ライフサイエンスコーパス: PcG

1 PcG complexes modify chromatin, but also interact with b

2 PcG function was originally viewed as being solely repre

3 PcG hyperactivity in B-cell lymphomas is caused by overe

4 PcG proteins are organized into multiprotein complexes t

5 PcG proteins form condensates in the cell nucleus, and t

6 PcG proteins regulate expression of homeotic genes and a

7 PcG-mediated repression does not play a significant role

8 that transcription factor YY1 functions as a PcG protein.

9 ectively, these findings reveal a role for a PcG complex in promoting mRNA transcription.

10 LT-HSC activity and that UBAP2L is part of a PcG subcomplex comprising BMI1, we propose a model in wh

11 netic silencing and opened new visions about PcG functions in cells.

12 Knock-down of YY1 abrogated PcG recruitment, which was not compensated by exogenous

13 advancements in targeted strategies against PcG as promising therapeutics for B-cell malignancies.

14 AP-Enhancer of zeste [E(z)], we captured all PcG-repressive complex 1 (PRC1) or PRC2 core components

15 e show that one role of H3K27me3 is to allow PcG complexes anchored at PREs to interact with surround

16 Although PcG proteins have been traditionally described as epigen

17 TRs instead possess a functionally analogous PcG protein, EMF1.

18 establish a direct link between lamin A and PcG epigenetic silencing and indicate that lamin A-depen

19 WDED NUCLEI1 (CRWN1), and the chromatin- and PcG-associated component, PROLINE-TRYPTOPHANE-TRYPTOPHAN

20 t genes that are co-regulated by cohesin and PcG proteins.

21 wn leads to PcG protein foci disassembly and PcG protein dispersion.

22 inding of key epigenetic writers/erasers and PcG complexes to restrict tumor development.

23 I-1, suggesting opposing roles for PEITC and PcG proteins in control of tumor progression.

24 ctions; for instance, between repressors and PcG proteins.

25 TrxG and PcG complexes play key roles in the epigenetic regulatio

26 In contrast, the TrxG and PcG proteins Trithorax and Enhancer-of-Zeste, which are

27 Although trxG is known to antagonize PcG, emerging data reveal that trxG can also repress gen

28 w two central regulatory mechanisms, such as PcG and microRNA, assemble to achieve a developmental ou

29 anscription through PREs disrupts associated PcG complexes, contributing to the establishment of the

30 (TET2), additional sex combs like 1 (ASXL1), PcG enhancer of zeste homolog 2 (EZH2) and DNA methyltra

31 How this modification becomes established at PcG-repressed loci is generally not known, but it has be

32 ith this, tissue-specific DNA methylation at PcG target genes is substantially reduced in Dnmt3a KO e

33 le in shaping H2AK119 mono-ubiquitylation at PcG targets and underpins an activity-based communicatio

34 Because PcG-associated aberrant DNA methylation is a hallmark of

35 estive of functional diversification between PcG proteins.

36 These tbx genes were decorated by broad PcG domains in wildtype whole embryo lysates.

37 structures characteristic of those bound by PcG complexes, consistent with the possibility that RNA

38 ~75% of hypermethylated genes are marked by PcG in the context of bivalent chromatin in both ESCs an

39 Aberrant epigenetic modification by PcG is strongly correlated with the severity and invasiv

40 of Drosophila PREs that can be recognized by PcG complexes, and RNA-DNA strand exchange as a PRC2 act

41 lysine 118 (H2AK118ub) outside of canonical PcG target regions, dependent on the RING/Sce subunit of

42 that forms of chromatin other than canonical PcG/TrxG transitions take over key roles during neural d

43 ely limited pool of experimentally confirmed PcG target genes.

44 n which at least 2 different BMI1-containing PcG complexes regulate HSC activity, which are distingui

45 targets the NFI-A promoter region containing PcGs binding sites and miR-223 complementary DNA sequenc

46 In contrast, PcG members restrain senescence by epigenetically repres

47 esults strongly suggest that Scm coordinates PcG complexes and polymerizes to produce broad domains o

48 n A/C is evolutionarily required for correct PcG protein nuclear compartmentalization.

