ライフサイエンスコーパス: anaphase

1 hromatid pairs, which separate accurately at anaphase.

2 o localize Aurora B to microtubules prior to anaphase.

3 quator and cell poles, in both metaphase and anaphase.

4 bitory signal that prevents progression into anaphase.

5 d in the cleavage furrow after completion of anaphase.

6 le assembly is completed before the onset of anaphase.

7 separase triggers chromosome segregation in anaphase.

8 mosome entanglements to allow segregation at anaphase.

9 defects, giving rise to chromatin bridges at anaphase.

10 relocate to the middle of the spindle before anaphase.

11 t-range compaction of chromatin during early anaphase.

12 etaphase, whereas disjunction takes place in anaphase.

13 hromatids together until their separation at anaphase.

14 that grow out from the spindle poles during anaphase.

15 t of the centrosome-independent force during anaphase.

16 chromosome arms, a process peaking later in anaphase.

17 e relaxation of the polar cell cortex at mid anaphase.

18 commonplace but are often corrected prior to anaphase.

19 mitosis and dephosphorylated at the onset of anaphase.

20 cytoplasmic surface of the SPBs during late anaphase.

21 and defective chromosome segregation during anaphase.

22 ch elicits severe chromosome interlinking in anaphase.

23 ment of quasi-diagonal metaphase spindles in anaphase.

24 emodeling between prophase, prometaphase and anaphase.

25 ed into small, nondeveloping polar bodies at anaphase.

26 time they are made until their separation at anaphase.

27 f collapse and recovery before proceeding to anaphase.

28 ientation and anchoring at the first meiotic anaphase.

29 upon chromosome alignment is thought to time anaphase [1-3], is functional during the rapid mitotic c

30 yotes, chromosome segregation occurs through anaphase A, in which chromosomes move toward stationary

31 Following anaphase, ac-SMC3 is deacetylated by HDAC8.

32 rom telomeres, whereas disjunction occurs at anaphase after the phosphorylation of condensin subunit

33 hromosomes, and its deacetylation by Hos1 in anaphase allows re-use of Smc3 in the next cell cycle.

34 in and microtubule (MT) cytoskeletons during anaphase and cytokinesis (C phase) is largely unknown.

35 in the transition of cells from metaphase to anaphase and is one of the main components of the spindl

36 The splitting of chromosomes in anaphase and their delivery into the daughter cells need

37 cells form ultra-fine bridges (UFBs) during anaphase and these bridges are generated as a result of

38 Aberrant SKAP expression can prolong anaphase and this may contribute to developmental defect

39 side of the SPBs during metaphase and early anaphase and to the cytoplasmic surface of the SPBs duri

40 bition, lung cancer cells develop multipolar anaphase and undergo multipolar cell division with the r

41 undergo sister chromatid non-disjunction in anaphase, and frequently abort cytokinesis.

42 ssary for sister chromatid separation during anaphase, and this is regulated by evolutionarily conser

43 comes abnormally narrow, leading to impaired anaphase B and incomplete chromosome segregation.

44 ween long microtubule-microtubule sliding in anaphase B and sliding of interphase microtubules during

45 Elongation of the mitotic spindle during anaphase B contributes to chromosome segregation in many

46 ge in MT dynamics observed experimentally at anaphase B onset.

47 sliding filament mechanism underlying proper anaphase B spindle elongation and chromosome segregation

48 e length control to describe the dynamics of anaphase B spindle elongation using experimental data fr

49 s of pre-anaphase B spindles and the rate of anaphase B spindle elongation.

50 , kinesin-5 localizes all along ipMTs of the anaphase B spindle in the presence of Feo, including at

51 the steady-state length and dynamics of pre-anaphase B spindles and the rate of anaphase B spindle e

52 t in Drosophila embryos, the latter process (anaphase B) depends on a persistent kinesin-5-generated

53 We show that, during anaphase B, Imp1-mediated transport of the AAA-ATPase Cd

54 osomes move toward stationary spindle poles, anaphase B, in which chromosomes move at the same veloci

55 During pre-anaphase B, this outward sliding of ipMTs is balanced by

56 the same velocity as the spindle poles in an anaphase B-like movement.

57 the mother cell compartment, cells arrest in anaphase because the mitotic exit network (MEN), an esse

58 G3 Terc(-/-)) show precocious development of anaphase-bridge formation, p21 up-regulation, and binucl

59 required for TOP2A recruitment to ultra-fine anaphase bridges (UFBs) in mitosis.

