome misalignment.

91 ell types, suggesting a general principle of metaphase chromosome organization.

92 DAPI lifetime variations in metaphase chromosome spreads allowed mapping of the diff

93 Metaphase chromosome spreads from human lymphocytes stim

94 luorescence in situ hybridization on mitotic metaphase chromosomes and interphase nuclei.

95 We show that holocentromeres of metaphase chromosomes are composed of multiple centromer

96 ommon fragile sites (CFSs) seen as breaks on metaphase chromosomes are distinct forms of structural c

97 on the distal end of one pair of homologous metaphase chromosomes compared with a faint hybridizatio

98 While wild-type metaphase chromosomes display residual levels of catenat

99 e distribution of H3K4me3 is the same across metaphase chromosomes from human primary lymphocytes and

100 t with shortening of the telomeric C strand, metaphase chromosomes showed loss of telomeres synthesiz

101 egulates kinetochore-microtubule dynamics of metaphase chromosomes, and we identify Hec1 S69, a previ

102 ns) show the same distributions across human metaphase chromosomes, showing that functional differenc

103 irely accounts for the extra volume found in metaphase chromosomes.

104 distribution of histone modifications across metaphase chromosomes.

105 omere fragility and altered the structure of metaphase chromosomes.

106 in mitosis, when ER membranes accumulate on metaphase chromosomes.

107 urface appearance with a volume smaller than metaphase chromosomes.

108 singly small percentage of the total mass of metaphase chromosomes.

109 respect to the substratum is established in metaphase coincident with maximal cell rounding, which e

110 Reduced RhoA activity at the metaphase cortex in HepG2 cells and Par1b-overexpressing

111 ated with robust LGN-NuMA recruitment to the metaphase cortex, spindle alignment with the substratum,

112 iding the assembly of a relatively isotropic metaphase cortex.

113 pensable for bridging actin filaments to the metaphase cortex.

114 microtubules were no more flared than their metaphase counterparts, but they were longer.

115 cally phosphorylated on threonine 103 by the metaphase cyclin-Cdk1 complex, in vivo and in vitro.

116 address clonal heterogeneity in AML based on metaphase cytogenetics.

117 Loss of Bub3 resulted in a metaphase delay that was not a consequence of aneuploidy

118 Metaphase describes a phase of mitosis where chromosomes

119 ling relation connecting microtubule flux to metaphase duration.

120 Philadelphia chromosome-negative (CCA/Ph(-)) metaphases emerge as patients with chronic phase chronic

121 During metaphase, forces on kinetochores are exerted by k-fibre

122 The involvement of Aurora A in events after metaphase has only been suggested because appropriate ex

123 Using polymer simulations, we found that metaphase Hi-C data are inconsistent with classic hierar

124 n, and disrupted chromosome alignment on the metaphase I (MI) plate.

125 ndles and misaligned chromosomes, leading to metaphase I arrest and failure of first polar body (PB1)

126 ctivated ATM kinase, leading to SAC mediated metaphase I arrest.

127 is unknown exactly how cell cycle arrest at metaphase I is achieved and how the fertilisation Ca(2+)

128 astl-null oocytes resume meiosis I and reach metaphase I normally but that the onset and completion o

129 quired for spindle maintenance, we monitored metaphase I spindles after a fast-acting mei-1(ts) mutan

130 uring prophase I, released at the prophase I/metaphase I transition, and reassociates with rDNA befor

131 brate groups have mature eggs that arrest at metaphase I, and these species do not possess the CaMKII

132 esis and extends to the entire chromosome at metaphase I, but is exclusively limited to the centromer

133 monstrate that parthenogenetic activation of metaphase I-arrested eggs by MEK inhibition, independent

134 independent mechanism removes cohesin before metaphase I.

135 ith extensive interchromosome connections at metaphase I.

136 gradually increases through prometaphase and metaphase I.

137 o, spontaneously activated, and they escaped metaphase II (MII) arrest and progressed to pronuclear,

138 e first time, produced meiotically competent metaphase II (MII) oocytes after in vitro maturation (IV

139 ter microinjecting the CRISPR/Cas9 system in metaphase II (MII) oocytes and zygote stage embryos.

140 r loss accumulated with age and unfertilized metaphase II (MII) oocytes exhibited irregularities of t

141 nsfer of first polar body (PB1) genomes from metaphase II (MII) oocytes into enucleated donor MII cyt

142 se oocytes from the germinal vesicle (GV) to metaphase II (MII) stages.