49 , we show here that lamin A loss deregulated PcG positioning in muscle satellite stem cells, leading

50 anscription through a PRE sequence displaces PcG proteins and provides a universal mechanism for indu

51 tone H3 lysine-4 demethylase form a distinct PcG complex, termed EMF1c, that plays PRC1-like roles an

52 hlighted by the fact that a lack of distinct PcG proteins results in embryonic lethality accompanied

53 The essential Drosophila PcG protein, Posterior Sex Combs (PSC), compacts chromat

54 ene, a mammalian homologue of the Drosophila PcG protein SCM, encodes two protein isoforms: SCML2A th

55 In Drosophila, PcG proteins are bound to DNA fragments called Polycomb

56 lls produced in vitro do not fully eliminate PcG-mediated repression on endocrine-specific genes, pro

57 mutant SAM disrupts clustering of endogenous PcG complexes and chromatin interactions while elevating

58 An essential PcG complex, PRC1, compacts chromatin and inhibits chrom

59 nt with the possibility that RNA facilitates PcG recruitment or maintenance at these sites.

60 Linking transcription factors, PcG proteins and paused Pol II states, these data identi

61 the cis-regulatory elements is critical for PcG recruitment, while high GC content and high conserva

62 ve biochemical and theoretical framework for PcG and TrxG regulation has the potential to reconcile s

63 sequence-independent feedback mechanism for PcG protein recruitment.

64 ) proteins, and that MIR31HG is required for PcG-mediated repression of the INK4A locus.

65 La cells showed that YAF2 is responsible for PcG recruitment to DNA, which is mediated by YY1 DNA bin

66 These findings identify a novel role for PcG proteins in promoting cancer cell survival via repre

67 The Polycomb Group (PcG) and Trithorax Group (TrxG) proteins are the central

68 Polycomb group (PcG) and trithorax Group (trxG) proteins maintain the "O

69 The highly-conserved Polycomb group (PcG) and trithorax group (trxG) proteins play major role

70 ncoding RNAs are involved in Polycomb group (PcG) and Trithorax group (TrxG) regulation has been on a

71 We identify silencers of the Polycomb group (PcG) as principal contributors to this mechanism and sho

72 2, a component of repressive Polycomb Group (PcG) complexes like PRC2, is increased on reactivation o

73 Polycomb group (PcG) complexes PRC1 and PRC2 are well known for silencin

74 Polycomb group (PcG) complexes such as PRC1 mediate transcriptional repr

75 in which CpG islands recruit Polycomb group (PcG) complexes; however, which subset of CGIs is selecte

76 Here, we show that a Polycomb group (PcG) component, Enhancer of Zeste [E(z)], a histone tran

77 y the opposing activities of Polycomb group (PcG) factors and trithorax group (trxG) factors.

78 of these domains depends on Polycomb Group (PcG) functions, which include trimethylation of lysine 2

79 encing through the so-called Polycomb Group (PcG) mechanism.

80 The Polycomb Group (PcG) of chromatin modifiers regulates pluripotency and d

81 The polycomb group (PcG) of proteins are epigenetic repressors and lamin A i

82 and differentiation are the Polycomb group (PcG) of proteins, organized in the nucleus as microscopi

83 mpanied by repression of the polycomb group (PcG) protein BMI1 and induction of cellular senescence.

84 The Polycomb group (PcG) protein BMI1 is a key factor in regulating hematopo

85 The Polycomb group (PcG) protein Bmi1 is an essential epigenetic regulator o

86 The Polycomb group (PcG) protein BMI1 is essential for the activity of both

87 The Polycomb group (PcG) protein family is a well-known group of epigenetic

88 regulators belonging to the Polycomb Group (PcG) protein family.

89 ften in association with the polycomb group (PcG) protein Polycomb (Pc), a subunit of polycomb repres

90 onditional knock-out (KO) of Polycomb Group (PcG) protein YY1 results in pro-B cell arrest and reduce

91 DFO1 interacts with the rice polycomb group (PcG) proteins (OsMSI1 and OsiEZ1).

92 Polycomb group (PcG) proteins are a group of evolutionarily conserved pr

93 Polycomb group (PcG) proteins are best known for their role in maintaini

94 Polycomb Group (PcG) proteins are crucial for epigenetic inheritance of

95 Polycomb Group (PcG) proteins are epigenetic repressors essential for co

96 Polycomb group (PcG) proteins are epigenetic transcriptional factors tha

97 Polycomb group (PcG) proteins are key chromatin regulators implicated in

98 The Polycomb group (PcG) proteins are key regulators of development in Droso

99 Among the distinct factors, Polycomb group (PcG) proteins are major negative regulators of gene expr

100 Polycomb group (PcG) proteins are responsible for maintaining the silenc

101 s key epigenetic regulators, polycomb group (PcG) proteins are responsible for the control of cell pr

