ライフサイエンスコーパス: XIST

1 ionally deleted from Xi in somatic cells (Xi(Xist)).

2 NOG, SOX2 and SSEA1 and lacked expression of Xist.

3 r of this process is the long non-coding RNA Xist.

4 tion 36 causes a significant derepression of Xist.

5 involved in the imprinting that silences Xm-Xist.

6 but is excluded from chromatin condensed by XIST.

7 maternal H3K27me3 as the imprinting mark of Xist.

8 mplex 2; second, Tsix enables PRDM14 to bind Xist.

9 ineage, for overlapping binding sites within Xist.

10 an mammals is mediated by the non-coding RNA Xist.

11 and the X-linked, X-inactivation transcript Xist.

12 nd in mice demonstrated robust regulation of XIST.

13 some silencing induced by the non-coding RNA Xist.

14 le mammals driven by the long noncoding RNA, Xist.

15 of the long noncoding RNAs HOTAIR, SRA, and Xist.

16 Binding of YY1 to the Xist 5' region before XCI competes with the Xist repress

17 nactivation, and that YY1 binds directly the Xist 5' region to trigger the activity of the Xist promo

18 XIST A-repeat forms complex inter-repeat duplexes that n

19 wn-regulated X-inactive specific transcript (XIST), a key player in X-chromosome inactivation that en

20 Xist, a long non-coding RNA crucial for both forms of XC

21 XIST, a long noncoding RNA (lncRNA) essential for X chro

22 Combining a brain-specific genetic Xist ablation with short-term 5-aza-2'-deoxycytidine (Az

23 During X-inactivation, Xist accumulates in cis on the future inactive X chromos

24 sgenic mouse cells show that XACT influences XIST accumulation in cis.

25 Xist antisense long non-coding RNA, XistAR (Xist Activating RNA), which is encoded within exon 1 of

26 d at the Xist promoter region, preventing Xm-Xist activation by RNF12.

27 Although the Xist activator RNF12/RLIM is present as a maternal facto

28 ed, binds CTCF, and extricates CTCF from one Xist allele.

29 on affects gene reactivation status along Xi(Xist), alters chromatin configuration and interferes wit

30 Xist, an essential lncRNA for X chromosome inactivation

31 late a comprehensive protein interactome for Xist, an RNA required for Xi silencing.

32 on of Tsix and PRC2 leads to derepression of Xist and in turn silencing of the single X chromosome in

33 , which interacts via the A-repeat domain of Xist and is required for gene silencing.

34 preferentially recognizes m(6)A residues on XIST and is required for XIST function.

35 tion (XCI) depends on the long noncoding RNA Xist and its recruitment of Polycomb Repressive Complex

36 nt changes the 3D structure of DNA, enabling Xist and its silencing proteins to spread across the X t

37 ng structure-function interrelationships for Xist and other lncRNAs in cells.

38 However, XIST and other X-linked genes were expressed from both c

39 y an unbiased proteomics approach to isolate Xist and PRC2 regulators and identified ATRX.

40 the Xi and support a functional tethering of Xist and PRC2.

41 ation (H3K27me3), indicating co-migration of Xist and PRC2.

42 gulation of the lncRNA (long non-coding RNA) Xist and recruitment of specific chromatin modifiers.

43 nactivation center (Xic), which includes the Xist and Tsix genes.

44 , and consequently, enhanced accumulation of Xist and variable numbers of inactivated X chromosomes d

45 changes in nuclear structure are mediated by Xist and whether they are required for silencing.

46 show that Tsix is dispensable for inhibiting Xist and X-inactivation in the early embryo and in cultu

47 mechanism involving antagonistic activity of XIST and XACT in controlling X chromosome activity in ea

48 ne or more X-inactivation escapees activates Xist and, separately, helps trigger X-linked gene silenc

49 in nuclear architecture (e.g., FIRRE, NEAT1, XIST, and others), the vast majority remain poorly under

50 xl10 including chemokines, the noncoding RNA Xist, and proteins involved in metabolic processes.

51 Here we discover an Xist antisense long non-coding RNA, XistAR (Xist Activat

52 ntify a mixed modality approach combining an Xist antisense oligonucleotide and a small-molecule inhi

53 changes, and protein-RNA interactions within Xist are poorly understood.

