Article

  • The EMBO Journal (2005) 24, 347 - 357
  • doi:10.1038/sj.emboj.7600516

Published online: 16 December 2004

Histone modifications defining active genes persist after transcriptional and mitotic inactivation

Antigone Kouskouti1 and Iannis Talianidis1

  1. Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology Hellas, Herakleion, Crete, Greece

Correspondence to:

Iannis Talianidis, Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology Hellas, PO Box 1527, Vassilika Vouton, 71110 Herakleion, Crete, Greece. Tel.: +30 2810 391163; Fax: +30 2810 391101; E-mail: talianid@imbb.forth.gr

Received 15 September 2004; Accepted 22 November 2004


We examined various histone modifications across the promoter and the coding regions of constitutively active hepatic genes in G0/G1-enriched, mitotically arrested and alpha-amanitin-blocked cells. Gene activation correlated with localized histone hyperacetylation, H3-K4 tri- or dimethylation and H3-K79 dimethylation and localized nucleosome remodeling at the promoter and the 5' portion of the coding regions. Nucleosomes at more downstream locations were monomethylated at H3-K4. CBP, PCAF, Brg-1, SNF2H and FACT were recruited to the coding regions in a gene-specific manner, in a similarly restricted promoter-proximal pattern. Elongator, however, associated with the more downstream regions. While all factors were dissociated from the chromatin after transcriptional inactivation by alpha-amanitin, the histone modifications remained stable. In mitotic cells, histone modifications on parental nucleosomes were preserved and were regenerated in a transcription-dependent manner at the newly deposited nucleosomes, as the cells entered the next G1 phase. The findings suggest that histone modifications may function as molecular memory bookmarks for previously active locations of the genome, thus contributing to the maintenance of active chromatin states through cell division.

  • Keywords:

    • active chromatin,
    • histone modifications,
    • transcriptional memory
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