ライフサイエンスコーパス: meiotic

1 entral spindle push chromosomes apart during meiotic anaphase in oocytes.

2 indle orientation and anchoring at the first meiotic anaphase.

3 transcriptional control of mRNA fate in late meiotic and haploid spermatogenic cells.

4 rate distribution of genetic material during meiotic and mitotic cell divisions.

5 CA2 in promoting homologous recombination in meiotic and mitotic cells.

6 Thus, specific meiotic and mitotic subunits endow septin complexes with

7 y of the genes encoding for well-established meiotic and post-meiotic proteins are already present in

8 egulation for somatic differentiation in pre-meiotic anthers.

9 the male germline causes infertility due to meiotic arrest and impaired inactivation of sex chromoso

10 Fertilization releases the meiotic arrest and initiates the events that prepare the

11 activation by Aly, a component of the testis-meiotic arrest complex, to transcripts for male germ cel

12 orulation, indicating that the processing of meiotic breaks requires both Mre11 and Sae2 nuclease act

13 enpH did not affect spindle organization and meiotic cell cycle progression after germinal vesicle br

14 e transcriptional states through mitotic and meiotic cell cycles.

15 Similar defects in meiotic cell division and reproductive ploidy stability

16 rom the tetraploid primary spermatocytes via meiotic cell division.

17 stem cell proliferation and differentiation, meiotic cell divisions and extreme chromatin condensatio

18 ce cell cycle resumption and transition of a meiotic cell into a mitotic one.

19 e somatic anther tissue is critical for male meiotic cell wall formation and thus plays an important

20 Meiotic cells contain a second chromosomal passenger com

21 Expression in meiotic cells is associated with a strong decrease in re

22 esions that can disrupt genome integrity, so meiotic cells regulate their number, timing, and distrib

23 beta-TrCP-deficient spermatogonia increased meiotic cells with a concomitant reduction of apoptosis.

24 n mammals, surveillance mechanisms eliminate meiotic cells with defective synapsis, thereby minimizin

25 the level of 8-oxo-guanine in the nucleus of meiotic cells, reflecting oxidative stress and affecting

26 n, chromosome segregation and cytokinesis in meiotic cells.

27 est that CLS-2-dependent microtubules of the meiotic central spindle, located between the segregating

28 Here, we aimed to correlate meiotic centromere dynamics and early telomere behaviour

29 esses preceding L1 integration in triggering meiotic checkpoints and germ-cell death.

30 y programming of the oocyte epigenome primes meiotic chromatin for subsequent functions in late proph

31 e-specific gene expression programs and post-meiotic chromatin reorganization.

32 ic chromosomes, it seems to diffuse out once meiotic chromosomal condensation is completed.

33 ic chromosomes, it seems to diffuse out once meiotic chromosomal condensation is completed.

34 Thus, meiotic chromosome axes are hubs for regulated proteolys

35 Meiotic chromosome axes form a platform for the assembly

36 we investigate the molecular organization of meiotic chromosome axes in Caenorhabditis elegans throug

37 se the proteins that are associated with the meiotic chromosome axis protein, ASY1, in Brassica olera

38 This pattern parallels enrichment for the meiotic chromosome axis proteins Hop1 and Red1.

39 elationship between crossover patterning and meiotic chromosome behavior.

40 Initially, homolog alignment is promoted by meiotic chromosome movements feeding into intimate homol

41 el genes important at distinct stages of the meiotic chromosome segregation and differentiation progr

42 332 and the two forms of PP2A by quantifying meiotic chromosome segregation defects in double or trip

43 crossover designation, and ensuring accurate meiotic chromosome segregation.

44 e(s) responsible for force generation during meiotic chromosome separation in oocytes is unclear.

45 etween non-B form DNA structures and Hop1 in meiotic chromosome synapsis and recombination.