54 We show that m(6)A formation in XIST, as well as in cellular mRNAs, is mediated by RNA-b

55 ing (SHAPE-MaP) to examine these features of Xist at single-nucleotide resolution both in living cell

56 ion controls mono-allelic fixation of YY1 to Xist at the onset of XCI.

57 Although Xist attracts some interactors, it repels architectural

58 (XR-PID), a 600 nt sequence encompassing the Xist B-repeat element.

59 Xist binding is linearly proportional to PRC2 density an

60 Here we generate high-resolution maps of Xist binding on the X chromosome across a developmental

61 lyses have provided significant insight into Xist binding patterns and chromatin organization of the

62 During the maintenance of XCI, Xist binds broadly across the X chromosome.

63 silencing, we ectopically induced endogenous Xist by ablating the antisense repressor Tsix in mice.

64 Thus, Jpx activates Xist by evicting CTCF.

65 s additional, Tsix-independent repression of Xist by maintaining pluripotency.

66 C0T-1 RNA has several properties similar to XIST chromosomal RNA but is excluded from chromatin cond

67 x anchor domain of CIZ1 and the E repeats of Xist CIZ1-null mice, although viable, display fully pene

68 ges onwards show hallmarks of XCI, including Xist clouds and H3K27me3 foci, and have full embryogenic

69 ts efficient PRC2 and H3K27me3 enrichment to Xist-coated chromatin.

70 on from the inactive X (Xi) precedes loss of XIST coating.

71 During XCI, Xist coats the future inactive X chromosome (Xi) and rec

72 These findings suggest a model in which Xist coats the X chromosome by searching in three dimens

73 Xist-deficient hematopoietic stem cells (HSCs) show aber

74 nviability of female embryos that inherit an Xist deletion from the father.

75 s overexpression of CIZ1 likewise results in Xist delocalization.

76 ferentiation, and XCI of hESCs can be either XIST-dependent (class II) or XIST-independent (class III

77 ion, highlighting a key role for Polycomb in Xist-dependent chromosome silencing.

78 successful reprogramming can occur from the XIST-dependent class II nuclear state but not class III

79 Deletion of XR-PID abolishes Xist-dependent Polycomb recruitment, in turn abrogating

80 to Xist RNA lacking XR-PID is sufficient for Xist-dependent Polycomb recruitment.

81 Localization of XIST, depletion of Cot-1 RNA, perinuclear localization,

82 ring a paternally derived Xist mutation (X/X(Xist-)) die owing to failure of imprinted XCI and, presu

83 Here, we show that Xist directly interacts with the Lamin B receptor, an in

84 trophectodermal stem cells derived from X/X(Xist-) embryos completely reverse normal imprinted XCI p

85 Xist evicts cohesins from the Xi and directs an Xi-speci

86 embryonic day (E) 6.5, we find that the X/X(Xist-) ExE lacks the transcriptional regulator CDX2, a f

87 CIZ1 interacts with a specific region within Xist exon 7-namely, the highly repetitive Repeat E motif

88 ells contained two active X chromosomes with XIST expression and chromosome-wide transcriptional damp

89 s erosion of XCI is characterized by loss of XIST expression and foci of H3-K27-trimethylation, as we

90 Loss of maternal H3K27me3 induces maternal Xist expression and maternal XCI in preimplantation embr

91 and embryonic cells related to mono-allelic XIST expression and non-random X inactivation highlight

92 he Xi and a genetic circuitry that maintains XIST expression and X-chromosome inactivation in differe

93 Tsix is instead required to prevent Xist expression as trophectodermal progenitor cells diff

94 We also provide evidence that loss of XIST expression is not the primary cause of XCI instabil

95 Loss of XIST expression is strongly correlated with upregulation

96 Although ectopic high-level Xist expression on autosomes can be compatible with viab

97 how that 24 h after synchronous induction of Xist expression, acquired PRC2 binding sites map predomi

98 ce on the Xi during reprogramming, and, like Xist expression, is erased only after pluripotency genes

99 coding sequence an antisense RNA that drives Xist expression.

100 , and ES-cloned embryos show RNF12-dependent Xist expression.

101 in the extra-embryonic ectoderm (ExE) of X/X(Xist-) female embryos.