60 subsequent formation of telomeric ultrafine anaphase bridges (UFBs), ultimately leading to stochasti

61 wever, we observed only a marginal effect on anaphase bridges and centrosome number, which could be d

62 mitosis, exhibit the formation of ultra-fine anaphase bridges and micronuclei.

63 diomyocytes with dysfunctional telomeres and anaphase bridges and positive for the cell-cycle arrest

64 Levels of anaphase bridges were also elevated, implicating failed

65 strand synthesis in early mitosis, ultrafine anaphase bridges, and G1-specific p53-binding protein 1

66 educed telomere-dysfunction-induced foci and anaphase bridges, indicating improved telomere capping.

67 During mitosis, they form anaphase bridges, resulting in chromosome breakage by an

68 a new subclass of human ribosomal ultrafine anaphase bridges.

69 bly checkpoint kinase Mps1 not only inhibits anaphase but also corrects erroneous attachments that co

70 t mitosis, biasing chromosome segregation in anaphase by causing daughter cells with old centrosomes

71 ic checkpoint complex" (MCC), which prevents anaphase by targeting Cdc20, the activator of the anapha

72 Mechanisms of CDK2-mediated anaphase catastrophe and how activated KRAS enhances thi

73 target and centrosome protein CP110 induced anaphase catastrophe of lung cancer cells.

74 ll division leading to apoptosis, defined as anaphase catastrophe.

75 critical mediator of CDK2 inhibition-driven anaphase catastrophe.

76 pression antagonized CDK2 inhibitor-mediated anaphase catastrophe.

77 tractile actin belt at the apex that governs anaphase cell flattening.

78 zation and bundling activity of Mklp2 at the anaphase central spindle.

79 nificantly reduced brain size, with frequent anaphase chromatin bridge formation observed in apical n

80 ct the outer kinetochore before the start of anaphase chromosome separation.

81 and Ndc80 submodules add copies to form an "anaphase configuration" kinetochore.

82 ormed between segregating chromosomes during anaphase, cooperates with astral microtubules to positio

83 ytene chromosomes persist into metaphase, an anaphase delay prevents tissue malformation and apoptosi

84 ics such as cell shape, cell size, metaphase/anaphase delays, and mitotic abnormalities including spi

85 ochore components prevents the error-induced anaphase delays.

86 Chromosome segregation during anaphase depends on chromosome-to-pole motility and pole

87 the mother cell compartment, cells arrest in anaphase due to inhibition of the MEN by the mother cell

88 to daughter cells was not due to changes of anaphase duration or nuclear shape but solely to the dow

89 local softening of the cortex, facilitating anaphase elongation and orderly cell division.

90 adation insufficient to guarantee that early anaphase events occur in the correct order.

91 provides robustness to the temporal order of anaphase events.

92 g UBE2C, whereas mutant p53 causes premature anaphase exit by increasing UBE2C expression in the pres

93 In all cases, dicentric breakage requires anaphase exit, ruling out stretching by the elongated mi

94 feature tilted metaphase spindles, lack this anaphase flattening mechanism and as a consequence maint

95 Our model is that during anaphase, "free" importins, whose gradient inversely cor

96 chromatin bridges and lagging chromosomes in anaphase, frequently leading to cytokinesis failure, mul

97 First, univalents lagged during anaphase I and their movement was biased toward the cort

98 omosome was preferentially eliminated during anaphase I of female meiosis.

99 g sister chromatids separate precociously in anaphase I revealed no direct role of these proteins on

100 logous chromosomes until their separation at anaphase I.

101 hromatid arms when the homologs segregate at anaphase I.

102 ister-chromatid cohesion at the metaphase II/anaphase II transition.

103 tric partitioning event occurs shortly after anaphase II, and both microtubules and actin partition i

104 t can slide away from the cell middle during anaphase in a myosin V-dependent manner.

105 lex in vitro and affects the timely onset of anaphase in cells.

106 ndle at the cell center during metaphase and anaphase in one- and two-cell Caenorhabditis elegans emb

107 pindle push chromosomes apart during meiotic anaphase in oocytes.

108 ce, they bypass mitotic arrest and embark on anaphase in spite of incorrect chromosome segregation, g

109 Moreover, this mechanism can prevent anaphase in the absence of kinetochore signalling.

110 to maintain faithful timing and execution of anaphase in the absence of securin.