46 We postulate that some meiotic chromosome-regulatory functions contribute to a

47 enable long-range signal transduction along meiotic chromosomes and underlie the rapid evolution of

48 We conclude that proteasome functions along meiotic chromosomes are evolutionarily conserved.

49 A key protein involved in the segregation of meiotic chromosomes is produced 'just in time' by the re

50 poisomerase II is not the major component of meiotic chromosomes, even though mitosis and meiosis sha

51 compromises its TRIP13-mediated removal from meiotic chromosomes, highlighting a conserved mechanism

52 vealed that it is not the major component of meiotic chromosomes, it seems to diffuse out once meioti

53 ed for individualization and condensation of meiotic chromosomes, it seems to diffuse out once meioti

54 Meiotic clade AAA ATPases (ATPases associated with diver

55 Meiotic clade AAA ATPases function as hexamers that can

56 data further suggest that the two different meiotic cohesin complexes are distinctly arranged within

57 ssociation of PRDM9-bound complexes with the meiotic cohesin REC8 and the synaptonemal complex protei

58 eletion of the upregulated gene encoding the meiotic cohesin Rec8 or the cyclin Crs1 suppresses UPD i

59 hesin binding and suppresses ctf7-associated meiotic cohesion defects, demonstrating that WAPL and CT

60 , a germ cell-specific gene activated during meiotic commitment.

61 Meiotic completion promotes GNU dephosphorylation and PN

62 een the sets of segregating chromosomes, the meiotic contractile ring forms on the cortex adjacent to

63 We show here that meiotic crossover patterning is lost in Drosophila melan

64 small chromosome 4, which normally never has meiotic crossovers [3].

65 work has identified three pathways limiting meiotic crossovers in Arabidopsis thaliana that rely on

66 Collectively, our results suggest that meiotic crossovers in potato are largely determined by t

67 Meiotic crossovers shuffle parental genetic information,

68 The vast majority (81%) of meiotic crossovers were mapped to less than 5 kb.

69 e genomic and epigenomic features underlying meiotic crossovers.

70 gai-t6 mutant revealed that defects in male meiotic cytokinesis are not caused by alterations in mei

71 We found that INP1 assembly occurs after meiotic cytokinesis at the interface between the plasma

72 GA specifically affects the process of male meiotic cytokinesis leading to meiotic restitution and t

73 red for functional RMA biosynthesis and male meiotic cytokinesis.

74 of reverse transcription did not rescue the meiotic defect.

75 omplex formation, elevation of Cyclin B, and meiotic defects consistent with premature PNG activation

76 This mutation may provoke meiotic defects leading to a depleted follicular stock,

77 But the meiotic defects when Dam1 is not phosphorylated are not

78 he microtubules, in response to a variety of meiotic defects, demonstrating that errors can be detect

79 germ cells exhibit excessive DNA damage and meiotic defects.

80 x/cyclosome that regulates multiple steps in meiotic development, including exit from MII.

81 periods of time in the prophase of the first meiotic division (prophase I).

82 prometaphase I but recovers after the first meiotic division and persists, uniquely for metaphase, i

83 e-copy genome into gametes during the second meiotic division is coordinated by a conserved casein ki

84 rate chromosome segregation during the first meiotic division relies on the formation of crossovers b

85 At the first meiotic division, anaphase-promoting complex/cyclosome a

86 on from prophase into metaphase of the first meiotic division, resulting in male infertility.

87 accurate chromosome segregation at the first meiotic division.

88 accurate chromosome segregation at the first meiotic division.

89 facilitate homolog segregation at the first meiotic division.

90 ivial because in both mice and humans oocyte meiotic divisions are prone to chromosome segregation er

91 Genome haploidization involves two meiotic divisions following a single round of DNA replic

92 Live imaging of meiotic divisions in condensin-depleted cells showed rep

93 ion involves genome duplication prior to the meiotic divisions.

94 When programmed meiotic DNA double-strand breaks (DSBs) undergo recombin

95 LinE proteins also promote the formation of meiotic DNA double-strand breaks (DSBs), the precursors

96 ing prophase I exit to repair any persisting meiotic DNA double-strand breaks.