102 PRC2 and Xist foci are not randomly distributed but showed statis

103 During initial establishment, Xist follows a two-step mechanism, but during maintenanc

104 In female cells undergoing XCI de novo, Xist follows a two-step mechanism, initially targeting g

105 delled the process by inducing expression of XIST from nine different locations in human HT1080 cells

106 s m(6)A residues on XIST and is required for XIST function.

107 racts, allowing a reappraisal of ideas about Xist function.

108 The non-coding RNA XIST functions as a cis-acting silencer when expressed f

109 which is encoded within exon 1 of the mouse Xist gene and is transcribed only from the inactive X ch

110 Thus, the Xist gene carries within its coding sequence an antisens

111 For example, low expression of the Xist gene correlated with cisplatin hypersensitivity in

112 Maternal imprinting at the Xist gene is essential to achieve paternal allele-specif

113 oncoding X-inactivation-specific transcript (Xist gene) is responsible for mammalian X-chromosome dos

114 Instead, Xist identifies these regions by exploiting the three-di

115 Thus, Xist imprinting is directed by sequences within a 200-kb

116 However, the mechanism underlying Xist imprinting is unclear.

117 However, Xist imprinting occurs efficiently only when it is in an

118 To investigate the mechanism of Xist imprinting, we introduce Xist transgenes (Tg) into

119 1 (YY1) in the transcriptional activation of Xist in both human and mouse.

120 Here we delete Xist in the blood compartment of mice and demonstrate th

121 mice an RLIM-independent mechanism activates Xist in the embryo proper.

122 ne reactivation occurs to 6% genes along Xi(Xist) in a recognizable pattern.

123 two opposing long non-coding RNAs, Tsix and Xist, in mice.

124 s can be either XIST-dependent (class II) or XIST-independent (class III).

125 Our data suggest Xist-independent mechanisms of dosage compensation and d

126 g Xist-mediated gene silencing and reversing Xist-induced chromatin inaccessibility.

127 Xist-induced Jarid2 recruitment occurs chromosome-wide i

128 cofactor Jarid2 is an important mediator of Xist-induced PRC2 targeting.

129 On reconversion to primed status, XIST-induced silencing restores monoallelic gene express

130 and an autosomally encoded protein dictates Xist induction.

131 During initiation of XCI, Xist initially transfers to distal regions across the X

132 which expression of the long non-coding RNA XIST initiates the heterochromatinization and silencing

133 Interestingly, when Xist is acutely stripped off from the Xi in post-XCI cel

134 containing the conserved B and F repeats of Xist is critical for Jarid2 recruitment via its unique N

135 g a single active X-chromosome by repressing Xist is crucial for embryonic development in mice.

136 Xist is depleted from genes that escape XCI but may conc

137 Xist is essential for both the random and imprinted form

138 Here we show that, in human cells, XIST is highly methylated with at least 78 N(6)-methylad

139 Xist is not found in metatherians (marsupials), and how

140 In the imprinted form, Xist is paternally marked to be expressed in female embr

141 tions as an X inactivation master regulator; Xist is selectively upregulated from the prospective ina

142 sent as a maternal factor, maternal Xist (Xm-Xist) is repressed during preimplantation phases to esta

143 ific loci on the X chromosome, including the XIST lincRNA locus.

144 estigated the localization mechanisms of the Xist lncRNA during X-chromosome inactivation (XCI), a pa

145 Thus, Xist lncRNA engages with proteins in a modular and devel

146 Eed (-/-) TSCs lack H3K27me3 and Xist lncRNA enrichment on the inactive X chromosome.

147 cally regulates Tsix, the major repressor of Xist lncRNA.

148 t studies have improved our understanding of Xist localization and the proteins with which it interac

149 silencing and histone modifications but not Xist localization, and Drosophila Split ends homolog Spe

150 Here we show that the Xist locus is coated with a broad H3K27me3 domain that i

151 ive X is protected from silencing by its own Xist locus, and the possibility of different solutions f

152 The X-linked Xist long non-coding RNA functions as an X inactivation

153 The 18-kb Xist long noncoding RNA (lncRNA) is essential for X-chro

154 The Xist long noncoding RNA (lncRNA) is essential for X-chro

155 The Xist long noncoding RNA orchestrates X chromosome inacti

156 X-inactive specific transcript (Xist) long noncoding RNA (lncRNA) is thought to catalyze

157 We propose that Xist loss results in X reactivation and consequent genom

158 male-specific embryo lethality and abrogates Xist-mediated gene repression, highlighting a key role f

159 actors include HnrnpK, which participates in Xist-mediated gene silencing and histone modifications b

160 ent Polycomb recruitment, in turn abrogating Xist-mediated gene silencing and reversing Xist-induced

161 METTL3), an m(6)A methyltransferase, impairs XIST-mediated gene silencing.

162 tes of PRC2 deposition do not correlate with Xist-mediated gene silencing.