111 unexpected events of error correction during anaphase in wild-type or mutant cells.

112 that C. elegans oocytes delay key events in anaphase, including AIR-2/Aurora B relocalization to the

113 ected centralspindlin oligomerization during anaphase induces contractile ring assembly at the membra

114 ally found in association with securin, this anaphase inhibitor is dispensable for murine life while

115 C regulator that promotes the assembly of an anaphase inhibitor through a sequential multi-target pho

116 Overall our studies reveal that anaphase inhibitors are diffusible and active outside th

117 esulted in a Cyclin B3-only mitosis in which anaphase initiated prior to chromosome alignment.

118 The impact of Cyclin B3 on anaphase initiation appeared to decline with development

119 which targets for degradation inhibitors of anaphase initiation.

120 ets for degradation securin, an inhibitor of anaphase initiation.

121 osome (APC/C), whose action is necessary for anaphase initiation.

122 disengagement) between two centrioles during anaphase is considered a licensing event for the next ro

123 mulation of Cdc5 at the daughter SPB in late anaphase is controlled by Bfa1.

124 mosomes move towards the polar cortex at mid anaphase, kinetochore-localized PP1-Sds22 helps to break

125 Kif2a-depleted animal caps have anaphase lagging chromosomes in stage 9 and 10 embryos a

126 of the Rho-interacting kinase citron to the anaphase midzone.

127 chromatin region during prophase but during anaphase move to surround segregating DNA.

128 During anaphase, MTs are incorporated into an anti-parallel arr

129 os1 has a more immediate effect in the early anaphase of budding yeast.

130 tein that is translationally repressed until anaphase of MII.

131 erlapping microtubules, during metaphase and anaphase of mitosis.

132 se 1 (PP1) to kinetochores to promote timely anaphase onset [12].

133 to the dissolution of sister chromatids and anaphase onset [1].

134 Chromosome segregation and anaphase onset are initiated through the action of the m

135 Most of these defects are corrected before anaphase onset by a mechanism involving Aurora B kinase,

136 faithful chromosome segregation by delaying anaphase onset even when a single kinetochore is unattac

137 ent, the BUB-1/BUB-3 complex promotes timely anaphase onset in Caenorhabditis elegans embryos.

138 ciated (Ska) complex is essential for normal anaphase onset in mitosis.

139 necessary to recruit Mad1:Mad2 to, and delay anaphase onset in response to, unattached kinetochores i

140 ttachment to spindle microtubules, and delay anaphase onset in response.

141 Proper spindle positioning at anaphase onset is essential for normal tissue organizati

142 ole for the BUB-1/BUB-3 complex in promoting anaphase onset that is distinct from its well-studied fu

143 which enriches at attachment sites prior to anaphase onset to dampen chromosome motion.

144 ), a conserved signaling pathway that delays anaphase onset until all chromosomes are attached to spi

145 events chromosome missegregation by coupling anaphase onset with correct chromosome attachment and te

146 w via two distinct cortical Myosin flows: at anaphase onset, a polarity induced, basally directed Myo

147 -C2alpha causes spindle alterations, delayed anaphase onset, and aneuploidy, indicating that PI3K-C2a

148 ake produces a checkpoint-dependent delay in anaphase onset, and inducing dietary restriction when th

149 From nuclear envelope breakdown until anaphase onset, GTSE1 binds preferentially to the most s

150 protein phosphatase 1 (PP1) to chromatin at anaphase onset, in a similar manner as RepoMan.

151 At anaphase onset, ring removal shifts the balance between

152 ter kinetochore component recruited prior to anaphase onset.

153 struction of securin and cyclin and delaying anaphase onset.

154 osome bound to Cdc20 (APC/C(Cdc20)) to delay anaphase onset.

155 removes SCIs from cohesed chromatids at the anaphase onset.

156 dle checkpoint signaling kinases and promote anaphase onset.

157 tly center themselves in the XY-plane before anaphase onset.

158 nd that completion of the dance is linked to anaphase onset.

159 produces an inhibitory signal that prevents anaphase onset.

160 an association between cortical contact and anaphase onset.

161 inetochores to generate a signal that delays anaphase onset.

162 al from an unattached kinetochore to inhibit anaphase onset.

