ライフサイエンスコーパス: metaphase

1 F, accumulate to the spindle equator in late metaphase.

2 st species undergo a long, natural arrest in metaphase.

3 eric and pericentromeric regions during (pro)metaphase.

4 by the orientation of its mitotic spindle at metaphase.

5 acts as a switch preventing MKLP2 binding in metaphase.

6 and increase spindle steady-state length at metaphase.

7 mitotic exit when cells are stressed during metaphase.

8 1 is required for normal progression through metaphase.

9 omosomes oscillate to align precisely during metaphase.

10 d the centrosomes must be dissolved to reach metaphase.

11 ite2 functions in spindle positioning during metaphase.

12 pacts when spindle forces are maximal during metaphase.

13 vesiculation is required for progression to metaphase.

14 es fully attached to spindle microtubules at metaphase.

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

16 polar attachment of replicated chromatids in metaphase.

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

18 hase with almost no cells progressing beyond metaphase.

19 ile MDCK cells progress from prometaphase to metaphase.

20 ccumulates at the mother spindle pole during metaphase.

21 hromatin that bridges sister kinetochores in metaphase.

22 o bind CENP-C and localize to centromeres in metaphase.

23 uces the activity of KIF18A and KIF15 during metaphase.

24 to inner centromeres and become depleted by metaphase.

25 ent manner, thereby inactivating Aurora B in metaphase.

26 DK1-bound cyclin B1 is destroyed only during metaphase.

27 amplified centromere tension specifically at metaphase.

28 hromosomes at the oldest spindle pole during metaphase.

29 hia chromosome translocation in 17 out of 20 metaphases.

30 In metaphase, ~40% of the Dam1C/DASH assemblies are complet

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

32 ne attachment to chromatin is induced during metaphase, after chromosomes have been singularized and

33 Lack of proper metaphase alignment is an indicator of defective chromos

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

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

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

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

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

39 s are byproducts of Cdk1 inactivation at the metaphase-anaphase transition, controlled by the spindle

40 ysis of cyclin B, securin and geminin at the metaphase-anaphase transition, followed by slow proteoly

41 At the metaphase-anaphase transition, MPS1 S281 dephosphorylati

42 rpolarize from the G2/M transition until the metaphase-anaphase transition.

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

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

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

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

47 is cleaved and distributed to kinetochores (metaphase and anaphase), spindle midzone/cleavage furrow

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

49 Coordinated cortical flows that begin near metaphase and are dependent on the actin cytoskeleton ra

50 Consequently, these cells stalled in metaphase and cytokinesis and ultimately underwent mitot

51 omes and mitotic spindles positioning during metaphase and delays the transition from metaphase to an

52 vely form as cells enter mitosis, peaking at metaphase and disassembling as cells exit mitosis.

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

54 uired for proper chromosome alignment during metaphase and for a fully functional spindle assembly ch

55 decondensation of satellite DNA sequences at metaphase and increased sister chromatid recombination e

56 Fixed human metaphase and interphase chromosomes were labeled with t

57 both centromeric localization of the CPC in metaphase and MKLP2-dependent transport in anaphase.

58 r envelope breakdown prior to progression to metaphase and subsequent division.

59 d that Kif4 localizes to chromosomes through metaphase and then largely redistributes to the spindle

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

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

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

63 ora B on the chromosomes during prophase and metaphase and, in addition, impairs the localization of

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

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

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

67 n of KKIP5 alleviates the DNA damage-induced metaphase arrest and causes chromosome mis-segregation a

68 MMS-induced DNA damage triggers a metaphase arrest by modulating the abundance of the oute

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

70 h1) kinase and Bub1 is sufficient to trigger metaphase arrest that is dependent on Mad1, Mad2, and Ma

71 n subunit SCC1, mimicking DNA damage-induced metaphase arrest, whereas depletion of KKIP5 alleviates

72 ow oocytes maintain a bipolar spindle during metaphase arrest.

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

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

75 A quantitative proteomic comparison between metaphase-arrested cell lysates and chromosome-sorted sa

76 solation of unfixed, native chromosomes from metaphase-arrested cells using flow cytometry and perfor

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

78 During (pro)metaphase, Aurora B is concentrated at the inner centrom

79 on partially suppresses an MMS or HU-induced metaphase block.

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

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

82 Separase is inhibited prior to metaphase by the tightly bound securin protein, which co

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

84 TOP2A from cells arrested in prometaphase or metaphase cause dramatic loss of compacted mitotic chrom

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

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

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

88 Depletion of FACT in metaphase cells prevents cohesin accumulation at pericen

89 e used electron tomography of well-preserved metaphase cells to obtain structural evidence about inte

90 entify all C. maxima chromosomes in the same metaphase cells using multiple rounds of sequential fluo

91 ications as demonstrated in somatic root tip metaphase cells, in the pachytene stage of meiosis, and

92 identify all poplar chromosomes in the same metaphase cells, which led to the development of poplar

93 P4 as major determinants of ER morphology in metaphase cells.

94 over a kinetochore-based, DNA damage-induced metaphase checkpoint in T. brucei.