163 In this study, we have analyzed Xist-mediated recruitment of PRC2 using two approaches,

164 nscription, SHARP and HDAC3 are required for Xist-mediated recruitment of the polycomb repressive com

165 ion whether Lamin B receptor is required for Xist-mediated silencing because they claim that our cell

166 a, and that this interaction is required for Xist-mediated silencing by recruiting the inactive X to

167 tificial tethering of YTHDC1 to XIST rescues XIST-mediated silencing upon loss of m(6)A.

168 discuss recent advances in our knowledge of Xist-mediated silencing, focusing on Xist spreading, the

169 m(6)A formation and recognition required for XIST-mediated transcriptional repression.

170 extensive efforts to define the mechanism of Xist-mediated transcriptional silencing, we still do not

171 eins--SHARP, SAF-A and LBR--are required for Xist-mediated transcriptional silencing.

172 from non-coding regions is not subjected to Xist-mediated transcriptional silencing.

173 wide transcriptional dampening and initiated XIST-mediated X inactivation upon differentiation.

174 n-coding RNA X-inactive specific transcript (XIST) mediates the transcriptional silencing of genes on

175 e maintenance phase, corresponding to 50-100 Xist molecules per Xi and contrasting with the chromosom

176 ntly, females harboring a paternally derived Xist mutation (X/X(Xist-)) die owing to failure of impri

177 aive state (differentiation) happened via an XIST-negative XaXa intermediate.

178 The XIST non-coding RNA coats chromosome 21 and triggers sta

179 ructure, via motifs spanning one-half of all Xist nucleotides.

180 Xist-null females are born at lower frequency and are sm

181 Therefore, Xist-null mice can develop to term in spite of a deficie

182 idespread loss of Xi-associated H3K27me3 and XIST occurs in fused cells and precedes the bi-allelic e

183 f the long noncoding RNAs (lncRNAs) XACT and XIST on active X chromosomes in both early human pre-imp

184 Accumulation of the noncoding RNA Xist on one X chromosome in female cells is a hallmark o

185 d by the antisense RNA Tsix, which represses Xist on the active X chromosome.

186 Our analysis reveals that Xist-PRC2 complexes are less numerous than expected and

187 inding protein and is titrated away from the Xist promoter by Jpx RNA.

188 The high levels of H3K9me3 at the Xist promoter region are lost in embryonic stem (ES) cel

189 ion embryos, that H3K9me3 is enriched at the Xist promoter region, preventing Xm-Xist activation by R

190 facilitate an increase in H3K27me3 over the Xist promoter, indicating that additional mechanisms exi

191 six cotranscriptionally and extends over the Xist promoter.

192 thylation (H3K27me3) is established over the Xist promoter.

193 by which Tsix blocks PRC2 recruitment to the Xist promoter.

194 ist 5' region to trigger the activity of the Xist promoter.

195 stripped off from the Xi in post-XCI cells, Xist recovers quickly within both gene-rich and gene-poo

196 , and the hemizygous (unpaired) state of the Xist region promotes its imprinting in the male germ lin

197 ed in a fundamental and conserved pathway of Xist regulation that ensures the asymmetric transcriptio

198 Xist 5' region before XCI competes with the Xist repressor REX1, whereas DNA methylation controls mo

199 Xist requires its silencing domain to spread across acti

200 itionally, artificial tethering of YTHDC1 to XIST rescues XIST-mediated silencing upon loss of m(6)A.

