ライフサイエンスコーパス: micromere

1 ghter of the four m(1) micromeres (the m(12) micromeres).

2 n of the comb rows (the e(1), e(2), and m(1) micromeres).

3 icromere) to observe the progeny of a single micromere.

4 the micromeres--the precursors of the small micromeres.

5 ated in the 3D cell but not in the overlying micromeres.

6 ression of two inductive signals produced by micromeres.

7 nd early blastula stages, and exclusively in micromeres.

8 ted by removal of two opposing first quartet micromeres.

9 cation in the absence of induction-competent micromeres.

10 r are necessary for activation of foxN2/3 in micromeres.

11 rough the formation of the fourth quartet of micromeres.

12 ng formation of each of the four quartets of micromeres.

13 ment is normally restricted to the 1a and 1c micromeres.

14 d natural fate maps for the first quartet of micromeres.

15 te in the lineage descendant from the embryo micromeres.

16 ised of eight cells-four macromeres and four micromeres.

17 the production of gametes, termed the small micromeres.

18 volving the derivatives of the first quartet micromeres.

19 a signaling also activates foxY in the small micromeres.

20 eractions, presumably from the first quartet micromeres.

21 ion signals, neither of which is required in micromeres.

22 The first quartet micromeres (1a, 1b, 1c and 1d) contribute to the head of

23 er spiralians studied to date (first-quartet micromeres: 1a, 1c).

24 different lineal precursors (second-quartet micromeres: 2a, 2c) compared to those in all other spira

25 Here we show that D quadrant micromeres (2d and 4d) of the oligochaete annelid Tubife

26 of the bilateral daughters (M teloblasts) of micromere 4d in the leech Helobdella sp. Austin, a clite

27 rochozoan species arises from the progeny of micromere 4d, which is assumed to be homologous with a s

28 ivisions and the definitive fate maps of the micromeres, a group of 25 small cells that arise during

29 The reduction in small micromere ABC transporter activity is mediated by a puls

30 Unexpectedly, we found small micromeres accumulate 2.32 times more of the ABC transpo

31 In the sea urchin embryo, the micromeres act as a vegetal signaling center.

32 ss homeodomain transcription factor which in micromeres acts as a repressor of a repressor: the gene

33 When such beta-catenin-blocked micromeres also express Pmar1, all observed micromere fu

34 t, in addition to e1 micromeres, the four m1 micromeres also make significant contributions to the ct

35 a (Cc-hb) is expressed maternally and in all micromere and macromere cells throughout cleavage.

36 latory region, which initiates expression in micromere and macromere descendant cells early in cleava

37 dent of the earlier expression of foxN2/3 in micromeres and is independent of signals from PMCs.

38 drant via cell-cell interactions between the micromeres and macromeres at the 24- to 36-cell stage.

39 ere derived from the transplanted D quadrant micromeres and not from the host embryo.

40 e gate (DNG), the subcircuit which specifies micromeres and skeletogenic cells in Strongylocentrotus

41 equires an inductive interaction between the micromeres and the D macromere.

42 between the derivatives of the first quartet micromeres and the vegetal macromeres specify which macr

43 Micromeres and their immediate descendants have three kn

44 In the sea urchin embryo, the large micromeres and their progeny function as a critical sign

45 controlled downregulation of SoxB1, first in micromeres and then in macromere progeny.

46 e blimp1/krox gene is expressed in the large micromeres and veg2 descendents.

47 teus, contacts between the progeny of animal micromeres and vegetal macromeres are established during

48 el whereby beta-catenin enters the nuclei of micromeres and, as a consequence, the micromeres produce

49 ell stage there are four macromeres and four micromeres, and each of these cells is uniquely identifi

50 ivatives of the second and third quartets of micromeres, and endomesoderm, which is formed from the f

51 in the early blastula only in the four small micromeres, and later only expressed in that coelomic po

52 accumulates selectively in the 16-cell stage micromeres, and then is restricted to the small micromer

53 r the localization of delta transcription in micromeres, and thereby for the conditional specificatio

54 essor: the gene is named pmar1 (paired-class micromere anti-repressor).

55 ning in the first interphase after the large micromeres are born.