163 x/cyclosome, a ubiquitin ligase required for anaphase onset.

164 tants support chromosome alignment but delay anaphase onset.

165 an bind both PP1 and microtubules to promote anaphase onset.

166 when cohesin Scc1 is cleaved by separase at anaphase onset.

167 se oscillations begin to subside soon before anaphase onset.

168 This, in turn, facilitates anaphase-onset by ubiquitin-mediated degradation of mito

169 In anaphase, p120 is enriched at the cleavage furrow where

170 lls and revealing a mechanism that regulates anaphase progression.

171 repressed genes is Emi1, an inhibitor of the anaphase promoting complex (APC) which is degraded durin

172 ndent protein kinase (Cdk) families, and the Anaphase Promoting Complex (APC).

173 oach by isolating the complexes for the rice ANAPHASE PROMOTING COMPLEX SUBUNIT 10 (APC10) and CYCLIN

174 Here we show that Parkin interacts with anaphase promoting complex/cyclosome (APC/C) coactivator

175 is mediated by increased destruction by the anaphase promoting complex/cyclosome (APC/C) during meio

176 The SAC prevents the anaphase promoting complex/cyclosome (APC/C) ubiquitin l

177 Assembly Checkpoint (SAC) that inhibits the Anaphase Promoting Complex/Cyclosome (APC/C) ubiquitin l

178 cycle onset is controlled by activity of the Anaphase Promoting Complex/Cyclosome (APC/C), a multisub

179 MCC inhibits the ubiquitin ligase anaphase promoting complex/cyclosome (APC/C), whose acti

180 MCC), which inhibits Cdc20 to inactivate the Anaphase Promoting Complex/Cyclosome (APC/C).

181 well-established substrate receptors for the Anaphase Promoting Complex/Cyclosome (APC/C).

182 factor (MPF) by inhibiting ubiquitin ligase anaphase promoting complex/cyclosome (APC/C).

183 nce of ubiquitylation events mediated by the anaphase-promoting complex (APC) based on short redundan

184 pindle assembly checkpoint, which results in anaphase-promoting complex (APC) inhibition.

185 ing the metaphase-anaphase transition by the anaphase-promoting complex (APC), which recognizes the d

186 etochores into the cytoplasm, inhibiting the anaphase-promoting complex (APC).

187 The anaphase-promoting complex (APC/C) is a multimeric RING

188 o the mitotic spindle with activation of the anaphase-promoting complex (APC/C), the E3 ubiquitin lig

189 int complex (MCC), a potent inhibitor of the anaphase-promoting complex (APC/C).

190 tivation of the E2 Ube2S by its RING-E3, the anaphase-promoting complex (APC/C); while phosphorylatio

191 In eukaryotes, the anaphase-promoting complex (APC/C, also known as the cyc

192 ulatory subunit of the ubiquitin ligase Cdh1-anaphase-promoting complex (Cdh1-APC), profoundly impair

193 nd thereby promoting SPOP degradation by the anaphase-promoting complex activator FZR1.

194 reakdown, and provides an effective block to anaphase-promoting complex activity, and consequently th

195 e groups that control the M phase, including anaphase-promoting complex genes, via aberrant transcrip

196 ve identified additional novel roles for the anaphase-promoting complex in diverse aspects of neurona

197 perspective on future investigations of the anaphase-promoting complex in neurobiology.

198 discuss the functions and mechanisms of the anaphase-promoting complex in neurogenesis, glial differ

199 The anaphase-promoting complex in partnership with its activ

200 lti-subunit E3 ubiquitin ligase known as the anaphase-promoting complex or cyclosome (APC/C [2]).

201 The anaphase-promoting complex or cyclosome (APC/C) is a ubi

202 The anaphase-promoting complex or cyclosome (APC/C) is the u

203 The anaphase-promoting complex or cyclosome (APC/C), a multi

204 role for a master cell-cycle regulator, the anaphase-promoting complex or cyclosome (APC/C), in the

205 ochores during prometaphase and inhibits the anaphase-promoting complex or cyclosome (APC/C), thus en

206 ed kinetochores and inhibits the Cdc20-bound anaphase-promoting complex or cyclosome (APC/C), to dela

207 R1-Bub3, Mad2, and Cdc20, which inhibits the anaphase-promoting complex or cyclosome bound to Cdc20 (

208 ago, the first post-mitotic function of the anaphase-promoting complex, a major cell cycle-regulated

209 erview of the function and regulation of the anaphase-promoting complex, an E3 ubiquitin ligase that

210 The anaphase-promoting complex, or cyclosome (APC/C), is a u

211 romiscuous E3 ligase inhibitor targeting the anaphase-promoting complex, which increases cell mitogen

212 ll cycle-associated E3-ubiquitin ligase, the anaphase-promoting complex.

