ライフサイエンスコーパス: meiosis II

1 to the sister kinetochores of dyads (during meiosis II).

2 g from opposite poles (biorientation) during meiosis II.

3 e body that lies between the two spindles of meiosis II.

4 but are maintained around centromeres until meiosis II.

5 egation of chromosomes at both meiosis I and meiosis II.

6 f chromosome segregation between mitosis and meiosis II.

7 ion in tam was delayed in both pachytene and meiosis II.

8 factor (CSF)-mediated arrest at metaphase of meiosis II.

9 surprisingly, does not halt progression into meiosis II.

10 eiosis I and from centromeric regions during meiosis II.

11 leading edge of the prospore membrane during meiosis II.

12 s, Ady3p remains associated with SPBs during meiosis II.

13 arate in meiosis I and segregate randomly in meiosis II.

14 ll four spindle pole bodies of a cell during meiosis II.

15 MPF) activity corresponding to meiosis I and meiosis II.

16 but also to stimulate cyclin B synthesis in Meiosis II.

17 are kept together until their separation in meiosis II.

18 ed cases mainly originated through errors in meiosis II.

19 st meiotic division but not the mitotic-like meiosis II.

20 Such oocytes entered S phase rather than meiosis II.

21 o nondisjunction of sister chromatids during meiosis II.

22 uring meiosis I and sister chromatids during meiosis II.

23 hout meiosis I and disappears at anaphase of meiosis II.

24 tic nuclear division most closely resembling meiosis II.

25 S332 mutant males enhances nondisjunction at meiosis II.

26 sis I and then from the centromere region in meiosis II.

27 essential for cohesion at the centromeres in meiosis II.

28 tric cellular division associated with sperm meiosis II.

29 ced, and nuclei become fragmented soon after meiosis II.

30 ular focus at centrioles until completion of meiosis II.

31 m segregation errors at meiosis I as well as meiosis II.

32 dial microtubule arrays (RMAs) at the end of meiosis II.

33 ons originate in meiosis I and two-thirds in meiosis II.

34 premature division in synchrony with female meiosis II.

35 easing the incidence of single chromatids at meiosis II.

36 iosis I, and then from the pericentromere in meiosis II.

37 ctivator, Ssp2, that binds Smk1/Isc10 during meiosis II.

38 and triads and tetrads as final products of meiosis II.

39 by NDT80 but not translated until the end of meiosis II.

40 hromatids together until their separation in meiosis II.

41 d chromosome missegregation in meiosis I and meiosis II.

42 ion of spindle microtubules in meiosis I and meiosis II.

43 e resumption of meiosis I and progression to meiosis II.

44 I but also the fate of sister chromatids at meiosis II.

45 drive against non-recombinant chromatids at meiosis II.

46 netochores isolated from cells in mitosis or meiosis II.

47 grate, rather than separate as in mitosis or meiosis II.

48 in preventing centriole disengagement during meiosis II.

49 ing a transient interphase-like state before meiosis II.

50 and an infrequent chromosome disjunction in meiosis II.

51 ds of nuclear divisions called meiosis I and meiosis II.

52 x was not required to initiate resumption of meiosis II.

53 is I but contributes to the timely exit from meiosis II.

54 the signaling pathway is active only during meiosis II.

55 ion of DNA replication between meiosis I and meiosis II.

56 for factors necessary to maintain SCC until meiosis II.

57 mains where cohesion will be protected until meiosis II.

58 eracting protein Cks30A to drive anaphase in meiosis II.

59 During meiosis II, activated cyclin E-Cdk2 significantly inhibi

60 extra Y was generated by non-disjunction at meiosis II after a normal chiasmate meiosis I.

61 -zygotic mitotic error or non-disjunction at meiosis II after a nullichiasmate meiosis I.

62 tic spindle abnormalities with completion of meiosis II after fertilization.

63 the DYRK kinase MBK-2, which is activated at meiosis II after fertilization.