56 Subsequently, micromeres are formed first at the aboral pole and later

57 It is initially activated as soon as the micromeres are formed, in response to Otx and beta-Caten

58 As is the early NSM, the small micromeres are in direct contact with Delta expressing s

59 the 2-cell stage, and later the 2 unlabeled micromeres are removed at the 16-cell stage, the remaini

60 If micromeres are removed from hosts at the fourth cleavage

61 Indeed, we find that embryos in which micromeres are removed respond by significant up-regulat

62 To test the proposition that the small micromeres are the definitive primordial germ cell linea

63 micromeres, the parent blastomeres of small micromeres, are deleted.

64 extended to include second and third quartet micromeres as well as the mesentoblast cell (4d) and som

65 The gut is formed by all the fourth quartet micromeres as well as the vegetal macromeres (4A, 4B, 4C

66 ormed both transplantations and deletions of micromeres at the 16-cell stage and demonstrated that th

67 ows are derived exclusively from the four e1 micromeres at the 16-cell stage.

68 Removal of the first quartet micromeres at the 8-cell stage also leads to the develop

69 lacteus by removing specific combinations of micromeres at the eight-cell stage.

70 Here, we have deleted small micromeres at the fifth division and have raised the res

71 Expression of foxN2/3 mRNA begins in micromeres at the hatched blastula stage and then is los

72 hatched blastula stage and then is lost from micromeres at the mesenchyme blastula stage.

73 lanted to the animal pole and the absence of micromeres at the vegetal pole results in the failure of

74 t fourth cleavage of sea urchin embryos four micromeres at the vegetal pole separate from four macrom

75 irst, in Helobdella sp. (Galt), the clone of micromere b" does not normally die, and contributes a su

76 (2) The clones of micromeres b" and b"' (2b and 3b in traditional nomencla

77 At the fourth cleavage, micromeres bearing altered pmar1 activity were combined

78 as identified and found to be transcribed in micromeres beginning at the fourth cleavage of sea urchi

79 s rescued if they later receive transplanted micromeres between the eighth and tenth cleavage.

80 All muscle cells are derived from micromeres born at the oral pole of endomesodermal precu

81 n be rescued to assume the normal c" fate if micromere c" or its clone are ablated in early developme

82 Second, in Helobdella sp. (Galt), micromere c"' makes no definitive contribution, whereas

83 ith respect to the embryonic midline and the micromere cap, epiboly fails, and the HRO-NOS knockdown

84 t significance of extrinsic signals from the micromere cell lineages.

85 s were constructed consisting of two labeled micromeres combined with micromereless 4th cleavage host

86 All four of these micromeres contribute to the apical organ and generate f

87 h as the coelomic pouches to which the small micromeres contribute.

88 purpuratus, both in the intact embryo and in micromere cultures.

89 some primary mesenchyme-specific proteins in micromere cultures; withholding serum severely depresses

90 ed gonads and visible gametes, whereas small micromere-deleted animals formed small gonads that lacke

91 Quantitative PCR results indicate that small micromere-deleted animals produce background levels of g

92 Adults from control and micromere-deleted embryos developed gonads and visible g

93 egulatory network was not activated in small micromere-deleted embryos.

94 not overexpress Vasa, as did embryos from a micromere deletion, implying the compensatory gene regul

95 Thus, e1 micromere derivatives not only generate comb plates but

96 a-catenin in vegetal nuclei does not require micromere-derived cues.

97 We show that the micromere-derived signal is necessary for the downregula

98 that animal cells are less responsive to the micromere-derived signal than vegetal cells.

99 tenin also plays a role in the production of micromere-derived signals.

100 all vegetal cell fates and the production of micromere-derived signals.

101 endodermal and mesodermal tissues including micromere-derived skeletogenic mesenchyme.

102 n, nuclear Cc-hb protein is expressed in the micromere-derived surface epithelium that undergoes epib

103 mesenchyme cells (PMCs and SMCs), and small micromere descendants (SMDs) of the sea urchin Lytechinu

104 a link between the induction of mesoderm by micromere descendants and the Notch signaling pathway.