102 Polycomb group (PcG) proteins are transcriptional repressors of genes in

103 Polycomb group (PcG) proteins are transcriptional repressors that are im

104 Polycomb Group (PcG) proteins assemble a chromatin state that maintains

105 genes through cobinding with Polycomb group (PcG) proteins at transcriptional start sites, whereas it

106 both tumors overexpress the polycomb group (PcG) proteins BMI-1 and EZH2, which contribute to tumori

107 rectly repress expression of Polycomb group (PcG) proteins CBX7, embryonic ectoderm development (EED)

108 how nuclear organization and Polycomb group (PcG) proteins contribute to epigenetically inheritable p

109 ion and segregation, and the Polycomb group (PcG) proteins for their roles in epigenetic gene silenci

110 Polycomb Group (PcG) proteins form memory of transient transcriptional r

111 The Polycomb Group (PcG) proteins form several complexes with important and

112 Polycomb group (PcG) proteins function as chromatin-based transcriptiona

113 Polycomb group (PcG) proteins initiate the formation of repressed chroma

114 Polycomb Group (PcG) proteins maintain transcriptional repression throug

115 Polycomb Group (PcG) proteins mediate heritable gene silencing by modify

116 The Polycomb group (PcG) proteins modulate nucleosomes to maintain repressio

117 Polycomb Group (PcG) proteins organize chromatin at multiple scales to r

118 Polycomb group (PcG) proteins play critical roles in the epigenetic inhe

119 Polycomb group (PcG) proteins play important roles in regulating develop

120 Polycomb group (PcG) proteins play vital roles in plant development via

121 The Polycomb group (PcG) proteins regulate stem cell differentiation via the

122 Polycomb group (PcG) proteins repress master regulators of development a

123 Polycomb group (PcG) proteins silence gene expression by chemically and

124 isions in Drosophila require Polycomb group (PcG) proteins to maintain the silent state and Trithorax

125 e balanced activities of the Polycomb group (PcG) proteins within the PRC1 and PRC2 complexes, and th

126 idence has demonstrated that polycomb group (PcG) proteins, a subset of histone-modifying enzymes kno

127 1HG genomic regions and with Polycomb group (PcG) proteins, and that MIR31HG is required for PcG-medi

128 The polycomb group (PcG) proteins, Bmi-1 and Ezh2, are important epigenetic

129 nome architecture, including Polycomb group (PcG) proteins, form subnuclear structures.

130 c-induced transformed cells, polycomb group (PcG) proteins, including BMI1 and SUZ12, were activated

131 dy of evidence suggests that Polycomb group (PcG) proteins, key regulators of lineage specific gene e

132 , and bind to the repressive Polycomb group (PcG) proteins, often in the context of bivalent chromati

133 izes epigenetic silencing by Polycomb group (PcG) proteins, stimulates enhancer-dependent transcripti

134 silencing is carried out by Polycomb group (PcG) proteins, which must be correctly recruited only to

135 iched with promoter-proximal Polycomb Group (PcG) proteins, yet lacking the classical H3K27me3 PcG si

136 S regions and gene bodies of Polycomb group (PcG) target developmental genes, while Dnmt3b has a domi

137 maintains downregulation of Polycomb Group (PcG) target genes in lhp1 mutants, while it sustains hig

138 uire stable silencing by the polycomb group (PcG) to prevent misexpression during differentiation and

139 rget genes are also bound by Polycomb group (PcG) transcriptional repressor proteins and change durin

140 he first genes composing the Polycomb group (PcG) were identified 50 years ago in Drosophila melanoga

141 meotic (Ph), a member of the Polycomb Group (PcG), is a gene silencer critical for proper development

142 sensitive to activity of the Polycomb Group (PcG), suggesting that PcG attenuation upon polarity loss

143 Polycomb group (PcG)-mediated repression is an evolutionarily conserved

144 We identify removal of Polycomb group (PcG)-mediated repression on stage-specific genes as a ke

145 n trithorax-group (TrxG) and polycomb-group (PcG) chromatin states are vital for the differentiation

146 Polycomb-group (PcG) complexes are multiprotein, evolutionarily conserve

147 c of males with mutations in Polycomb-group (PcG) genes.