213 Here, we show that inactivation of the anaphase-promoting complex/cyclosome (APC(Cdh1)) has the

214 uch E3 is the gigantic, multisubunit 1.2-MDa anaphase-promoting complex/cyclosome (APC), which contro

215 ubiquitination activities of CDC20-activated anaphase-promoting complex/cyclosome (APC/C(CDC20)).

216 ntriole disengagement depend on separase and anaphase-promoting complex/cyclosome (APC/C) activity, w

217 o-EM and biochemistry show that the human E3 anaphase-promoting complex/cyclosome (APC/C) and its two

218 duration is determined by activation of the anaphase-promoting complex/cyclosome (APC/C) bound to it

219 Here we show that Arabidopsis anaphase-promoting complex/cyclosome (APC/C) coactivator

220 The anaphase-promoting complex/cyclosome (APC/C) controls a

221 several means, including inactivation of the anaphase-promoting complex/cyclosome (APC/C) E3 ubiquiti

222 y-destroyed cyclins-Cyclins A and B-restrain anaphase-promoting complex/cyclosome (APC/C) function, w

223 Here, we demonstrate that the anaphase-promoting complex/cyclosome (APC/C) in complex

224 The anaphase-promoting complex/cyclosome (APC/C) is a large

225 The anaphase-promoting complex/cyclosome (APC/C) is a large

226 The anaphase-promoting complex/cyclosome (APC/C) is a massiv

227 The anaphase-promoting complex/cyclosome (APC/C) is a member

228 The Anaphase-Promoting Complex/Cyclosome (APC/C) is an E3 ub

229 The checkpoint system acts on the Anaphase-Promoting Complex/Cyclosome (APC/C) ubiquitin l

230 The anaphase-promoting complex/cyclosome (APC/C) ubiquitin l

231 ostnatal deletion of Cdh1, a cofactor of the anaphase-promoting complex/cyclosome (APC/C) ubiquitin l

232 bub3Delta cells had impaired binding of the anaphase-promoting complex/cyclosome (APC/C) with its ac

233 MCC inhibits the anaphase-promoting complex/cyclosome (APC/C), a ubiquiti

234 Cdc20, a cofactor of the E3 ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C), accumulate

235 A multi-subunit ubiquitin ligase, the anaphase-promoting complex/cyclosome (APC/C), regulates

236 es with the function of the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C), which, tog

237 n the proteasome after ubiquitylation by the anaphase-promoting complex/cyclosome (APC/C)-cadherin 1

238 proteins inhibit Cdc20, an activator of the anaphase-promoting complex/cyclosome (APC/C).

239 ork that inhibits premitotic activity of the anaphase-promoting complex/cyclosome (APC/C).

240 checkpoint complex (MCC), which inhibits the anaphase-promoting complex/cyclosome (APC/C).

241 ase by targeting Cdc20, the activator of the anaphase-promoting complex/cyclosome (APC/C).

242 MCC formation inhibits the anaphase-promoting complex/cyclosome (Cdc20-APC/C), ther

243 At the first meiotic division, anaphase-promoting complex/cyclosome associated with Cdc

244 This is achieved through inhibition of the anaphase-promoting complex/cyclosome by a kinetochore-de

245 proliferation, including most targets of the anaphase-promoting complex/cyclosome complex, a set of g

246 BubR1M that contribute to Cdc20 binding and anaphase-promoting complex/cyclosome inhibition: a destr

247 a meiosis-specific targeting subunit of the anaphase-promoting complex/cyclosome that regulates mult

248 iated by the 1.2-MDa ubiquitin ligase APC/C (anaphase-promoting complex/cyclosome) and its coactivato

249 CC is a critical checkpoint inhibitor of the anaphase-promoting complex/cyclosome, a ubiquitin ligase

250 The relevant ubiquitin ligase, the anaphase-promoting complex/cyclosome, also targets cycli

251 y preventing degradation of cyclin B1 by the anaphase-promoting complex/cyclosome, but some cells eva

252 te and characterize recombinant forms of the anaphase-promoting complex/cyclosome, cohesin, and kinet

253 bility of RNF157 during the cell cycle in an anaphase-promoting complex/cyclosome-CDH1-dependent mann

254 le ensuring timely activation of separase by anaphase-promoting complex/cyclosome-dependent degradati

255 ugating enzyme that donates ubiquitin to the anaphase-promoting complex/cyclosome.