143 hinery increases dramatically, preparing the metaphase II (MII)-arrested egg for fertilization.

144 l nuclear transfer (SCNT) into unfertilized, metaphase II (MII)-arrested oocytes attests to the cytop

145 ed in oocytes after their entry into meiotic metaphase II and declines again upon exit into interphas

146 s is thought to be restricted to maintaining metaphase II arrest through stabilizing Cdk1 activity.

147 n APC/C(cdc20) inhibitor, links release from metaphase II arrest with the Ca(2+) transient and its de

148 nogenetic activation, which indicates proper metaphase II arrest.

149 s (germinal vesicle stage), matured oocytes (metaphase II eggs) and 2-cell stage embryos.

150 eling chaperone specifically enriched in the metaphase II human oocyte, is necessary for reprogrammin

151 Metaphase II mouse oocytes (n = 240), with and without c

152 fusion between a haploid spermatozoon and a metaphase II oocyte.

153 acetylation (H3K27ac) in mouse immature and metaphase II oocytes and in 2-cell and 8-cell embryos.

154 dose of gonadotropin or the total number of metaphase II oocytes retrieved did not affect developmen

155 logue of transcripts in germinal vesicle and metaphase II oocytes, and in embryos at the four-cell, e

156 We found that oocytes in metaphase II show homogeneous chromatin folding that lac

157 e stimulated to resume meiosis and mature to metaphase II, a sequence of events that prepares the ooc

158 erm displayed a reduced ability to fertilize metaphase II-arrested eggs in vitro.

159 cium oscillations, followed by activation of metaphase II-arrested oocytes.

160 f meiosis I and an increase in aneuploidy at metaphase II.

161 is exclusively limited to the centromere at metaphase II.

162 gly reduced CRM and ZmBs repeat sequences at metaphase II.

163 but is restricted to the inner centromere at metaphase II.

164 release of sister-chromatid cohesion at the metaphase II/anaphase II transition.

165 The ability of human metaphase-II arrested eggs to activate following fertili

166 is, we first investigated ER localization in metaphase-II Mater(tm/tm) (hypomorph) oocytes and found

167 n during mating and spindle alignment during metaphase in budding yeast.

168 During metaphase in the early Caenorhabditis elegans embryo, th

169 that spindles in every cell tend to align at metaphase in the long length of the apical surface excep

170 n generated by pericentromere stretch during metaphase in wild-type cells and in mutants with disrupt

171 ohesin enriched, are separated by >800 nm at metaphase in yeast.

172 meiotic division and persists, uniquely for metaphase, in MII-arrested oocytes.

173 nactive centromere cannot maintain H3T3ph at metaphase, indicating that a functional centromere is re

174 A delay in the completion of metaphase induces a stress response that inhibits furthe

175 complexes surrounding the central spindle in metaphase is a consequence of the size of the DNA loops

176 tion as generally envisioned, progression to metaphase is a discontinuous process involving chromosom

177 nd inactivation of both pools of Mps1 during metaphase is essential to ensure prompt and efficient SA

178 hing of the pericentromeric chromatin during metaphase is thought to generate a tension-based signal

179 prometaphase to their fully matured form at metaphase, just before anaphase onset.

180 In two of these cases in which the metaphase karyotype showed additional material of unknow

181 icroarray and in some cases is better than a metaphase karyotype.

182 ions, mosaicism, and trisomy 20 diagnosed by metaphase karyotype.

183 We performed metaphase karyotyping and next-generation sequencing (NG

184 Metaphase karyotyping is an established diagnostic stand

185 plexes in live mouse hippocampal neurons and metaphase kinetochores in dividing human cells.

186 at recruiting the checkpoint protein Mad1 to metaphase kinetochores is sufficient to reactivate the c

187 dimerization to enhance Aurora B activity at metaphase kinetochores.

188 second sister can persistently generate this metaphase-like tension before biorientation, likely stab

189 Proper length control of the metaphase mitotic spindle is critical to this process an

190 However, in contrast to this model, metaphase mitotic spindles with inactive kinesin-14 minu

191 ilures of Discs Large apical localization in metaphase neuroblasts.

192 structure and function of chromosomes during metaphase of 2,572 dividing cells, and developed a softw

193 find that oocytes with DNA damage arrest at metaphase of the first meiosis (MI).