148 Polycomb-group (PcG) proteins function to ensure correct deployment of d

149 heterochromatin mediated by Polycomb-group (PcG) proteins has been reported as well.

150 one deacetylases (HDACs) and Polycomb-group (PcG) proteins.

151 proteins, yet lacking the classical H3K27me3 PcG signature.

152 How PcG activities are targeted to PREs to maintain represse

153 How PcG complexes form repressive chromatin domains remains

154 recent advances, we review evidence for how PcG and TrxG patterns change dynamically during cell typ

155 se findings radically change our view of how PcG repression is targeted and suggest that PRC1 and PRC

156 Our findings reveal how PcG repression is potentially inherited in vertebrates.

157 ography-tandem mass spectrometry to identify PcG interaction partners, we confirmed the existence of

158 rder structures, thereby leading to impaired PcG protein repressive functions.

159 ses detachment from chromatin and defects in PcG protein-mediated higher-order structures, thereby le

160 eview, we will illustrate recent findings in PcG-mediated gene regulation, with special focus on the

161 h both RNA and DNA, and RNA is implicated in PcG targeting and function.

162 However, the role of the Ph SAM polymer in PcG-mediated gene silencing was uncertain.

163 M1BP-regulated genes results in reduction in PcG binding, the release of paused Pol II, increases in

164 nt a model of YAF2-dependent and independent PcG DNA recruitment by YY1.

165 eins, and such binding is dependent on a key PcG component SUZ12.

166 Hypothalamic expression of two key PcG genes, Eed and Cbx7, decreased and methylation of th

167 ast stage of differentiation, the locus lost PcG binding and H3K27me3, gained JMJD3 recruitment, and

168 we determined that components of three major PcG protein complexes are present at an engrailed PRE in

169 A mammalian PcG protein, enhancer of zeste homolog 2 (Ezh2), trigger

170 We manipulated PcG clusters by disrupting the polymerization activity o

171 During hematopoietic differentiation, many PcG proteins are fundamental for proper lineage commitme

172 this effector of senescence to the SA-miRNA/PcG self-regulatory loop.

173 tion to transcriptional activity in most non-PcG target genes and intergenic regions and is governed

174 orm of epigenetic memory required for normal PcG chromatin domain function in gene regulation.

175 However, despite the complete absence of PcG-associated epigenetic mark and proteins, only minor

176 myogenic program because of an alteration of PcG protein-mediated transcriptional repression.

177 ecular regulatory mechanisms at the basis of PcG-mediated epigenetic silencing and opened new visions

178 e putative human PRE has enriched binding of PcG proteins, and such binding is dependent on a key PcG

179 focusing on the compositional complexity of PcG complexes, and we briefly discuss the ongoing clinic

180 a on other loci, speaks to the complexity of PcG targeting in mammals.

181 tantially expedite experimental discovery of PcG target genes by providing an effective initial scree

182 and polymerizes to produce broad domains of PcG silencing.

183 ps were frequently located within domains of PcG-repressed chromatin.

184 Mutation and dysregulation of PcG genes cause developmental defects and cancer.

185 rvation level are also important features of PcG target genes.

186 mical principles underlying the formation of PcG condensates remain unknown, and their determination

187 ll-established cancer-associated function of PcG proteins.

188 ecently described non-classical functions of PcG complexes in stem cells and cancer.

189 was also associated with hypomethylation of PcG target genes that are typically hypermethylated in c

190 to facilitate experimental identification of PcG target genes, here we propose a novel computational

191 targets that are regulated independently of PcG.

192 transformation was blocked by inhibition of PcG function.

193 Interplays of PcG and miRNA deregulations often establish a vicious si

194 f PcG-mediated gene silencing, interplays of PcG with other epigenetic regulators such as miRNAs duri

195 is crucial to understanding the mechanism of PcG recruitment to PREs.

196 Unfortunately, the molecular mechanism of PcG-mediated epigenetic regulation remained elusive, par

197 essive complexes (PRC) nor the mechanisms of PcG and trxG-mediated gene silencing and activation are

198 by overexpression or recurrent mutations of PcG genes and deregulation of microRNAs (miRNAs) or tran

199 Organization of PcG proteins into small, abundant clusters on chromatin

200 We characterized the organization of PcG target genes in ESCs and neural progenitors using 5C

201 was partially reversed by overexpression of PcG member BMI-1, suggesting opposing roles for PEITC an

202 its own transcription via the recruitment of PcG complexes to the FMR1 locus.