97 In females, meiotic DNA replication and recombination occur in fetal

98 restored by inhibiting cep-1/p53, endogenous meiotic double strand breaks, or the expression of MIRAG

99 wild populations are derived from programmed meiotic double strand breaks, which precede chromosomal

100 s, reflecting oxidative stress and affecting meiotic double-strand break repair, chromosome synapsis

101 gous recombination (HR) repair of programmed meiotic double-strand breaks (DSBs) requires endonucleol

102 ome axes in promoting interhomolog repair of meiotic double-strand breaks by inhibiting intersister r

103 aracteristic of a bias in the frequencies of meiotic double-strand DNA breaks at the hotspot near the

104 the wtf multigene family proliferated due to meiotic drive and highlights the power of selfish genes

105 ges, e.g., competition among sperm/pollen or meiotic drive during gamete/spore production.

106 Here, we demonstrate a complex landscape of meiotic drive genes on chromosome 3 of the fission yeast

107 parasites on evolution and infertility, few meiotic drive loci have been identified or mechanistical

108 ggest nonrandom union of gametes rather than meiotic drive or preferential lethality.

109 ion typically occurs among sperm/pollen, and meiotic drive typically occurs during either spermatogen

110 ecific degradation of PRDM9 binding sites by meiotic drive, which steadily increases asymmetric PRDM9

111 evolution to include gametic competition and meiotic drive.

112 heir transmission through a process known as meiotic drive.

113 the suppression of transposable elements or meiotic drive.

114 Meiotic drivers are selfish genes that bias their transm

115 Thus, selfish meiotic drivers exploit the asymmetry inherent in female

116 nd the related SCs of other species regulate meiotic DSB formation to form crossovers crucial for mei

117 n the genome coined "hot spots." In mammals, meiotic DSB site selection is directed in part by sequen

118 m synapsed chromosomes, suggesting that many meiotic DSBs are normally repaired by intersister recomb

119 Since the meiotic error rate increases almost exponentially after

120 ng of both polar bodies to identify maternal meiotic errors and karyomapping to fingerprint the paren

121 genomically imbalanced, often as a result of meiotic errors inherited in the oocyte, these aneuploidi

122 m, kinetochores could be involved in sensing meiotic errors using an unconventional mechanism that do

123 These findings link meiotic exit to Smk1 activation and spore wall assembly.

124 ccurs over a wide range of abundances during meiotic exit.

125 rowth/proliferation is overly simplistic, as meiotic factors are not a feature of most embryonic tiss

126 ogenesis, and we extend this to propose that meiotic factors could be powerful sources of targets for

127 after their prolonged arrest is crucial for meiotic fidelity and subsequent development.

128 s reveal a novel role of CenpH in regulating meiotic G2/M transition by acting via the APC/C(Cdh1)-cy

129 How the meiotic gene expression program temporally restricts kin

130 Hence, Snf2 exerts systems level control of meiotic gene expression through two temporally distinct

131 modeler Swi/Snf in regulation of splicing of meiotic genes and find that the complex affects meiotic

132 nation machinery promotes island assembly at meiotic genes.

133 Autoimmune responses to meiotic germ cell antigens (MGCA) that are expressed on

134 erentiation into late primordial germ cells, meiotic germ cells and ovarian follicles.

135 with recombinant human GDF9 and BMP15, these meiotic germ cells are further induced to form ovarian F

136 ch haploid cells normally arise only as post-meiotic germ cells that serve to ensure a diploid genome

137 criptomic profile and expressed several post-meiotic germ line related markers, showed meiotic progre

138 e AAA+ ATPase TRIP13 regulates both MAD2 and meiotic HORMADs by disassembling these HORMA domain-clos

139 dle assembly checkpoint protein MAD2 and the meiotic HORMADs, assemble into signaling complexes by bi

140 However, other chromatin features needed for meiotic hot spot specification are largely unknown.

141 onical sex chromosome dosage compensation or meiotic inactivation.

142 SC destruction relieved meiotic inhibition of the ubiquitous recombinase Rad51,

143 l proximity: spermatogonial differentiation, meiotic initiation, initiation of spermatid elongation,

144 nsitions, spermatogonial differentiation and meiotic initiation, were known to be coregulated by an e

145 r multiple centromere associations formed in meiotic interphase undergo a progressive polarization (c

146 Using meiotic mapping, we localized the fro locus to the previ

147 clin A2 and failing to properly express many meiotic markers.

