ライフサイエンスコーパス: PcG

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

2 PcG proteins are organized into multiprotein complexes t

3 PcG proteins are present at elevated levels in cancer ce

4 PcG proteins regulate expression of homeotic genes and a

5 PcG-mediated repression does not play a significant role

6 Featured prominently are (1) PcG-controlled nonskin lineage genes, whose expression i

7 that transcription factor YY1 functions as a PcG protein.

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

9 Our findings highlight a PcG/MBT collaboration that attains repressive chromatin

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 TRs instead possess a functionally analogous PcG protein, EMF1.

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

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

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

20 Bindings of both HDAC and PcG to Arf are disrupted by inactivation of p53 and can

21 lts indicate that p53 recruits both HDAC and PcG to Arf locus to repress its expression, and this rep

22 show that p53 is required for both HDAC and PcG to repress Arf expression.

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

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

34 estive of functional diversification between PcG proteins.

35 rowth-control genes between Polycomb bodies (PcGs) and interchromatin granules (ICGs) in response to

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

37 t saturation of the INK4b-ARF-INK4a locus by PcG complexes.

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

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

42 ely limited pool of experimentally confirmed PcG target genes.

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

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

45 In contrast, PcG members restrain senescence by epigenetically repres

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

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

48 rrent activation and repression of different PcG target genes.

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

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

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

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

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

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

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

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

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

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

59 sociated proteins copurified with Cbx family PcG proteins from mouse embryonic stem (ES) cells.

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

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

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

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

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

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

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

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

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

69 The genomic binding sites of Polycomb group (PcG) complexes have been found to cluster, forming Polyc

70 2, a component of repressive Polycomb Group (PcG) complexes like PRC2, is increased on reactivation o

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

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

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

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

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

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

77 The polycomb group (PcG) genes encode a family of proteins that methylate an

78 Here, we uncover a role of Polycomb Group (PcG) genes in the temporally precise repression of WUS e

79 differentiation genes by the Polycomb group (PcG) machinery is emerging as a key feature of precursor

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

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

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 chanism of repression by the Polycomb group (PcG) protein Enhancer of zeste [E(Z)], which is involved

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

89 sertion region 1 (Bmi1) is a Polycomb Group (PcG) protein important in gene silencing.

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

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

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

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 The Polycomb group (PcG) proteins are epigenetic suppressors of gene express

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

98 Polycomb group (PcG) proteins are essential for accurate axial body patt

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

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

101 Polycomb group (PcG) proteins are required for the epigenetic maintenanc

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

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

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

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

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

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

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

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

110 Polycomb group (PcG) proteins control the epigenetic inheritance of tran

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

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

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

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

115 For example, the Polycomb Group (PcG) proteins maintain developmental gene silencing usin

116 Polycomb Group (PcG) proteins maintain transcriptional repression throug

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

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

119 Polycomb group (PcG) proteins play an important role in the control of d

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

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

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

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

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

125 1HG genomic regions and with Polycomb group (PcG) proteins, and that MIR31HG is required for PcG-medi

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

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

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

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

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

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

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

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

134 tone deacetylases (HDAC) and polycomb group (PcG) proteins.

135 Evidence is presented that Polycomb group (PcG) repressors can influence paused Pol II.

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

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

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

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

140 leg (Scm) is a member of the Polycomb group (PcG), a set of transcriptional repressors that maintain

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

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

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

149 Polycomb protein group (PcG)-dependent trimethylation on H3K27 (H3K27me3) regula

150 proteins, yet lacking the classical H3K27me3 PcG signature.

151 How PcG complexes form repressive chromatin domains remains

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

153 Recent findings have identified PcG proteins both as targets for modification by the sma

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

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

156 Importantly, PcG-mediated repression may serve as a precursor for the

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

158 types susceptible to switches in identity in PcG mutants.

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

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

161 auses a concentration-dependent reduction in PcG protein (Bmi-1, Ezh2) expression in SCC-13 skin canc

162 the ncRNAs TUG1 and MALAT1/NEAT2, located in PcGs and ICGs, respectively.

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

164 ocus and recruiting, directly or indirectly, PcG that methylates histone H3 Lys-27 at WUS.

165 some-dependent mechanism, thereby inhibiting PcG-dependent pro-survival epigenetic events.

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

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

168 e underlying epigenetic mechanisms that link PcG function with ANRIL, which impose gene silencing to

169 how the developmental program reverses local PcG action to allow expression of terminal differentiati

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

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

172 We manipulated PcG clusters by disrupting the polymerization activity o

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

174 y we have analysed the function of the mouse PcG protein polycomblike 2 (Pcl2), one of three homologu

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

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

177 We infer that the ability of PcG proteins to compact chromatin in vitro can be predic

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

179 ypothesis that compaction is a key aspect of PcG function.

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

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

182 n by predicting the compacting capability of PcG proteins from species other than Drosophila and mice

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

184 C1)-like 4 (PRC1L4), given the copresence of PcG proteins RING1, RING2, and PCGF6/MBLR.

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

186 and polymerizes to produce broad domains of PcG silencing.

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

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

189 e impact of SFN on the level and function of PcG proteins in skin cancer cells has not been assessed.

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

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

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

193 targets that are regulated independently of PcG.

194 transformation was blocked by inhibition of PcG function.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 progression associates with reinstatement of PcG-dependent repression.

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

212 The important role of PcG in mediating repression of the INK4b-ARF-INK4a locus

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

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

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

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

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

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

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

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

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

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

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

224 on the balance between repression (Polycomb-PcG) and activation (Trithorax-TrxG) of a developmentall

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

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

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

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

229 Polycomb group proteins (PcG) function as transcriptional repressors of gene expr

230 The Polycomb group of proteins (PcG) is important for transcriptional repression and sil

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

232 Agents that reduce PcG protein level are regarded as potentially cancer-pre

233 may suppress cancer progression by reducing PcG protein level via a proteasome-dependent mechanism,

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

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

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

237 ich drives seed coat development by removing PcG function.

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

239 e regulatory elements in removing repressive PcG complexes.

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

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

242 Some PcG proteins covalently modify histones, which contribut

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

244 In mammalian systems, PcG proteins participate in the control of pluripotency,

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

246 ferentiation and in disease states, and that PcG expression is regulated by agents that influence cel

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

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

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 We also show that PcG acts downstream of AG and probably in parallel with

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

255 Recent studies show that PcG proteins are expressed in epidermis, that their leve

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

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

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

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

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

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

262 The PcG proteins recognize target genomic loci through cis D

263 ly lower than in native tissues, and (2) the PcG-regulated Ink4a/Inkb/Arf locus.

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

265 essential, nonredundant role in clearing the PcG complex and H3K27me3 from the CpG island.

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

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

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

269 omb-repressive complex 1 (PRC1) class of the PcG are conserved from flies to humans and inhibit trans

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

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

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

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

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

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

276 a pattern virtually identical to that of the PcG protein, Psc.

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

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

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

280 distribution of expression suggest that the PcG proteins have a central role in maintaining the bala

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

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

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

284 Thus, PcG targeting elements overlap with enhancers.

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

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

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

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

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

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

291 conferred repression that was dependent upon PcG expression.

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

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

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

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