ライフサイエンスコーパス: polar body

1 ortion of the cytoplasm underlying the first polar body.

2 sition of the contractile ring of the second polar body.

3 tivity that precedes extrusion of the second polar body.

4 tic cleavage or produces an abnormally large polar body.

5 ment was biased toward the cortex and future polar body.

6 e disposal of half of the chromosomes into a polar body.

7 ective disposal of half the chromosomes in a polar body.

8 nt to the maternal chromatin and the forming polar body.

9 nd abundant macroH2A is present in the first polar body.

10 favor of C57BL/6 alleles at Om in the second polar body.

11 ose to the animal pole, marked by the second polar body.

12 e was preferentially extruded with the first polar body.

13 2 also remains associated with both extruded polar bodies.

14 ly removed from the oocyte by extrusion into polar bodies.

15 to facilitate extrusion of chromosomes into polar bodies.

16 olution of a sperm cell equivalent to female polar bodies.

17 is that results in a large egg and two small polar bodies.

18 ortex to allow expulsion of chromosomes into polar bodies.

19 al and generate a large oocyte and two small polar bodies.

20 cell stages lack macroH2A except in residual polar bodies.

21 sposal of three haploid chromosome sets into polar bodies.

22 ns, resulting in one large egg and two small polar bodies.

23 GV-stage, and MII-arrested), pronuclei, and polar bodies.

24 o that extra chromosomes can be deposited in polar bodies.

25 thout transitioning to anaphase or producing polar bodies.

26 eral endoderm cells that originated near the polar body (a marker of the blastocyst axis of symmetry)

27 t the contractile ring of the forming second polar body about 1.5 h post-activation.

28 At least one polar body, almost invariably the second, persists intac

29 nhk-1-/- mutant females arrest with aberrant polar bodies and mitotic spindles, revealing that mitosi

30 ads was found in the oocytes with analyzable polar bodies and no FISH errors.

31 The whole genomes of the polar bodies and oocytes are amplified by multiple displ

32 wn of the germinal vesicle, the formation of polar bodies and the formation of the egg pronucleus.

33 That the distribution of degenerating polar bodies and their presumed debris was similar to in

34 ndergo asymmetric cell division to produce a polar body and cleave to form two-cell embryos upon fert

35 observed beyond second cleavage, the second polar body and conceptus could remain coupled ionically

36 1) distribution of chromatids into the first polar body and M-II oocytes.

37 on of meiosis and the emission of the second polar body and precedes the decline in MAP kinase activi

38 sting into the MII stage oocyte, the oocytic polar bodies, and the two-cell embryo, extinction becomi

39 leted the first meiotic division extruding a polar body, and became competent for fertilization by sp

40 intracellular calcium, extrusion of a second polar body, and progression to meiotic stages beyond MII

41 sition with reference to the egg surface and polar bodies are given off at this new site.

42 Polar bodies are not extruded, but remain in the embryo

43 As a result, polar bodies are not produced, pronuclei fail to form, a

44 red, a chitin eggshell is not formed, and no polar bodies are produced.

45 e time course for the emission of the second polar body are significantly delayed/inhibited.

46 cell division in the ovary, exhibit abnormal polar bodies, are detached from the cumulus granulosa ce

47 ding moiety in the jelly coat near the first polar body as it is being given off and also a discrete

48 tion and programmed degradation of the first polar body as new and important roles for the Mos/MAPK p

49 l amount of material either from the animal (polar body-associated) or the vegetal (opposite) pole of

50 somes are expelled into small, nondeveloping polar bodies at anaphase.

51 cells located either near to or opposite the polar body at the 8-cell stage of the mouse embryo retai

52 therefore be related to the position of the polar body at the 8-cell stage, and by implication, to t

53 due to unequal segregation of alleles to the polar body at the second meiotic division.

54 ntry and aster disassembly also required for polar body biogenesis.

55 Polar body biopsy was performed on metaphase II (MII) oo

56 pulsion of the entire meiotic spindle into a polar body by negatively regulating the rho pathway rath

57 myosin II isotypes concentrate in the second polar body cleavage furrow and the sperm incorporation c

58 The chromosomes in the oocyte and first polar body complement each other and provide an internal

59 ond meiotic spindle in relation to the first polar body; consequently, microinjection targeting is im

60 Considering that a polar body contains few mitochondria and shares the same

61 erhaps dynein-driven, is causally related to polar body contractile ring formation, with anaphase ent

62 ed that spatial organization of the putative polar body contractile ring was determined by the periph

63 s were frequently captured by the ingressing polar body contractile ring.

64 Unlike mitotic contractile rings, polar body contractile rings assemble over one spindle p

65 tric cytokinetic events that extrude the two polar bodies during oocyte meiosis, but is dispensable f

66 ndle to detach from the cortex and prevented polar body emission after activation.

67 that Ca(2+) influx is sufficient to support polar body emission and pronucleus formation after only

68 rations had no effect on spindle function or polar body emission.

69 of CaMKIIgamma that are required for second polar body emission.

70 n the egg and in defining the future site of polar body emission.

71 as part of the contractile apparatus during polar body emission.

72 ellular calcium levels interferes with first-polar-body emission in mice and frogs.

73 tion, but the exact role of Ca(2+) in second-polar-body emission remains unknown.

74 e subsequent irreversible progression to the polar body extruded stage.

75 Cdk1-cyclin B1 activity falls at the time of polar body extrusion and after MAP kinase has been inhib

76 sitioning of the meiotic spindle, defects in polar body extrusion and chromosome segregation, and abn

77 se chromosomes with the subsequent events of polar body extrusion and cytokinesis.