201 In these contexts, the XIST RNA adopts an unusual, highly dispersed organizatio

202 Despite induction of wild-type Xist RNA and accumulation of histone H3-K27me3, many Tsi

203 existing models for Polycomb recruitment by Xist RNA and establish precedence for H2AK119u1 in initi

204 n et al proposed that an interaction between Xist RNA and Lamin B receptor (LBR) is necessary and suf

205 During XCI, the long noncoding Xist RNA and Polycomb proteins spread along the inactive

206 ons argue against direct interaction between Xist RNA and PRC2 proteins and, as such, prompt a reappr

207 Here we view Xist RNA and the Xi at 20-nm resolution using STochastic

208 The mechanisms by which Xist RNA associates with the X chromosome to mediate alt

209 TORM) shows a tight association of CIZ1 with Xist RNA at the single-molecule level.

210 Thus, whereas Xist RNA can inactivate the X chromosome in females it m

211 Here, we report that female mice lacking Xist RNA can, surprisingly, develop and survive to term.

212 f X(DeltaTsix)Y male cells displayed ectopic Xist RNA coating compared with X(DeltaTsix)X female cell

213 Recent genome-wide Xist RNA distribution studies suggest that this long non

214 erlapping Xist RNA, leads to a deficiency in Xist RNA expression in cis during the initiation of X in

215 uitment of both PRC1 and PRC2 in response to Xist RNA expression.

216 s an important intermediate between PRC2 and Xist RNA for the initial targeting of the PRC2 complex t

217 The Xist RNA forms complex well-defined secondary structure

218 with X(DeltaTsix)X cells, despite equivalent Xist RNA induction and coating.

219 We find that ectopic Xist RNA induction and subsequent X-linked gene silencin

220 Focal localization of Xist RNA is also disrupted in activated B and T cells is

221 lycomb repressive complexes PRC1 and PRC2 by Xist RNA is an important paradigm for chromatin regulati

222 Although Xist RNA is essential for the recruitment of PRC2 to the

223 The noncoding Xist RNA is expressed and initiates XCI only when more t

224 ar mechanism for PCGF3/5-PRC1 recruitment by Xist RNA is not understood.

225 cordingly, synthetically tethering hnRNPK to Xist RNA lacking XR-PID is sufficient for Xist-dependent

226 oblast cells derived from CIZ1-null embryos, Xist RNA localization is disrupted, being highly dispers

227 a strong female bias, and observed different XIST RNA localization patterns, evidence of biallelic ex

228 d a more global view of Xist's function, how Xist RNA localizes to the inactive X chromosome (Xi) and

229 Without ATRX, PRC2 cannot load onto Xist RNA nor spread in cis along the X chromosome.

230 Thus, Xist RNA not only is required to maintain XCI but also s

231 Only approximately 50 hubs of Xist RNA occur on the Xi in the maintenance phase, corre

232 To test the impact of Xist RNA on X-linked gene silencing, we ectopically indu

233 Here we define the Xist RNA Polycomb Interaction Domain (XR-PID), a 600 nt

234 The Xist RNA structure modulates protein interactions in cel

235 ale cells phenocopies one another in causing Xist RNA to delocalize from the Xi and disperse into the

236 hromosome inactivation (XCI) is triggered by Xist RNA to equalize gene expression between the sexes.

237 ng protein that directly interacts with RepA/Xist RNA to promote loading of PRC2 in vivo.

238 protein CIZ1 is critical for localization of Xist RNA to the Xi chromosome territory.

239 major role in ensuring stable association of Xist RNA within the Xi territory.

240 ion of XistAR, while sparing the overlapping Xist RNA, leads to a deficiency in Xist RNA expression i

241 Despite the absence of H3K27me3 and Xist RNA, only a subset of the inactivated X-linked gene

242 ne a key pathway for Polycomb recruitment by Xist RNA, providing important insights into mechanisms o

243 XCI is initiated in cis by the noncoding Xist RNA, which coats the inactive X chromosome (Xi) fro

244 XCI is orchestrated by Xist RNA, whose expression in early development leads to

245 ckout and knockdown approaches, we find that Xist RNA-binding proteins, YY1 and hnRNPU, are critical

246 target loci in mESCs and is also involved in Xist RNA-mediated silencing, the latter suggesting a wid

247 The Xist RNA-protein particle assembles in two steps coupled

248 male mammals is inactivated by the noncoding Xist RNA.

249 ishment of heterochromatin by the non-coding XIST RNA.

250 e relative localization of PRC2 proteins and Xist RNA.

251 the A-repeat region located at the 5' end of Xist RNA.

252 xpression of X inactive-specific transcript (Xist) RNA during the earliest stages of X inactivation i

253 r regulator, X-inactive specific transcript (Xist) RNA, which localizes in cis along the entire lengt

254 and interacts directly with Tsix, Xite, and Xist RNAs.

