Concerted epigenetic signatures inheritance at PcG targets through replication (Articolo in rivista)

Type

• Articolo in rivista (Classe)
• Prodotto della ricerca (Classe)

Label

• Concerted epigenetic signatures inheritance at PcG targets through replication (Articolo in rivista) (literal)

Anno

• 2012-01-01T00:00:00+01:00 (literal)

Alternative label

• Lanzuolo Chiara1,2,3; Lo Sardo Francesca1,2; Orlando Valerio1,2 (2012)
  Concerted epigenetic signatures inheritance at PcG targets through replication
  in Cell cycle (Georget. Tex.)
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Lanzuolo Chiara1,2,3; Lo Sardo Francesca1,2; Orlando Valerio1,2 (literal)

Pagina inizio

• 1296 (literal)

Pagina fine

• 1300 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 11 (literal)

Rivista

• Cell cycle (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note

• In press - April 1, 2012 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali

• 4 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

• 7 (literal)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• 1) Dulbecco Telethon Institute at IRCCS Santa Lucia Foundation; 2) Epigenetics and Genome Reprogramming; Rome, Italy; 3) CNR Institute of Neurobiology and Molecular Medicine; IRCCS Santa Lucia Foundation(*); Rome, Italy (literal)

Titolo

• Concerted epigenetic signatures inheritance at PcG targets through replication (literal)

Abstract

• Polycomb group of proteins (PcG), by controlling gene silencing transcriptional programs through cell cycle, lock cell identity and memory. Recent chromatin genome-wide studies indicate that PcG targets sites are bivalent domains with overlapping repressive H3K27me3 and active H3K4me3 mark domains. During S phase, the stability of epigenetic signatures is challenged by the replication fork passage. Hence, specific mechanisms of epigenetic inheritance might be provided to preserve epigenome structures. Recently, we have identified a critical time window before replication, during which high levels of PcG binding and histone marks on BX-C PRE target sites set the stage for subsequent dilution of epigenomic components, allowing proper transmission of epigenetic signatures to the next generation. Here, we extended this analysis to promoter elements, showing the same mechanism of inheritance. Furthermore, to gain insight into the inheritance of PREs bivalent marks, we analyzed dynamics of H3K4me3 deposition, a mark that correlates with transcriptionally active chromatin. Likewise, we found an early S-phase enrichment of H3K4me3 mark preceding the replication-dependent dilution. This evidence suggests that all epigenetic marks are inherited simultaneously to ensure their correct propagation through replication and to protect the “bivalency” of PREs. (literal)

Prodotto di

• ex ME.P02.010.001 / Patologie del S.N. e Fattori di Crescita (ME.P02.010.004) (Modulo)

Autore CNR

• CHIARA LANZUOLO (Unità di personale interno)

Incoming links:

Prodotto

• ex ME.P02.010.001 / Patologie del S.N. e Fattori di Crescita (ME.P02.010.004) (Modulo)

Autore CNR di

• CHIARA LANZUOLO (Unità di personale interno)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Cell cycle (Rivista)