95 ypanosomes employ a novel DNA damage-induced metaphase checkpoint to maintain genomic integrity.

96 s, constituting the molecular trigger of the metaphase checkpoint when Topo II is catalytically inhib

97 eviously described function to clear ER from metaphase chromatin.

98 complexes on mitotic chromosomes, defects in metaphase chromosome alignment, and elevated rates of ch

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

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

101 Metaphase chromosome spreads from human lymphocytes stim

102 lly the presence of anticancer drug sites in metaphase chromosomes and cellular nuclei.

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

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

105 associated domain)-like structures in G1 and metaphase chromosomes are reduced in the absence of FACT

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

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

108 situ hybridization (FISH) and immuno-FISH on metaphase chromosomes from karyotypically normal primary

109 We also find that compact metaphase chromosomes have a densely packed core along t

110 romatin and generate infrared maps of single metaphase chromosomes revealing detailed information on

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

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

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

114 re complex environment of intact and damaged metaphase chromosomes, unravelling their structural feat

115 ols to decipher the molecular composition of metaphase chromosomes.

116 urface appearance with a volume smaller than metaphase chromosomes.

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

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

119 distribution of histone modifications across metaphase chromosomes.

120 that allows visualization of COs directly on metaphase chromosomes.

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

122 d contribute to the growth of the cap into a metaphase compartment.

123 cortical actin caps that grow into dome-like metaphase compartments for dividing syncytial nuclei.

124 at a C. elegans one-cell stage centrosome at metaphase contains >10,000 microtubules with a total pol

125 iding the assembly of a relatively isotropic metaphase cortex.

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

127 ing through mitosis and found that prolonged metaphase delay is sufficient to disrupt Ace2 asymmetry

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

129 ling relation connecting microtubule flux to metaphase duration.

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

131 1 inhibition does not necessarily compromise metaphase establishment, but instead its maintenance.

132 Accurate chromosome alignment at metaphase facilitates the equal segregation of sister ch

133 AA reconstruction, integrated with metaphase fluorescence in situ hybridization (FISH) and

134 hat M18BP1 may identify centromeric sites in metaphase for subsequent CENP-A nucleosome assembly in i

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

136 targeting of SET to the kinetochores during metaphase hyperactivates Aurora B via PP2A inhibition, a

137 Depletion of Bub3 also results in shorter metaphase I and metaphase II due to premature localizati

138 ass I crossovers, resulting in univalents at metaphase I and pollen sterility.

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

140 Further, this study demonstrated that metaphase I arrest of Wdr62-deficient spermatocytes was

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

142 ial for maintaining a bipolar spindle during metaphase I arrest.

143 Mutant oocytes appear normal until metaphase I but then display a highly penetrant failure

144 om B73 in different stages of prophase I and metaphase I during meiosis.

145 ar architecture during the long prometaphase/metaphase I in Drosophila melanogaster oocytes.

146 A diploid-like behaviour at metaphase I involving bivalent configurations was predom

147 spindle microtubules during prometaphase and metaphase I of female meiosis [9, 10].

148 eases chromosome misalignment at the meiosis metaphase I plate, and causes chromosome mis-segregation

149 ntly associates with Exo1 at the prophase-to-metaphase I transition, enables the formation of MutLgam

150 n form complex multivalent configurations at metaphase I, and in turn alter allelic segregation ratio

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

152 including improper alignment of bivalents at metaphase I, unequal chromosome segregation during anaph

153 on is active in meiotic prophase, but not in metaphase I.

154 independent mechanism removes cohesin before metaphase I.

155 o properly congress or orient chromosomes in metaphase I.

156 to the formation of chromosome aggregates at metaphase I.

157 satellite transcripts in both prophase-I and metaphase-I chromosomes.

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

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

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

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

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

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

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

165 i-deficient mice show elevated aneuploidy in metaphase II and spermatid death.

166 Bub3 also results in shorter metaphase I and metaphase II due to premature localization of protein ph

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

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

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

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

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

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

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

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

175 is exclusively limited to the centromere at metaphase II.

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

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

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

179 kinetochore regions and affected over 30% of metaphase-II-arrested (MII) kinetochores in aged women a

180 c centromere and kinetochore organization in metaphase-II-arrested eggs from three mammalian species,

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

182 During metaphase in the early Caenorhabditis elegans embryo, th

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

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

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

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

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

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

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

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

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

192 Metaphase karyotyping is an established diagnostic stand

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

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

195 Surprisingly, mutations which disrupt the metaphase M18BP1/CENP-C interaction cause defective nucl

196 ilures of Discs Large apical localization in metaphase neuroblasts.