64 ter formation of bipolar domains, whereas in meiosis II, AIR-1 is necessary to recruit PAR-2 onto the

65 More severely affected embryos skipped meiosis II altogether and exhibited striking defects in

66 I, the protein kinase is dispensable during meiosis II and does not even phosphorylate its meiosis I

67 g meiosis I division and remained low during meiosis II and following mitoses.

68 Consequently, some cells fail to undergo meiosis II and form dyads, while some, as they progress

69 APC/C(Cdc20) activity as the cells complete meiosis II and form spores.

70 initiate growth at the spindle poles during meiosis II and grow to encapsulate daughter nuclei.

71 iming of the translation of several mRNAs in meiosis II and is required to maintain meiotic commitmen

72 to arrest unfertilized eggs at metaphase of meiosis II and seems to be the long-sought mediator of C

73 tromeric cohesion is lost as cells exit from meiosis II and sister chromatids can then separate.

74 is removed from chromosomes normally during meiosis II and sister chromatids separate, suggesting th

75 potentially led to subsequent disruptions in meiosis II and spermiogenesis.

76 are sequestered away from chromosomes during meiosis II and subsequently eliminated.

77 stage VI oocytes blocks progression through meiosis II and the establishment of CSF arrest.

78 pindle microtubules throughout meiosis I and meiosis II, and dissociates from the meiotic spindle in

79 es blocks the establishment of CSF arrest in meiosis II, and immunodepletion of either protein blocke

80 uch as nondisjunction (NDJ) in meiosis I and meiosis II, and premature separation of sister chromatid

81 ed to kinetochores during both meiosis I and meiosis II, and the electrophoretic mobility of Bub1 upo

82 aintain c-mos and MAP kinase activity during meiosis II, and to establish the metaphase arrest at the

83 ermatocytes in meiosis I to spermatocytes in meiosis II, and to move chromosomes from one spindle to

84 We present evidence that, as cells exit from meiosis II, APC/C(Ama1) mediates Cdc20p destruction.

85 tivation, xFizzy-ablated oocytes progress to Meiosis II as shown by cyclin E synthesis, further accum

86 ll imaging indicate that PDS5 play a role in meiosis II as well.

87 ogous chromosomes are segregated, and during meiosis II, as in mitosis, sister chromatids are partiti

88 In meiosis II, Aurora B controls KT-MT attachment but appea

89 Lastly, we found that during meiosis II, autophagy degrades Rim4, an amyloid-like tra

90 equired that an LRE3 mRNA transcribed before meiosis II be carried separately from its precursor LRE3

91 NP-E epitopes, not the absence of CENP-E, in meiosis II because a different polyclonal antibody raise

92 osomes can switch from meiosis I behavior to meiosis II behavior.

93 pears to promote centromeric cohesion during meiosis II but is not essential for kinetochore function

94 disrupts sister chromatid segregation during meiosis II but not homologous chromosome segregation dur

95 it and for the maintenance of cohesion until meiosis II, but is independent of the ability of Eco1 to

96 he activity of APC(Ama1) is inhibited before meiosis II, but the substrates specifically targeted for

97 ent trigger for cyclin B1 destruction during meiosis II; but it played no role during meiosis I and f

98 vertebrate eggs are arrested in metaphase of meiosis II by cytostatic factor (CSF), an activity that

99 rtilization, vertebrate eggs are arrested in meiosis II by cytostatic factor (CSF), which holds the a

100 g fertilization are arrested at metaphase of meiosis II by cytostatic factor (CSF).

101 tions for centromeric cohesin removal during meiosis II by promoting the degradation of Spo13, a prot

102 in afd1 meiocytes, all of the chromosomes at meiosis II carry single kinetochores.

103 dyads, while some, as they progress through meiosis II, cause a defect in chromosome integrity.

104 t the segregation of the Y chromatids during meiosis II, causing female-biased sex ratio in progeny.

105 ells, we detected chromosome breakage in the meiosis II cells.

106 ate Meikin at anaphase I result in defective meiosis II chromosome alignment in mouse oocytes.