194 prohibits the transition from prophase into metaphase of the first meiotic division, resulting in ma

195 letion results in chromosome misalignment in metaphase, often leading to catastrophic mitotic failure

196 At metaphase, one sister kinetochore couples to depolymeriz

197 rix, are severely reduced at kinetochores in metaphase oocytes following Rab5a knockdown.

198 omosome segregation, is severely impaired in metaphase oocytes following Sirt6 knockdown.

199 inesis only early in mitosis, but not during metaphase or cytokinesis.

200 In metaphase, p37 negatively regulates this function of PP1

201 During metaphase, phosphorylated Moesin (p-Moesin) is enriched

202 34A impairs mitotic progression by affecting metaphase plate alignment and pressure generation by del

203 , PLK-1-dependent chromosome congression and metaphase plate alignment are necessary for the disassem

204 y condensed chromosomes were not arranged on metaphase plate and chromosomal perturbations were obser

205 show defects in chromosome alignment at the metaphase plate and in spindle pole integrity.

206 Accumulation of SUMO conjugates on the metaphase plate and proper chromosome alignment depend o

207 Inactivation of the checkpoint prior to metaphase plate centering leads to asymmetric cell divis

208 , if the checkpoint is inactivated after the metaphase plate has centered its position, symmetric cel

209 ssion returns nonexchange chromosomes to the metaphase plate invalidates this interpretation and rais

210 ndicates that the equatorial position of the metaphase plate is essential for symmetric cell division

211 uplicated mitotic chromosomes aligned at the metaphase plate maintain dynamic attachments to spindle

212 e experimentally observed disordering of the metaphase plate occurs because phosphorylation increases

213 When we offset the metaphase plate position by creating an asymmetric centr

214 sm by providing cells enough time to correct metaphase plate position.

215 y, completion of chromosome alignment at the metaphase plate was significantly delayed.

216 f temperature shift, bivalents moved off the metaphase plate, and microtubule bundles within the spin

217 rs to be dependent on the position along the metaphase plate, both types of behavior are observed wit

218 are properly attached and bioriented at the metaphase plate, the checkpoint needs to be silenced.

219 There is also structure throughout the metaphase plate, with a steeper PEF potential well towar

220 r spindle with chromosomes aligned along the metaphase plate.

221 or (2) the absence of oscillations about the metaphase plate.

222 n and alignment of the maternal and paternal metaphase plates relative to each other.

223 iole distribution on each pole, we find that metaphase plates relocate to the middle of the spindle b

224 chromosomes, and their eventual alignment on metaphase plates.

225 While Mad2 delays anaphase separation of metaphase polytene chromosomes, Mad2's control of overal

226 o prevent cells from entering mitosis alters metaphase progression and centrosome number, resulting i

227 e that Bub3 has an unexpected role promoting metaphase progression in budding yeast.

228 chromosomes not involved in TFs in the same metaphases, regardless of the p53 status, indicating tha

229 he switch to more stable k-MT attachments in metaphase requires the proteasome-dependent destruction

230 Here we determine that the metaphase response to catenation in mammalian cells oper

231 Our model reproduces all the key features of metaphase sister kinetochore dynamics in PtK1 cells and

232 In metaphase, sister kinetochores on the surface of replica

233 r4 facilitates complete removal of Byr4 from metaphase SPBs in concert with Plo1, revealing an unexpe

234 ter chromatids maintain biorientation on the metaphase spindle are critical to the fidelity of chromo

235 ch a subset of dynamic microtubules from the metaphase spindle are selected and organized into a stab

236 Chromosome bi-orientation at the metaphase spindle is essential for precise segregation o

237 In diverse cell types, the metaphase spindle is maintained at characteristic consta

238 Metaphase spindle length is proposed to be regulated by

239 eletion strains showed large fluctuations in metaphase spindle length, suggesting a disruption of spi

240 tethering during DNA repair, and imply that metaphase spindle maintenance is a critical feature of t

241 As a proof of concept, we use ISI to measure metaphase spindle microtubule poleward flux in primary c

242 that She1 is required for the maintenance of metaphase spindle stability.

243 ined into the molecular building plan of the metaphase spindle using bulk and single-molecule measure

244 stic force contributors in the fission yeast metaphase spindle.

245 Misaligned metaphase spindles are believed to result in divisions i

246 We find that metaphase spindles first undergo a sustained rotation th

247 parallel spindle alignment of quasi-diagonal metaphase spindles in anaphase.