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

198 linker regions of DNA in the interphase and metaphase of eukaryotic cells are unprotected by histone

199 However, most germ cells were arrested at metaphase of meiosis I and no mature sperm were detected

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

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

202 hromosome paints from Varanus komodoensis to metaphases of nine species of monitor lizards.

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

204 At metaphase, one sister kinetochore couples to depolymeriz

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

206 In metaphase, p37 negatively regulates this function of PP1

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

208 34A impairs mitotic progression by affecting metaphase plate alignment and pressure generation by del

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

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

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

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

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

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

215 ted with chromosome-alignment defects at the metaphase plate leading to robust chromosome-segregation

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

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

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

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

220 s focused poles, chromosome alignment at the metaphase plate, and proper spindle length.

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

222 me congression from the spindle poles to the metaphase plate.

223 es have been singularized and aligned at the metaphase plate.

224 ines to quantify kinetochore misalignment at metaphase plates as well as lagging chromosomes at anaph

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

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

227 chromosomes, and their eventual alignment on metaphase plates.

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

229 nopus M18BP1 localizes to centromeres during metaphase-prior to CENP-A assembly-by binding to CENP-C

230 ing LMNB2 expression correspondingly altered metaphase progression and ploidy of daughter nuclei.

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

232 Inactivating Lmnb2 decreased metaphase progression, which led to formation of polyplo

233 usivity of GEMs was similar inside the dense metaphase spindle and the surrounding cytoplasm.

234 The metaphase spindle is a dynamic structure orchestrating c

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

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

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

238 conserved microtubule bundler Ase1/PRC1 for metaphase spindle organization, and simultaneous loss of

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

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

241 packed, dynamic microtubules, comprising the metaphase spindle.

242 otubule cytoskeleton self-organizes into the metaphase spindle: an ellipsoidal steady-state structure

243 Misaligned metaphase spindles are believed to result in divisions i

244 Metaphase spindles exert pole-directed forces on still-c

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

246 teractions among different classes of MTs in metaphase spindles from Chlamydomonas rheinhardti and tw

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

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

249 e been seen in even bigger spindles, such as metaphase spindles in Haemanthus endosperm and frog egg

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

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

252 mensurate with the inter-filament spacing in metaphase spindles.

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

254 53(-/-) lymphomas and MEFs, as determined by metaphase spread assay and spectral karyotyping analysis

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

256 Using metaphase spreads from human lymphoblastoid cell lines,

257 pressed entanglements; the transition to the metaphase state requires higher lengthwise compaction an

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

259 ural progenitors in mitosis, specifically in metaphase, suggesting shortened mitosis owing to prematu

260 Metaphase tension may be critical in preventing mitotic

261 role of centromere mechanics in controlling metaphase tension remains unknown.

262 iple aneuploid cell lines, leading to a weak metaphase tension signal.

263 n S352 and S274 in OE CMs, which peak during metaphase, that are ERK dependent and Hippo independent.

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

265 We find that at metaphase, the interface between the two pronuclei is co

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

267 Overexpression of KKIP5 arrests cells at metaphase through stabilizing the mitotic cyclin CYC6 an

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

269 anaphase chromosome mis-segregration, and in metaphase time.

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

271 ation of the spindle architecture during the metaphase to anaphase transition in cells.

272 , while most of the genome segregates at the metaphase to anaphase transition, resolution of the ribo

273 ing metaphase and delays the transition from metaphase to anaphase.

274 n B and results in a pronounced delay at the metaphase-to-anaphase transition after chromosome alignm

275 5 in centromeric chromatin occurs during the metaphase-to-anaphase transition and coincides with the

276 Growth is only stopped as cells approach metaphase-to-anaphase transition and growth resumes in l

277 PP1 therefore facilitates the metaphase-to-anaphase transition by promoting APC/C(CDC2

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

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

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

281 /C) is reported to play an important role in metaphase-to-anaphase transition.

282 , cleaves the Scc1 subunit of cohesin at the metaphase-to-anaphase transition.

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

284 on of Cdc23 siRNA caused decreased ratios of metaphase-to-anaphase transition.

285 icle breakdown and showed defects during the metaphase-to-anaphase transition.

286 chromosomes until its cleavage triggered the metaphase-to-anaphase transition.

287 ion exhibited a delay in the prometaphase-to-metaphase transition and anaphase defects such as laggin

288 tor cells experience delayed prometaphase-to-metaphase transition and prolonged S-phase.

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

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

291 hromosome individualization from prophase to metaphase transition.

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

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

294 The remaining three metaphases were normal karyotype.

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

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

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

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

299 antitatively measure chromosome alignment at metaphase will facilitate understanding of the contribut

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