256 The anaphase promotion function required BUB-1's kinase doma

257 negatively regulating the Cdc Fourteen Early Anaphase Release (FEAR) pathway.

258 ion at kinetochores influences the timing of anaphase requires an understanding of how spindle checkp

259 Importantly, SCI removal in anaphase requires condensin and coincides with the hyper

260 While Mad2 delays anaphase separation of metaphase polytene chromosomes, M

261 lex/cyclosome by a kinetochore-derived "wait anaphase" signal known as the mitotic checkpoint complex

262 Thus, we propose that the diffusible 'wait anaphase' signal could be the MCC itself, and explain ho

263 d kinetochores generating a diffusible 'wait anaphase' signal that inhibits the APC/C in the cytoplas

264 cells are fused with interphase cells, "wait anaphase" signals are diluted, resulting in premature mi

265 Here we report that "wait anaphase" signals are indeed able to diffuse outside the

266 Our findings uncover an anaphase-specific function for these effector kinesins t

267 In budding yeast, alignment of the anaphase spindle along the mother-bud axis is crucial fo

268 If the anaphase spindle becomes misaligned in the mother cell c

269 The anaphase spindle determines the position of the cytokine

270 pt for kinesin-6 Klp9, which is required for anaphase spindle elongation.

271 se ingredients power the oscillations of the anaphase spindle in budding yeast, but in A. gossypii, t

272 hore microtubules in metaphase and then with anaphase spindle midzone.

273 microtubules at the centre of the elongating anaphase spindle.

274 We find that metaphase and anaphase spindles elongate at the same rate when confine

275 r efficient dissolution of cohesion in early anaphase; subsequent Smc3 deacetylation, triggered by Sc

276 All anaphase substrates tested by this methodology are stabi

277 Swivel reduces as cells approach anaphase, suggesting an organisational change linked to

278 perturbations were observed when advance to anaphase, suggesting the importance of topoisomerase II

279 her to align all chromosomes before entering anaphase synchronously.

280 Before their resolution at 3-20 hr after anaphase, the chromatin bridges induced nuclear envelope

281 oting complex or cyclosome (APC/C), to delay anaphase, thereby preventing aneuploidy.

282 nd cyclin B competing for degradation during anaphase, this provides robustness to the temporal order

283 ubunits is created during S and destroyed at anaphase through Scc1 cleavage by separase.

284 hed during prometaphase remain intact during anaphase to facilitate separation, defining a novel form

285 hatase that counteracts CDK1 activity during anaphase to promote mitotic exit in Saccharomyces cerevi

286 lin, moving from poles to midzone during the anaphase-to-telophase transition.

287 ric chromatin occurs during the metaphase-to-anaphase transition and coincides with the removal of ch

288 n-6, has critical roles during the metaphase-anaphase transition and cytokinesis.

289 atids together from S phase to the metaphase-anaphase transition and ensures accurate segregation of

290 l cycle and is degraded during the metaphase-anaphase transition by the anaphase-promoting complex (A

291 y securin-bound separase at the metaphase-to-anaphase transition renders it resistant to re-inhibitio

292 At the metaphase-to-anaphase transition, the CPC dissociates from centromere

293 ting to the coordination of the metaphase-to-anaphase transition.

294 in mitotic checkpoint signaling, preventing anaphase until all chromosomes are properly attached to

295 e spindle assembly checkpoint (SAC) prevents anaphase until all kinetochores attach to the spindle.

296 curacy of chromosome segregation by delaying anaphase until correct bipolar attachment of chromatids

297 Our data show that in anaphase, when the spindle elongates, PP1/Repo-Man promo

298 in G2 phase and released to the cytoplasm in anaphase, where it accumulates at the bud neck.

299 that the Dam1 submodule is unchanged during anaphase, whereas MIND and Ndc80 submodules add copies t

300 icrotubules and prevents precocious onset of anaphase, which can lead to aneuploidy.