78 th a Trk receptor inhibitor suppressed first polar body extrusion and the progression of zygotes into

79 Polar body extrusion during oocyte maturation is critica

80 In the absence of ALADIN, polar body extrusion is compromised due to problems in s

81 homologous chromosomes do not segregate, and polar body extrusion is prevented.

82 Polar body extrusion occurred at the ring center, the di

83 est in meiosis-1; despite cell cycle arrest, polar body extrusion occurred roughly on schedule.

84 ssed exclusively in oocytes to enhance first polar body extrusion of oocytes and to promote the in vi

85 As polar body extrusion progressed, P-Tyr-containing protei

86 nced and the advance to anaphase I and first polar body extrusion takes place without delay.

87 GVBD and polar body extrusion were reduced significantly (P < 0.0

88 reticulum and Lamin, and disappear following polar body extrusion.

89 t before completing MI, marked by failure of polar body extrusion.

90 ndle but still permits spindle migration and polar body extrusion.

91 tor that permitted ring assembly but blocked polar body extrusion.

92 This was independent of actual first polar body extrusion.

93 from starfish oocytes by extrusion into the polar bodies for successful embryo development.

94 n eggs can be fertilized only at the site of polar body formation and first acquire this ability duri

95 Polar body formation is an essential step in forming hap

96 ite where the meiotic apparatus attaches and polar body formation occurs following fertilization.

97 This new site of polar body formation sets up a new animal-vegetal axis t

98 breakdown, disappeared at the time of first polar body formation, and then reappeared as larger clus

99 antibody, alone or coinjected, blocks second polar body formation, in vitro fertilization, or cytokin

100 -4 and EGG-5, we observe defects in meiosis, polar body formation, the block to polyspermy, F-actin d

101 ine the precise role of calcium signaling in polar body formation, we used live-cell imaging coupled

102 and first acquire this ability during second polar body formation.

103 d with local events occurring at the site of polar body formation.

104 culin-B permitted all events except ring and polar body formation.

105 in the ring center, respectively, inhibiting polar body formation.

106 ciated with the egg surface where the second polar body forms, which disappears immediately after fer

107 ous telomere lengths, that human oocytes and polar bodies have nearly identical telomere lengths, and

108 the oocyte cortex ensures extrusion of small polar bodies in the two meiotic divisions, essential for

109 that fusions preferentially segregate to the polar body in laboratory mouse strains when the fusion c

110 time that the contractile ring of the second polar body is constricting.

111 lin B1 kinase activity declines and a second polar body is emitted.

112 ed by female meiosis associate together in a polar body-like structure, while a bipolar spindle is es

113 o the germinal vesicle is the site where the polar bodies normally form.

114 It is concluded that the second polar body normally remains attached to the conceptus th

115 The polar body nuclei do not associate with their normal mon

116 mbryos completed anaphase I but did not form polar bodies or assemble meiosis II spindles.

117 Prior to emission of the first and second polar bodies, PAR-3 is located within a central subdomai

118 down during oocyte maturation did not affect polar body (PB) extrusion.

119 The first polar body (PB) is extruded from the oocyte before ferti

120 f human female meiosis: the first and second polar bodies (PB1 and PB2) and the corresponding oocyte.

121 equencing the triads of the first and second polar bodies (PB1 and PB2) and the oocyte pronuclei from

122 icant pro-M I/M Iarrest and failure of first polar body (PB1) extrusion.

123 g to metaphase I arrest and failure of first polar body (PB1) extrusion.

124 oocytes following nuclear transfer of first polar body (PB1) genomes from metaphase II (MII) oocytes

125 The first polar body (pb1) is extruded when the MPF activity is lo

126 (GVBD) and failure in extrusion of the first polar body (PBE).

127 Moreover, the first polar body persists instead of degrading and sometimes u

128 ing experiments failed to detect movement of polar bodies relative to the surface of the conceptus du

129 an oocytes that give rise to mature eggs and polar bodies remains poorly understood.

130 he fertilized eggs failed to emit the second polar body, resulting in formation of three pronuclei.

131 xpected phenotype of initial ingression of a polar body ring with twice the diameter of wild type.

132 pe revealed a novel mechanism for minimizing polar body size.

133 of F-actin was observed during formation of polar bodies, suggesting the existence of a secondary me

134 ed, while those that originated opposite the polar body tended to become proximal.

135 bditis elegans led to the formation of large polar bodies that contain all maternal DNA, because the

136 Hence, according to the distribution of polar bodies, the axis of bilateral symmetry of the earl

137 -wide SNP genotyping and meiomapping of both polar bodies to identify maternal meiotic errors and kar

138 rodite oogenesis they segregate to the first polar body to yield nullo-X oocytes.

139 Our preclinical model demonstrates polar body transfer has great potential to prevent inher

140 nalysis confirms that the F1 generation from polar body transfer possesses minimal donor mtDNA carryo

141 me genomic material as an oocyte, we perform polar body transfer to prevent the transmission of mtDNA

142 r, pronuclear transfer, and first and second polar body transfer, in mice.

143 genotype remains stable in F2 progeny after polar body transfer.

144 nal spindle transfer, pronuclear transfer or polar body transfer: all involve the transfer of nuclear

145 tion in early blastocysts of these surviving polar bodies was highly non-random.

146 The corresponding polar bodies were also analyzed in 188 of these oocytes.

147 as did the finding that at all stages second polar bodies were attached to conceptuses by a thin, ext

148 d induce cyclin B1 destruction and the first polar body would be extruded.