105 LvDelta is expressed by micromere descendants during the blastula stage, a time

106 In this study, we demonstrate that these micromere descendants express LvDelta, a ligand for the

107 Spdri is shown to act in the micromere descendants in the pathways that result in the

108 ments, we show that expression of LvDelta by micromere descendants is both necessary and sufficient f

109 Signals from micromere descendants play a critical role in patterning

110 a late signaling function on the part of the micromere descendants that is needed to complete clearan

111 scription factors normally expressed only in micromere descendants, and also a set of downstream skel

112 ion gene batteries normally function only in micromere descendants.

113 d Sp-SoxE transcripts are localized in small micromere descendents at the tip of the archenteron duri

114 germ line determinants selectively in small micromere descendents supports the hypothesis that these

115 ratus, Vasa protein is enriched in the small micromeres despite a uniform distribution of vasa transc

116 n-D lineages, cleavage plane positioning and micromere division rates are relatively insensitive to c

117 "' makes no definitive contribution, whereas micromere dm' gives rise to cells equivalent to those ar

118 The PMC progeny of a single micromere do not disperse upon ingression, but instead r

119 No ectomesoderm is formed; the first three micromere duets generate only ectodermal derivatives.

120 exhibit abnormalities in the distribution of micromeres during cleavage.

121 activated MAPK is not required in the animal micromeres during subsequent stages of development.

122 ic lineages, both daughters of the four e(1) micromeres (e(11) and e(12)) and a single daughter of th

123 germline specification depends on the small micromeres, either directly as lineage products, or indi

124 Micromeres expressing Golgi-tethered GFP (galtase-GFP) w

125 Signaling-competent micromeres fail to induce SMCs if macromeres express dom

126 In addition, nuclear beta-catenin-deficient micromeres failed to induce a secondary axis when transp

127 (3) Two qualitative differences in micromere fates are seen between H. robusta (Sacramento)

128 imeras demonstrate that Snail is required in micromeres for PMC ingression.

129 y reported astral spreading during embryonic micromere formation suggests that related mechanisms are

130 In sea urchin embryos, small micromeres formed at the fifth division appear to be suc

131 us studies showed that ectopically implanted micromeres from the 16-cell embryo can induce ectopic gu

132 from this work shows how the specificity of micromere function depends on continuing global regulato

133 micromeres also express Pmar1, all observed micromere functions are rescued.

134 The third quartet micromeres generate clones situated in a bilaterally sym

135 Two of the micromeres generate the somatic mesoderm, a third microm

136 meres generate the somatic mesoderm, a third micromere generates the endoderm and the fourth micromer

137 romere generates the endoderm and the fourth micromere generates the germline.

138 Third quartet micromeres give rise to large areas of the foot, velum,

139 for the selective RNA retention in the small micromeres; GNARLE is required but not sufficient for th

140 This reveals the specific linkages of the micromere GRN forged in the evolutionary process by whic

141 An abrupt "break point" in the micromere GRN is thus revealed, on one side of which mos

142 era toxin B uptake experiments indicate that micromeres have higher rates of bulk and raft-associated

143 Thus, the Tubifex D quadrant micromeres have the ability to organize axis formation,

144 The micromeres have the capacity to induce a second axis if

145 This suggests that micromeres have the capacity to induce SMCs.

146 eriments suggest that only the first quartet micromeres have this ability.

147 ntly in 4d and finally in a subset of animal micromeres immediately following those stages.

148 o selective reporter enrichment in the small micromeres in blastulae.

149 pical organ, which arises from the 1c and 1d micromeres in C. apiculata.

150 Unlike most spiralians, the first quartet micromeres in the eight-celled embryo are larger than th

151 The role of animal first quartet micromeres in the establishment of the dorsal (D) cell q

152 We propose that the micromeres induce adjacent cells to form SMCs, possibly

153 Between the eighth and tenth cleavage micromeres induce SMCs through Notch.

154 The micromeres induce SMCs, most likely through direct conta

155 The macromere progeny receive the micromere induction signal through the Notch receptor.

156 tch pathway becomes competent to receive the micromere induction signal, and to transduce that signal

157 omere progeny to be competent to receive the micromere induction signal, beta-catenin must enter macr

158 for these cells to receive and transduce the micromere induction signal.