203 DSBs) but evidence for direct recruitment of PcG proteins at specific breaks remains limited.

204 g protein that is involved in recruitment of PcG proteins.

205 d illustrate the diversity and redundancy of PcG protein recruitment mechanisms.

206 udies have been focused on the regulation of PcG activity itself.

207 late transcription through the regulation of PcG protein epigenetic factors.

208 progression associates with reinstatement of PcG-dependent repression.

209 n, reduced Pc activity, and de-repression of PcG targets.

210 eview, we present an overview of the role of PcG proteins in normal and malignant hematopoiesis, focu

211 role in transmitting epigenetic silencing of PcG targets by linking PRC1 to formation of a repressive

212 these condensates are the physical sites of PcG-targeted gene silencing via formation of facultative

213 ylation preferentially targets the subset of PcG genes that are developmental regulators, and this ma

214 A subset of PcG target loci are compacted and cluster in the nucleus

215 ssium (Kv) channel genes are also targets of PcG regulation in stem cells.

216 Using reversible tethering of PcG proteins to ectopic sites in mouse embryonic stem ce

217 the differences that exist in the timing of PcG protein action between vertebrate species.

218 'cellular memory' of active transcription of PcG-regulated genes.

219 w, we summarize our current understanding of PcG-mediated gene silencing, interplays of PcG with othe

220 echanism of regulated protein degradation on PcG homeostasis and epigenetic activity.

221 s-induced death and that survival depends on PcG function.

222 hat phase-separated condensates can organize PcG-bound chromatin.

223 This action facilitates the binding of other PcG proteins to chromatin for purposes of transcriptiona

224 cus encoding PLZF, is repressed by Polycomb (PcG) and H3K27me3 in naive hMSCs.

225 In Drosophila, Polycomb (PcG) and Trithorax (TrxG) group proteins are assembled o

226 " hypermethylation, recruitment of polycomb (PcG)-RNAi complexes, and miR-223 promoter targeting acti

227 d cancer genes are occupied by the Polycomb (PcG) repressor complex in embryonic stem cells (ESCs).

228 m Drosophila argue that cohesin and the PRC1 PcG complex interact to control transcription of many ac

229 We report two novel prospective PcG-dependent regulatory elements within the human HOXB

230 Here, we analyzed Polycomb group protein (PcG) complex integrity in response to heat shock (HS).

231 ndidates that impact polycomb group protein (PcG)-regulated gene expression in vivo A novel lncRNA fr

232 Polycomb group proteins (PcG) are transcriptional repressors that control cell id

233 ed Polycomb Response Elements (PREs) recruit PcG proteins.

234 argeting: The same DNA elements that recruit PcG complexes to a repressed locus also encode transcrip

235 parasegment-specific signatures that reflect PcG function, chromatin from single parasegments was iso

236 inding proteins, JARID2 and YY1, to regulate PcG activity at these three elements.

237 iption factors such as c-MYC, which regulate PcG expression.

238 ich drives seed coat development by removing PcG function.

239 The genomic loci of repressed PcG targets formed discrete, small (20-140 Kb) domains o

240 it is now clear that modular and reversible PcG function is essential at most developmental genes.

241 Since PcG and TrxG are ubiquitous and lack apparent sequence s

242 ats, and transcription factor-binding sites (PcG/MIR/TFBS), was associated with reduced survival (HR,

243 Some PcG proteins covalently modify histones, which contribut

244 ion to loss of homeotic gene silencing, some PcG mutants also have small imaginal discs.

245 By FLAG-tagging PcG proteins and expressing them specifically where engr

246 ome inhibitor-treated cells and confirm that PcG protein levels are regulated by proteasome activity.

247 er spread interest for the contribution that PcG proteins revealed in the pathogenesis and progressio

248 We demonstrate that PcG targets coalesce in vivo, and that developmentally i

249 chromatin immunoprecipitation evidence that PcG proteins are bound to the Thor 5' region in vivo.

