Literature DB >> 2167251

The expression of the histone H1 (0) gene in the human hepatoma cell line HepG2 is independent of the state of cell proliferation.

C Hochhuth1, D Doenecke.   

Abstract

The H1 histone subtype H1 (0) is a characteristic component of the chromatin of several mammalian tissues. Since H1 (0) is synthesized in nondividing cells upon terminal differentiation, it has been mostly considered either as a prerequisite for or as a consequence of an arrest of DNA replication during the process of differentiation. In several H1 (0)-expressing systems studied until now, inducers of differentiation or inhibitors of DNA synthesis cause an increase of the ratio between H1 (0) and the other H1 proteins. We have studied the steady-state levels of histone H1 (0) mRNA under varied growth conditions in the human hepatoma cell lines HepG2 and Hep3B, and we show in the HepG2 system that H1 (0) is not confined to resting cells, that the H1 (0) gene appears to be expressed throughout the cell cycle and that established inducers of de novo H1 (0) synthesis fail to cause a further increase of the high H1 (0) level. This constitutive expression of H1 (0) appears to reflect the chromatin structure of the liver cells, from which the HepG2 hepatoblastoma cells initially may have evolved. In contrast to the situation in nondividing adult liver cells, the H1 (0) gene is transcribed in HepG2 at a high level, and this expression is compatible with DNA replication.

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Year:  1990        PMID: 2167251     DOI: 10.1111/j.1432-0436.1990.tb00448.x

Source DB:  PubMed          Journal:  Differentiation        ISSN: 0301-4681            Impact factor:   3.880


  2 in total

Review 1.  Growth regulation of human variant histone genes and acetylation of the encoded proteins.

Authors:  D Alvelo-Ceron; L Niu; D G Collart
Journal:  Mol Biol Rep       Date:  2000-06       Impact factor: 2.316

2.  Effects of antineoplastic phospholipids on parameters of cell differentiation in U937 cells.

Authors:  C Hochhuth; D Berkovic; H Eibl; C Unger; D Doenecke
Journal:  J Cancer Res Clin Oncol       Date:  1990       Impact factor: 4.553

  2 in total

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