159 ation pathway, and upstream of two important micromere induction signals.

160 In order to be receptive to the micromere inductive signal the macromeres first must tra

161 elopment in ctenophores and indicate that e1 micromeres influence the development of adjacent cell li

162 However, the eye-forming ability of the 1d micromere is not influenced by its close position to the

163 By contrast, when a transplanted micromere is placed at the vegetal plate after removing

164 If a labeled micromere is placed ectopically at the macromere/mesomer

165 MAPK function in the Ilyanassa micromeres is a recent cooption and, since the divergenc

166 hough vasa protein accumulation in the small micromeres is fixed, accumulation in other cells of the

167 ctivated in the progeny of the first quartet micromeres, just prior to the birth of the third quartet

168 functionally required in 3D and also in the micromeres known to require a signal from 3D.

169 Small micromeres lacking Sp-nanos1 and Sp-nanos2 undergo an ex

170 ectoderm, where the progeny of the 1a and 1d micromeres lie to the left of the median plane while tho

171 These control the specification of the micromere lineage and of the initial veg(2) endomesoderm

172 expressed exclusively by cells of the large micromere lineage beginning in the first interphase afte

173 trotus purpuratus is restricted to the large micromere lineage by a double negative regulatory gate.

174 ll observable developmental functions of the micromere lineage during the specification period.

175 f gene expression unique to the skeletogenic micromere lineage is set in train by activation of the p

176 nchyme cells of the embryo, beginning in the micromere lineage of the early blastula stage and contin

177 irects the specification of the skeletogenic micromere lineage of the sea urchin embryo.

178 and maintenance of multipotency in the small micromere lineage requires nanos, which may function in

179 generate a precociously specified embryonic micromere lineage that ingresses before gastrulation and

180 expressed with different timing in the small micromere lineage.

181 were caused to be activated in the embryonic micromere lineage.

182 rly by translational regulation to the small micromere lineage.

183 through the Notch receptor from the vegetal micromere lineages diverts adjacent mesendoderm to secon

184 ction cascade that is initiated by the large micromeres located at the vegetal pole.

185 In general, second quartet micromeres make major contributions to the shell-forming

186 The 1b micromere may not develop an eye during normal developme

187 Specification of sea urchin embryo micromeres occurs early in cleavage, with the establishm

188 erm, which is formed from the fourth quartet micromere of the D quadrant (4d).

189 The first-quartet micromere of the dorsal D lineage (1d) is smaller than t

190 ntral nervous system is mainly formed by the micromeres of the 1st and 2nd quartet, of which 1a, 1c,

191 mesoderm in C. fornicata is mainly formed by micromeres of the 3rd quartet (principally 3a and 3b), w

192 tropod Ilyanassa obsoleta, the first-quartet micromeres of the A, B and C lineages (1a, 1b, and 1c) a

193 The four small micromeres of the sea urchin embryo contribute only to t

194 signaling in macromeres and does not require micromere or veg2-inductive signals.

195 reless 4th cleavage host embryos; either the micromeres or the hosts contained alphaSpdri MASO.

196 ignaling mechanisms emanating from the small micromeres or their descendants.

197 We demonstrate that the micromeres play an important role in the induction of se

198 ion studies position Snail in the sea urchin micromere-PMC gene regulatory network (GRN), downstream

199 s reveal that, although most features of the micromere-PMC GRN are recapitulated in transfating NSM c

200 The micromere-PMC GRN governs the development of the larval

201 ty to fuse is autonomously programmed in the micromere-PMC lineage by the 16-cell stage.

202 ent of the GRN, unlike its deployment in the micromere-PMC lineage, is independent of the transcripti

203 t is due to mechanical constraint from other micromere-PMCs.

204 r normal development, as removal of all four micromeres prevented dorsoventral axis formation.

205 The micromere-primary mesenchyme cell (PMC) GRN drives the d

206 lei of micromeres and, as a consequence, the micromeres produce an inductive ligand.

207 ntinues to activate foxY expression in small micromere progeny.