250 Here we describe our novel finding that PcG-dependent repression of the Kv1.5 channel gene KCNA5

251 The prevalent model holds that PcG proteins bind PREs only in cells where the target ge

252 Our data question the idea that PcG protein recruitment provides a link between DSB repa

253 In summary, our results reveal that PcG condensates assemble through liquid-liquid phase sep

254 These results show that PcG binding per se does not determine the transcriptiona

255 per-resolution microscopy, here we show that PcG proteins are organized into hundreds of nanoscale pr

256 contributors to this mechanism and show that PcG proteins repress Kiss1, a puberty-activating gene.

257 These results thus suggest that PcG proteins can directly modulate cell growth in Drosop

258 of the Polycomb Group (PcG), suggesting that PcG attenuation upon polarity loss potentiates select ta

259 forced expression of Bmi-1, suggesting that PcG proteins, consistent with a prosurvival action, may

260 The PcG machinery can be divided into two major complexes: P

261 The PcG protein Enhancer of Zeste Homolog 2 (EZH2) works as

262 The PcG proteins recognize target genomic loci through cis D

263 We tested these two models at the PcG target gene engrailed.

264 t is precluded from binding its E-box by the PcG protein, CBX7.

265 cription through a PRE fails to dislodge the PcG proteins, nor does it remove repressive histone mark

266 of AEBP2 may have opposite functions for the PcG target genes, and may play significant roles in cell

267 b in fruit and provide new insights into the PcG-mediated epigenetic regulation of climacteric fruit

268 est findings regarding the properties of the PcG and COMPASS families and the insight they provide in

269 e integuments, leading to the removal of the PcG block on seed coat development.

270 n HOX clusters can recruit components of the PcG complexes and confer repression, similar to what has

271 focus on the multiple modes of action of the PcG complexes and describe their biological roles.

272 wever, little is known about the role of the PcG machinery in regulating the transition from juvenile

273 ect of HDACi, and restores expression of the PcG protein BMI1.

274 vity of the sterile alpha motif (SAM) of the PcG protein Polyhomeotic (Ph) or by increasing Ph levels

275 hylation module," comprises a portion of the PcG target genes that are down-regulated in cancer.

276 ch, namely the biochemical properties of the PcG/TrxG system and the application of theoretical mathe

277 These regions recruited the PcG proteins BMI1 and SUZ12 to a reporter construct in m

278 ears, increasing evidence indicates that the PcG complexes can also positively regulate gene transcri

279 REs via GTGT motifs and colocalizes with the PcG proteins Pleiohomeotic (Pho) and Polyhomeotic (Ph) a

280 Remarkably, both the integrity of the PcGs-RNAi complex and DNA sequences matching the seed re

281 This is achieved by the activity of three PcG repressive complex 2s (PRC2s) and the participation

282 Thus, PcG targeting elements overlap with enhancers.

283 s reveals that lamin A/C knock-down leads to PcG protein foci disassembly and PcG protein dispersion.

284 a molecular network from DNA recognition to PcG recruitment, highlighting the essential role of Ster

285 trast, the bulk of H2AK118ub is unrelated to PcG repression.

286 Traditionally, PcG complexes have been associated with maintenance of g

287 enic flies, implying that not only the trans PcG proteins but also certain features of the cis PREs a

288 and a subordinate role in establishing TrxG/PcG chromatin structure at sites unique to differentiate

289 However, the mechanisms underlying PcG recruitment in mammals remain unclear since few regu

290 conferred repression that was dependent upon PcG expression.

291 We also examined whether PcG proteins are bound to an engrailed PRE in cells wher

292 osome compaction is a key mechanism by which PcG proteins maintain gene silencing during mouse develo

293 ly used to inhibit growth of tumors in which PcG protein BMI1 is overexpressed or the PRC1 activity i

294 ce suggests a more complex scenario in which PcG proteins can have a dynamic effect on gene expressio

295 CNA5 promoter is marked in cancer cells with PcG-dependent chromatin repressive modifications that in

296 ce floral organ identity by cooperating with PcG proteins to regulate the H3K27me3-mediated epigeneti

297 s gene expression, acting cooperatively with PcG.

298 increasing cohesin stability interferes with PcG silencing at genes that are co-regulated by cohesin

299 ansformations similar to those observed with PcG loss-of-function mutations.

300 amino-acid YY1 REPO domain necessary for YY1 PcG function, and used this mutant (YY1DeltaREPO), to tr