107 somes attach to the spindle differently than meiosis II chromosomes and that they regulate chromosome

108 that meiosis I chromosomes become competent meiosis II chromosomes in anaphase of meiosis I, but not

109 ecise regulation of crossover number in each meiosis, (ii) considerably reduced recombination along c

110 Cold arrest induced a fraction of meiosis II crane fly spermatocytes to form (n + 1) and (

111 In contrast, in meiosis II, cytoplasm that contains upregulated factors

112 hat (i) these NAHR hot spots are specific to meiosis, (ii) deletions are generated at a higher rate t

113 se to DNA damage in fully mature eggs during meiosis II, despite the divisions being separated by jus

114 retained to ensure proper segregation during meiosis II, dissolution of arm cohesion would be require

115 nce diploid cells skip meiosis I and execute meiosis II division.

116 of recombination is apparently required for meiosis II division.

117 ng meiotic maturation arrest in metaphase of meiosis II due to a cytoplasmic activity termed cytostat

118 ggesting absence of checkpoint regulation of meiosis II entry.

119 atterns, including an increased frequency of meiosis II errors among eggs affected by errors in meios

120 e can also distinguish between meiosis I and meiosis II errors based on signatures spanning the centr

121 17% of Meiosis II errors were misclassified as Meiosis I, mainl

122 1) are prematurely active, and meiosis I and meiosis II events occur in a single meiotic division.

123 PTKs play an essential role in completion of meiosis II following fertilization and progression from

124 ewise, condensin activity is nonessential in meiosis II for telomere and chromosome arm separation.

125 Additionally, cytokinetic failure at meiosis II gives rise to bi-nucleated or even tetra-nucl

126 ed with the meiotic spindle at all stages of meiosis II; however, no concentration of labeling was ev

127 At the onset of meiosis II, Ime2 kinase activity rises and triggers a de

128 by Don1p, and Don1p rings are absent during meiosis II in ady3Delta/ady3Delta cells.

129 The extended meiosis II in cul-2 mutants induces polarity reversals t

130 enance of H1 kinase activity at metaphase of meiosis II in progesterone-treated oocytes.

131 During meiosis II in Saccharomyces cerevisiae, the cytoplasmic

132 During meiosis II in the yeast Saccharomyces cerevisiae, the cy

133 target of the MAPK pathway during M phase of meiosis II in Xenopus oocytes.

134 s: prophase of meiosis I and after exit from meiosis II, in spermatids.

135 l nuclear envelope breakdown' at anaphase of meiosis II, in which the nuclear envelope is structurall

136 pt chromosome behavior in male meiosis I and meiosis II, indicating that ZW10 function is common to b

137 ation suggests that the occurrence of NDJ in meiosis II is associated with the ploidy status of an eg

138 brate unfertilized eggs, metaphase arrest in Meiosis II is mediated by an activity known as cytostati

139 tention of cohesins around centromeres until meiosis II is required for the accurate segregation of s

140 detectable on spermatid mitochondria late in meiosis II, just prior to fusion, and disappears soon af

141 Errors in progression from meiosis I to meiosis II lead to aneuploid and polyploid gametes, but

142 activity at the transition from meiosis I to meiosis II led to accelerated completion of meiosis I an

143 ng the ability of some univalents to adopt a meiosis II-like orientation on the spindle.

144 bodies after the meiosis I division, and at meiosis II localizes to the new spore membrane as it sur

145 release, but its abrupt accumulation during meiosis II (M II) is also required for the establishment

146 nce events, such as chromatid segregation in meiosis II, many decades later.

147 The appearance of CSF arrest at Meiosis II may result from coexpression of cyclin E/Cdk2

148 ase PP2A-B55 is reactivated at the meiosis I/meiosis II (MI/MII) transition, resulting in the prefere

149 In meiosis II, microtubules nucleate in the vicinity of chr

150 eiosis I, Mastl-null oocytes failed to enter meiosis II (MII) because they reassembled a nuclear stru

151 ot caused by alterations in meiosis I (MI or meiosis II (MII) chromosome dynamics, but instead result

152 ncreased recombination has been reported for meiosis II (MII) errors involving chromosome 21.