208 These results demonstrate that micromere quartet identity, a hallmark of the ancient sp

209 the relative size and timing of formation of micromere quartets and none can be considered, by itself

210 axial relationships exhibited by successive micromere quartets are a characteristic of spiralian dev

211 ies of asymmetric divisions that produce the micromere quartets are particularly important for patter

212 d by all blastomeres of the first and second micromere quartets, as well as 3c and 3d.

213 d obligatorily from descendants of the small micromeres; rather, the germ cell lineage arises during

214 strate that the proximity of a first quartet micromere relative to the inducing D macromere is import

215 Generally, progeny of a single micromere remain in the quadrant of origin.

216 If beta-catenin signaling is blocked, the micromeres remain unspecified and are unable to signal t

217 We demonstrate that micromeres require nuclear beta-catenin to exhibit SMC i

218 in the skeletogenic descendants of the large micromeres; second, after about 20 h in the oral ectoder

219 n nuclear beta-catenin in vegetal nuclei and micromere signaling, we performed both transplantations

220 show that the gene is not involved in early micromere signaling.

221 s mRNA accumulates specifically in the small micromere (sMic) lineage.

222 Here we demonstrate that small micromeres (SMics), which are formed at the fifth cell d

223 Thus, the micromere-specific control genes, which are the target o

224 togenic cell state is specified initially by micromere-specific expression of these regulatory genes,

225 se all of the cells of the embryo to express micromere-specific genes.

226 ed functions, including global repression of micromere-specific regulatory genes.

227 f which the regulatory apparatus is entirely micromere-specific.

228 derm specification places pmar1 early in the micromere specification pathway, and upstream of two imp

229 cription factor necessary for initiating the micromere specification program and for the expression o

230 has likely been used for euechinoid echinoid micromere specification since at least the Late Triassic

231 nent of the gene network that controls large micromere specification, the homeodomain protein Alx1.

232 ic regulatory gene network that accounts for micromere specificity.

233 terval when the progeny of the first quartet micromeres specify the D quadrant macromere.

234 tative in that more SMCs are induced by four micromeres than by one.

235 (12)) and a single daughter of the four m(1) micromeres (the m(12) micromeres).

236 e of pmarl is to prevent, exclusively in the micromeres, the expression of a repressor that is otherw

237 tracing to determine that, in addition to e1 micromeres, the four m1 micromeres also make significant

238 vision because animals are fertile even when micromeres, the parent blastomeres of small micromeres,

239 the vegetal plate after removing all 4 host micromeres, the resultant PMCs ingress and migrate into

240 ng 20-60 minutes after the appearance of the micromeres--the precursors of the small micromeres.

241 (v) presentation of a signal required by the micromeres themselves and of two different signals requi

242 romeres, and then is restricted to the small micromeres through gastrulation to larval development.

243 Transplantation of micromeres to animal cells resulted in the induction of

244 that the induction signal is passed from the micromeres to macromere progeny between the eighth and t

245 nth cleavage addition of induction-competent micromeres to micromereless embryos fails to specify SMC

246 The migration of the small micromeres to the coelomic pouches in the sea urchin emb

247 s disrupts the ordered distribution of small micromeres to the left and right coelomic pouches.

248 TC-stained hosts (in place of the endogenous micromere) to observe the progeny of a single micromere.

249 Micromere transplantation experiments revealed that the

250 Micromere transplantation experiments show that the gene

251 the greatest number of the remaining animal micromeres, ultimately became the D quadrant.

252 rilii, we investigated the lineage of the 4d micromere, using high-resolution long-term live imaging

253 In addition, the 1b micromere was found to be equivalent to 1a and 1c, but 1

254 After removing the micromeres, we observed a significant delay in the forma

255 ing endodermal canals) form when all four e1 micromeres were deleted.

256 When single micromeres were isolated and cultured in unsupplemented

257 four-cell stage, and specific first quartet micromeres were removed from discrete positions relative

258 hen either one or two adjacent first quartet micromeres were removed from one side of the embryo, the

259 pressor, pmar1, is activated specifically in micromeres, where it represses transcription of a second

260 its propensity for accumulation in the small micromeres, whereas overexpression of the Vasa-interacti

261 However, at fourth cleavage, the micromeres, which are partitioned by asymmetric division

262 Although isolated e(1) micromeres will spontaneously generate comb plates, cell