248 We conclude that metaphase spindles in epithelia engage in a stereotyped

249 even in the absence of astral microtubules, metaphase spindles in MDCK and HeLa cells are not random

250 nsin/MAP7 mutant neuroblasts display shorter metaphase spindles, a defect caused by a reduced microtu

251 as cells with shorter- or longer-than-normal metaphase spindles, generated through deletion or inhibi

252 helial cells, which typically feature tilted metaphase spindles, lack this anaphase flattening mechan

253 bly accurate predictions of the behaviors of metaphase spindles-the cytoskeletal structure, composed

254 tocol, we describe two methodologies, namely metaphase spread analysis and cell sorting, for the iden

255 53(-/-) lymphomas and MEFs, as determined by metaphase spread assay and spectral karyotyping analysis

256 ter chromatids, homologue pairs and from one metaphase spread to another.

257 Using metaphase spreads from human lymphoblastoid cell lines,

258 esulting from apoptosis that affects meiotic metaphase-stage spermatocytes.

259 ly, chromosomes globally compact, giving the metaphase state.

260 echanisms depending on the mitotic phase: in metaphase, Stu1 binds directly to the MT lattice, wherea

261 signaling upon S-phase progression, fragile metaphase telomeres that resemble the common fragile sit

262 When in metaphase, the duplicated cores align to opposite sides

263 -2 are displaced from the chromosome during metaphase, they dissociate from each other, but each enz

264 ytene chromosomes can also separate prior to metaphase through a spindle-independent mechanism termed

265 polar microtubules and spindle poles during metaphase through telophase, and partially co-localized

266 central role in the transition of cells from metaphase to anaphase and is one of the main components

267 required for proper chromosome alignment and metaphase to anaphase progression.

268 tages of the mitotic cell cycle, except from metaphase to mid-anaphase.

269 Aurora A function that takes place after the metaphase-to-anaphase transition and a new powerful tool

270 5 in centromeric chromatin occurs during the metaphase-to-anaphase transition and coincides with the

271 yeast Wee1 kinase, Swe1, also restrains the metaphase-to-anaphase transition by preventing Cdk1 phos

272 this anaphase inhibitor is destroyed at the metaphase-to-anaphase transition by ubiquitin-dependent

273 Therefore, the metaphase-to-anaphase transition in frog oocytes is not

274 of previously securin-bound separase at the metaphase-to-anaphase transition renders it resistant to

275 At the metaphase-to-anaphase transition, the CPC dissociates fr

276 ween APC/C(CDC20) and APC/C(CDH1) during the metaphase-to-anaphase transition, thereby contributing t

277 MISP depletion led to an impaired metaphase-to-anaphase transition, which depended on phos

278 nism contributing to the coordination of the metaphase-to-anaphase transition.

279 TRIP13 knockdown delays metaphase-to-anaphase transition.

280 mposes a Bub1 binding-dependent delay in the metaphase-to-anaphase transition.

281 in the number of cells that fail to undergo metaphase-to-anaphase transition.

282 Cdk1 drives both mitotic entry and the metaphase-to-anaphase transition.

283 suppression of lamin A/C phosphorylation and metaphase transition induced by the UPR was rescued by k

284 hromosome individualization from prophase to metaphase transition.

285 n of MDC1 causes a delay of the prometaphase-metaphase transition.

286 M disorganization and phosphorylation during metaphase, ultimately leading to mitotic catastrophe, mu

287 The spindle checkpoint arrests cells in metaphase until all chromosomes are properly attached to

288 Analysis of tumor metaphases using sequential telomere fluorescent in-situ

289 ations in transverse spindle position during metaphase was only 0.5% of the short axis of the cell.

290 In metaphase, we identified a homogenous folding state that

291 The remaining three metaphases were normal karyotype.

292 ensation defect was most striking at meiotic metaphase, when Tetrahymena chromosomes are normally mos

293 Telomere dispersion initiates in metaphase, whereas disjunction takes place in anaphase.

294 SENP1 delays sister chromatid separation at metaphase, whereas SENP2 knockdown produces no detectabl

295 d geminin are degraded simultaneously during metaphase, which directs Cdt1 accumulation on segregatin

296 mechanism for positioning the spindle during metaphase while assembly is completed before the onset o

297 spindle, especially to the spindle poles at metaphase, while it was concentrated at the midbody in t

298 e find that cells depleted of Ska3 arrest at metaphase with only partial degradation of cyclin B1 and

299 t or overexpression of Swe1 blocked cells in metaphase with reduced APC activity in vivo and in vitro

300 e of the inherent difficulties in generating metaphases within the malignant plasma cell clone.