153 l cases where the ratio of meiosis I (MI) to meiosis II (MII) errors is 3:1, a near 1:1 ratio exists

154 tion events and for proximal exchanges among meiosis II (MII) events.

155 Sister chromatid attachment during meiosis II (MII) is maintained by securin-mediated inhib

156 ciated with both maternal meiosis I (MI) and meiosis II (MII) non-disjunction events.

157 during the transition from meiosis I (MI) to meiosis II (MII) remain unclear.

158 transition of oocytes from meiosis I (MI) to meiosis II (MII) requires partial cyclin B degradation t

159 Meiosis II (MII) segregation leads to the separation of

160 as 2 - 3-fold less than that at metaphase of Meiosis II (MII), but MAP K activation was maximal at me

161 unction occurring at both meiosis I (MI) and meiosis II (MII).

162 structures that engulf haploid cells during meiosis II (MII).

163 o meiotic cell divisions, meiosis I (MI) and meiosis II (MII).

164 e parental origin and stage (meiosis I [MI], meiosis II [MII], or postzygotic mitotic) of the chromos

165 matid cohesion is lost at anaphase I, giving meiosis II missegregation.

166 hift may perturb segregation, leading to the meiosis II NDJ in this study, and is further evidence fo

167 Meiosis II NDJ occurred in 21 of 23 families.

168 and a published trisomy 21 map derived from meiosis II NDJ.

169 tal DNA available, at least four were due to meiosis II non-disjunction following a normal chiasmate

170 isomy with partial isodisomy was caused by a meiosis II nondisjunction event.

171 This study investigated the basis of meiosis II nondisjunction.

172 rmally colocalizes with cohesin; however, in meiosis II oocytes from older women, SGO2 is frequently

173 isjunction must occur either during paternal meiosis II or as a post-zygotic mitotic error, both of w

174 ch fertilized oocytes arrest in meiosis I or meiosis II or fail to complete the actin-based process o

175 e with opposed sister kinetochores (mitosis, meiosis II) or paired homologous kinetochores (meiosis I

176 metaphase I is not required for anaphase I, meiosis II, or the decondensation of the meiotic product

177 Finally, we found that meiosis II outer kinetochore assembly was solely depende

178 of the spindle pole body, referred to as the meiosis II outer plaque (MOP), is modified in both compo

179 Vesicle docking complexes, called meiosis II outer plaques (MOPs), form on each meiosis II

180 pindle organization, and the expression of a meiosis II post-fertilization marker.

181 mentally regulated DYRK2 kinase activated at meiosis II, primes T(186) for subsequent polo kinase-dep

182 the spindle poles eventually disappeared as meiosis II progressed to anaphase II.

183 ty acids at a time that correlates well with meiosis II progression, concomitant with phospholipid re

184 produced in prophase I indirectly regulates meiosis II progression, or that a very low level of CYCA

185 very low level of CYCA1;2 directly regulates meiosis II progression.

186 and consequently, the activation of MPF for meiosis II requires new cyclin synthesis, principally of

187 is I, followed by nondisjunction in maternal meiosis II, resulted in an oocyte with two copies of the

188 Both features are lost during meiosis II, resulting in sister chromatid disjunction an

189 , centrioles separate inappropriately during meiosis II, resulting in spermatids with disengaged cent

190 which disturbed spindle position during male meiosis II results in the incorporation of previously se

191 At the onset of meiosis II, Rim4 aggregates are abruptly degraded allowi

192 ion during meiosis I, and others showed more meiosis II segregation failures.

193 ombination during meiosis I, affected mainly meiosis II segregation.

194 sis I, homologues are segregated, whereas in meiosis II, sister chromatids are segregated.

195 , homologous chromosomes segregate, while in meiosis II, sister chromatids separate from each other.