148 id status and the expression of several post-meiotic markers.

149 and their male germ cells exhibit defects in meiotic maturation and sperm production.

150 ed physiological process during mouse oocyte meiotic maturation whose underlying mechanism is the tra

151 e transport into oocytes was detected during meiotic maturation.

152 s cell cycle progression during mouse oocyte meiotic maturation.

153 n and functions of Kif2a during mouse oocyte meiotic maturation.

154 but CHDH became highly active during oocyte meiotic maturation.

155 2, specifically interacts with the conserved meiotic Mer3 helicase, which recruits it to recombinatio

156 ome condensation defect was most striking at meiotic metaphase, when Tetrahymena chromosomes are norm

157 plate, is responsible for G2/M transition in meiotic mouse oocytes.

158 of Enhancer of rudimentary, is implicated in meiotic mRNA elimination during vegetative growth, but i

159 Maize meiotic mutants and minichromosomes were used to study t

160 in vivo analysis of recombination-defective meiotic mutants.

161 peats (LCRs) might predispose chromosomes to meiotic non-allelic homologous recombination (NAHR) even

162 ation and programmed reduction of H3K9me2 at meiotic onset, the transgene showed 1,400-fold increase

163 otic proteins are already present in the pre-meiotic phase.

164 ding of many still mysterious aspects of the meiotic process and help to explain the evolutionary bas

165 Later still, modifications to meiotic processes occurred within different groups of eu

166 complex (SC) and play central roles in other meiotic processes, including homologous pairing, recombi

167 ble state that ensures the repression of the meiotic program by Mmi1.

168 l, and intra-gametogenesis variations in the meiotic program, A. rhodensis is an ideal model for stud

169 tes Mmi1, thereby allowing expression of the meiotic program.

170 onary basis of functional adaptations to the meiotic program.

171 ermore, P4-PGRMC1 interaction blocked oocyte meiotic progression and decreased intra-oocyte cyclic AM

172 ate that mTORC1 has an essential role in the meiotic progression and silencing of sex chromosomes in

173 suggest that spindle size and the timing of meiotic progression are governed by cytoplasmic componen

174 Meiotic progression depends on tight physical and functi

175 Meiotic progression in mammalian preovulatory follicles

176 st-meiotic germ line related markers, showed meiotic progression, evidence of epigenetic reprogrammin

177 localization of pro-crossover factors during meiotic progression, revealing how the SC might act as a

178 led to male infertility because of aberrant meiotic progression.

179 chromosome architecture required for correct meiotic progression.

180 Control of protein turnover is critical for meiotic progression.

181 rmatogonia to stop mitosis and transition to meiotic prophase and the spermatocyte state.

182 h gap junctions into the oocyte, maintaining meiotic prophase arrest.

183 ossing over between homologs is initiated in meiotic prophase by the formation of DNA double-strand b

184 Rec8 is a prominent component of the meiotic prophase chromosome axis that mediates sister ch

185 us macromolecular assembly that forms during meiotic prophase I and mediates adhesion of paired homol

186 ocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during whic

187 In meiotic prophase I, homologous chromosome pairing is pro

188 ssed in spermatocytes at the early stages of meiotic prophase I, the limited period when PRDM9 is exp

189 mainly located at the pericentromere during meiotic prophase II but is restricted to the inner centr

190 teasome systems regulate the major events of meiotic prophase in mouse.

191 During meiotic prophase in Saccharomyces cerevisiae, expression

192 o demonstration that oxidative stress during meiotic prophase induces chromosome segregation errors a

193 Sa15 forms linear structures in meiotic prophase nuclei to which Zhp3 localizes.

194 approximately 300 genes coordinately during meiotic prophase, but different mRNAs within the NDT80 r

195 During Schizosaccharomyces pombe meiotic prophase, homologous chromosomes are co-aligned

196 Instead of continuing through meiotic prophase, the cells attempt an abnormal mitotic-

197 increase of retrotransposition in the early meiotic prophase.

