title: Exploring cellular memory molecules marking competent and active transcriptions.
abstract: BACKGROUND
  Development in higher eukaryotes involves programmed gene expression. Cell type-specific gene expression is established during this process and is inherited in succeeding cell cycles. Higher eukaryotes have evolved elegant mechanisms by which committed gene-expression states are transmitted through numerous cell divisions. Previous studies have shown that both DNase I-sensitive sites and the basal transcription factor TFIID remain on silenced mitotic chromosomes, suggesting that certain trans-factors might act as bookmarks, maintaining the information and transmitting it to the next generation.
  
  
  RESULTS
  We used the mouse globin gene clusters as a model system to examine the retention of active information on M-phase chromosomes and its contribution to the persistence of transcriptional competence of these gene clusters in murine erythroleukemia cells. In cells arrested in mitosis, the erythroid-specific activator NF-E2p45 remained associated with its binding sites on the globin gene loci, while the other major erythroid factor, GATA-1, was removed from chromosome. Moreover, despite mitotic chromatin condensation, the distant regulatory regions and promoters of transcriptionally competent globin gene loci are marked by a preserved histone code consisting in active histone modifications such as H3 acetylation, H3-K4 dimethylation and K79 dimethylation. Further analysis showed that other active genes are also locally marked by the preserved active histone code throughout mitotic inactivation of transcription.
  
  
  CONCLUSIONS
  Our results imply that certain kinds of specific protein factors and active histone modifications function as cellular memory markers for both competent and active genes during mitosis, and serve as a reactivated core for the resumption of transcription when the cells exit mitosis.
authors.affiliation: From National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China. xlgene@263.net <xlgene@263.net>
authors.forename: Li
authors.initials: L
authors.lastname: Xin
authors.forename: Guo-Ling
authors.initials: GL
authors.lastname: Zhou
authors.forename: Wei
authors.initials: W
authors.lastname: Song
authors.forename: Xue-Song
authors.initials: XS
authors.lastname: Wu
authors.forename: Gong-Hong
authors.initials: GH
authors.lastname: Wei
authors.forename: De-Long
authors.initials: DL
authors.lastname: Hao
authors.forename: Xiang
authors.initials: X
authors.lastname: Lv
authors.forename: De-Pei
authors.initials: DP
authors.lastname: Liu
authors.forename: Chih-Chuan
authors.initials: CC
authors.lastname: Liang
mesh_terms: D000107:Acetylation; D000818:Animals; D045744:Cell Line, Tumor; D033481:Chromosomes, Mammalian / Q000378:metabolism; D044127:Epigenesis, Genetic; D050982:GATA1 Transcription Factor / Q000378:metabolism*; D005914:Globins / Q000235:genetics*; D006657:Histones / Q000378:metabolism; D008745:Methylation; D051379:Mice; D008938:Mitosis; D050984:NF-E2 Transcription Factor, p45 Subunit / Q000378:metabolism*; D011401:Promoter Regions, Genetic; D015533:Transcriptional Activation
chemical_list: D050982:GATA1 Transcription Factor; C494689:Gata1 protein, mouse; D006657:Histones; D050984:NF-E2 Transcription Factor, p45 Subunit; D005914:Globins