196 , Ste segregates asymmetrically again during meiosis II, sparing half of the Y-bearing spermatids fro

197 e segregated from one another in mitosis and meiosis II, specific adaptations enable the segregation

198 revealed that autophagy inhibition prevents meiosis II-specific expression of Clb3 and leads to the

199 ts in modification of only one SPB from each meiosis II spindle and formation of a two-spored ascus,

200 of MT severing, caused a specific defect in meiosis II spindle disassembly.

201 meiosis I but frequent asymmetric failure of meiosis II spindle formation.

202 ; e.g., a meiosis I chromosome attached to a meiosis II spindle in its normal fashion and sister chro

203 rough the SPE-11 protein but assembly of the meiosis II spindle is initiated through an SPE-11-indepe

204 tribution in which the two newly synthesized meiosis II spindle pole bodies of MPC70/mpc70 strains la

205 eiosis II outer plaques (MOPs), form on each meiosis II spindle pole body (SPB) and serve as sites of

206 Ady3p forms ring-like structures around meiosis II spindles that colocalize with those formed by

207 sequential associations of the meiosis I and meiosis II spindles with the cell cortex so that extra c

208 ract spindles recapitulate the length of egg meiosis II spindles, by using mechanisms intrinsic to th

209 I but did not form polar bodies or assemble meiosis II spindles.

210 hromosomes, as well as mispositioning of the meiosis II spindles.

211 of microtubules established between the two meiosis II spindles.

212 regation in meiosis I much more than that in meiosis II, suggesting that checkpoint defects may contr

213 (1) the central MTOC that forms between the meiosis II tandem spindles and (2) the centrosomes of th

214 hose translation is delayed until the end of meiosis II, termed protected transcripts, the transcript

215 f spindle pole bodies (SPBs) at the onset of meiosis II that allows them to promote de novo membrane

216 Importantly, in meiosis II, the sole event required for cleavage of peri

217 Then, in meiosis II, the two are distributed, one to each future

218 During meiosis II, there was a dramatic re-localization, and th

219 function to inhibit centriole separation at meiosis II, thereby ensuring that the zygote inherits th

220 on from meiosis I to the metaphase arrest at meiosis II; therefore, one function of MAPK during norma

221 CSF) arrests vertebrate eggs in metaphase of meiosis II through several pathways that inhibit activat

222 icted to meiosis I, and Clb3-CDK activity to meiosis II, through 5'UTR-mediated translational control

223 membrane must be coordinated with the end of meiosis II to ensure proper cell division.

224 n plays a role in coupling the completion of meiosis II to gamete formation.

225 s also tightly regulated and is activated in meiosis II to resolve persistent Holliday junctions.

226 ane (PSM) that is synthesized de novo during meiosis II to sequester the dividing nuclei in sporulati

227 Xenopus but is required during the onset of meiosis II to suppress entry into S phase, to regulate t

228 ation of a cluster of genes at the meiosis I-meiosis II transition, including the critical determinan

229 kinase C (PKC) may regulate the meiosis I-to-meiosis II transition.

230 nt in stage VI oocytes and is expressed from meiosis II until gastrulation.

231 Consistent with a role for the MEN during meiosis II, we find that the signaling pathway is active

232 ivision) and sgo1 (shugoshin) mutants during meiosis II when the sister chromatids exhibit random dis

233 grossly normal, a defect becomes apparent in meiosis II when the two component spindles fail to coher

234 Unlike during mitosis and meiosis II, when sister chromatids attach to microtubule

235 mologs) segregate, is followed by equational meiosis II, where sister chromatids separate.

236 levels after the end of meiosis I and before meiosis II, which correlates temporally with changes in

237 vesicle breakdown and arrest at metaphase of meiosis II with a normal bipolar spindle.

238 (Ama1) functions to coordinate the exit from meiosis II with cytokinesis.

239 vertebrate eggs are arrested in metaphase of meiosis II with high cyclin B/Cdc2 activity to prevent p

240 Vertebrate eggs are arrested at metaphase of meiosis II with stable cyclin B and high cyclin B/Cdc2 k

241 s are unable to initiate either meiosis I or meiosis II, yet proceed to execute all subsequent develo