198 oscillations of the horsetail nucleus during meiotic prophase.

199 quence, NDC80 expression is repressed during meiotic prophase.

200 L-1 controls chromosome structure throughout meiotic prophase.

201 vel with specific organizational features of meiotic-prophase chromosomes.

202 role for the p53-like protein CEP-1 and the meiotic protein HIM-5 in maintaining genome stability in

203 itor maintenance by repressing production of meiotic proteins and use distinct mechanisms to repress

204 coding for well-established meiotic and post-meiotic proteins are already present in the pre-meiotic

205 physical and functional interactions between meiotic proteins is also limited.

206 le strategy for revealing previously unknown meiotic proteins, and we show how the PPI network can be

207 (PPI) network containing known and candidate meiotic proteins, including proteins more usually associ

208 inversions predispose chromosome 22q11.2 to meiotic rearrangements and increase the individual risk

209 instability is a failure to up-regulate the meiotic recombination 11 (Mre11) nuclease in S phase, wh

210 Meiotic recombination 11 homolog (MRE11) is downregulate

211 e very useful insights into the mechanism of meiotic recombination and the process of genome evolutio

212 eview, we focus on advances in understanding meiotic recombination and then summarize the attempts to

213 Gene conversions resulting from meiotic recombination are critical in shaping genome div

214 ed double-strand breaks (DSBs) that initiate meiotic recombination are dangerous lesions that can dis

215 DNA double-strand breaks that initiate meiotic recombination are exonucleolytically processed.

216 Rates of meiotic recombination are widely variable both within an

217 this end, we report the local stimulation of meiotic recombination at a number of chromosomal sites b

218 hat such rearrangement-mediated reduction of meiotic recombination can lead to genetically isolated h

219 9 (PRDM9) protein is a major determinant of meiotic recombination hot spots and acts through sequenc

220 s for histone acetylation marks at mammalian meiotic recombination hot spots.

221 fic KRAB-ZFPs, including genomic imprinting, meiotic recombination hotspot choice, and placental grow

222 Last, we pay special attention to the meiotic recombination in polyploidy, which is a common g

223 e genomic region, we found that interhomolog meiotic recombination in the array is reduced compared t

224 Meiotic recombination initiates following the formation

225 Meiotic recombination is a major driver of genetic diver

226 Meiotic recombination is an essential feature of sexual

227 pecies have revealed two mechanisms by which meiotic recombination is directed to the genome-through

228 Meiotic recombination is initiated by programmed double

229 Meiotic recombination is the foundation for genetic vari

230 In mammals, meiotic recombination occurs at 1- to 2-kb genomic regio

231 omes, that is, heterozygosity, can influence meiotic recombination pathways in cis and trans.

232 chromatin, increased gene density, elevated meiotic recombination rates and in the proximity of repe

233 Meiotic recombination shapes the genetic diversity trans

234 PRDM9 binding localizes almost all meiotic recombination sites in humans and mice.

235 ce motifs that predict consistent, localized meiotic recombination suppression around a subset of PRD

236 During meiotic recombination, a subset of programmed DNA double

237 rring in the p53(-) germline were incited by meiotic recombination, and transcripts produced from the

238 rge-scale variation in GC-content, caused by meiotic recombination, via the non-adaptive process of G

239 an integral part of a new regulatory step of meiotic recombination, which has implications to prevent

240 itability and genome stability are shaped by meiotic recombination, which is initiated via hundreds o

241 fied by successive megachunk integration and meiotic recombination-mediated assembly, producing a fun

242 hromosomes in pachytene cells, which undergo meiotic recombination.

243 much progress has been made in understanding meiotic recombination.

244 subtelomeric regions, it locally influences meiotic recombination.

245 known homeostatic mechanisms that act during meiotic recombination.

246 ures governing successive steps in mammalian meiotic recombination.

247 nd annealing, break-induced replication, and meiotic recombination.

248 other axis-associated protein with a role in meiotic recombination.

249 en found to link changes in SC dynamics with meiotic recombination.

250 romeric regions that are virtually devoid of meiotic recombination.