255 proaches have provided a more global view of Xist's function, how Xist RNA localizes to the inactive

256 Our results suggest that Xist silences transcription by directly interacting with

257 lly, XCR requires both DNA demethylation and Xist silencing, ensuring that only cells undergoing fait

258 ndreds of caRNAs, including previously known XIST, SNHG1, NEAT1, and MALAT1, as well as each caRNA's

259 ceptor (LBR) is necessary and sufficient for Xist spreading during X-chromosome inactivation.

260 We conclude that Xist spreading takes distinct stage-specific forms.

261 edge of Xist-mediated silencing, focusing on Xist spreading, the nuclear organization of the inactive

262 iched for SINE elements, predicted to impair XIST spreading.

263 es preclude assessment of the role of LBR in Xist spreading.

264 two-step mechanism, but during maintenance, Xist spreads rapidly to both gene-rich and gene-poor reg

265 How Xist spreads silencing on a 150-megabases scale is uncle

266 How Xist spreads, what are its binding sites, how it recruit

267 K36 methylase Setd2 leads to upregulation of Xist, suggesting H3K36me3 as a modification that contrib

268 dosage compensation can be achieved without Xist, supporting the idea of inherent genome balance.

269 smitted from a hemizygous father (+/Tg), the Xist Tg demonstrates paternal-specific expression in the

270 ic expression is recapitulated by the 200-kb Xist Tg.

271 cto corrected by manipulating a single gene, XIST (the X-inactivation gene).

272 orially target factors in the interactome of Xist, the noncoding RNA responsible for X inactivation.

273 ing one X in both sexes from inactivation by XIST, the noncoding RNA that silences the inactive X.

274 Upon deleting Xist, the Xi acquires the cohesin-binding and chromosoma

275 en proteins that specifically associate with Xist, three of these proteins--SHARP, SAF-A and LBR--are

276 o the nuclear lamina and by doing so enables Xist to spread to actively transcribed genes across the

277 that CIZ1 has an essential role in anchoring Xist to the nuclear matrix in specific somatic lineages.

278 promoting expression and/or localization of Xist to the Xi.

279 Of note, Xist transcript was significantly enriched in dopamine n

280 initiation of X-chromosome inactivation and XIST transcription in ES cells, also plays a role in mai

281 ranscriptional repressor, is an activator of Xist transcription.

282 In pre-XCI cells, CTCF protein represses Xist transcription.

283 ence of colocalization both in the inducible Xist transgene ES cell line and in normal XX somatic cel

284 er nucleases, we inserted a large, inducible XIST transgene into the DYRK1A locus on chromosome 21, i

285 use of an ES cell line carrying an inducible Xist transgene located on mouse chromosome 17, we show t

286 e mechanism of Xist imprinting, we introduce Xist transgenes (Tg) into the male germ line.

287 ntified regions, both proximal and distal to Xist/Tsix, that contribute to the choice of which X chro

288 y exclusive binding between Cdx2 and Oct4 in Xist underlies the switch between imprinted and random X

289 We show that loss of YY1 prevents Xist upregulation during the initiation and maintenance

290 P29, NNAT, PEG10, RTL1, IGF2, H19, MIM1, and XIST) were compared between embryos reaching the blastoc

291 (XCI) is initiated by the long noncoding RNA Xist, which coats the inactive X (Xi) and targets Polyco

292 CI is dependent upon the long non-coding RNA Xist, which is expressed from and coats the inactivated

293 One of the best-studied lncRNAs is Xist, which is required for transcriptional silencing of

294 t studies have established a requirement for Xist with inviability of female embryos that inherit an

295 ion pattern along the inactive X (Xi), after Xist (X-inactive specific transcript), a prototype long

296 and hnRNPU, are critical for recruitment of XIST/Xist RNA back to the Xi.

297 vation of lymphocytes triggers the return of XIST/Xist RNA transcripts and some chromatin marks (H3K2

298 ive T and B cells have dispersed patterns of XIST/Xist RNA, and they lack the typical heterochromatic

299 iched with heterochromatic modifications and XIST/Xist RNA, which equalizes gene expression between t

300 IM is present as a maternal factor, maternal Xist (Xm-Xist) is repressed during preimplantation phase