251 Thus, the poised state that allows rapid meiotic reentry in mouse GV oocytes may be determined by

252 protein level undergo minimal changes during meiotic reentry.

253 dings reveal an important connection between meiotic replication fork stability and chromosome segreg

254 ion or eviction as a defining feature of the meiotic resection landscape.

255 ocess of male meiotic cytokinesis leading to meiotic restitution and the production of diploid (2n) p

256 Meiotic resumption (G2/M transition) and progression thr

257 Restoring meiotic translation rescues the meiotic resumption defect of Cdh1-depleted oocytes.

258 The mechanism underlying meiotic resumption remains largely elusive.

259 xes were completely absent in oocytes during meiotic resumption, homologous chromosomes failed to seg

260 volved in specific meiotic stages, including meiotic resumption, spindle assembly, and spindle positi

261 r (MPF) activation, and severely compromised meiotic resumption.

262 ction in meiosis in that it is essential for meiotic resumption.

263 cGMP diffusion out of the oocyte, initiating meiotic resumption.

264 The results demonstrate that one meiotic role of Mps1 is to stabilize connections that ha

265 rate of Mps1, was necessary for its critical meiotic role.

266 nserved kinase, Mps1, result in catastrophic meiotic segregation errors but mild mitotic defects.

267 ous chromosomes is required for the faithful meiotic segregation of chromosomes and leads to the gene

268 Here we show that meiotic segregation of X chromosomes in the trioecious n

269 fic may allow functional compensation during meiotic sex chromosome activation.

270 [6-8] and a compensatory mechanism based on meiotic sex chromosome inactivation (MSCI) [6, 8-11].

271 romosome dosage compensation in the soma and meiotic sex chromosome inactivation in the germline.

272 -characterized example of meiotic silencing, meiotic sex chromosome inactivation, we reveal this AAD-

273 dy identifies TOPBP1 as a critical factor in meiotic sex chromosome silencing.

274 However, which partner facilitates the meiotic silencing properties of ATR is unknown.

275 ocusing on the best-characterized example of meiotic silencing, meiotic sex chromosome inactivation,

276 One such surveillance mechanism is meiotic silencing, the inactivation of genes located on

277 and CTF7 function as antagonists to regulate meiotic sister chromatid cohesion.

278 In contrast to somatic cells, the first meiotic spindle assembles in the absence of centriole-co

279 Accurate meiotic spindle assembly and chromosome segregation - es

280 that CSNK-1 prevents expulsion of the entire meiotic spindle into a polar body by negatively regulati

281 n at the opposite end of the embryo from the meiotic spindle while yolk granules are transported thro

282 esulting in sperm DNA within 2 microm of the meiotic spindle.

283 ents the sperm DNA from interacting with the meiotic spindle.

284 ical F-actin to prevent interaction with the meiotic spindle.

285 ted irregularities of the zona pellucida and meiotic spindle.

286 d oocytes supported the formation of de novo meiotic spindles and, after fertilization with sperm, me

287 demonstrating that it is a key regulator of meiotic splicing in S. cerevisiae.

288 otic genes and find that the complex affects meiotic splicing in two ways.

289 These programs include the initiation of meiotic sporulation, the formation of filamentous growth

290 at Rpl10l plays an essential role during the meiotic stage of spermatogenesis by compensating for MSC

291 ow that this protein is involved in specific meiotic stages, including meiotic resumption, spindle as

292 Meiotic synapsis and recombination between homologs perm

293 RingoA as an important activator of Cdk2 at meiotic telomeres, and provide genetic evidence for a ph

294 brane-trafficking system and a near-complete meiotic toolkit, possibly indicating a sexual cycle.

295 ase, results in the temporal deregulation of meiotic transcription and affects female fertility.

296 categories reflect differences in levels of meiotic transcription, which is linked to variation in r

297 ssociates with Mmi1, promotes suppression of meiotic transcripts expression in mitotic cells.

298 accharomyces cerevisiae, such as splicing of meiotic transcripts.

299 Restoring meiotic translation rescues the meiotic resumption defec

300 nding protein Rim4 are general regulators of meiotic translational delay, but how differential timing