Cell transformation by c-Ha-rasVal12 oncogene is accompanied by a decrease in histone H1 zero and an increase in nucleosomal repeat length

J Laitinen, L Sistonen, K Alitalo, E Hölttä

Research output: Contribution to journalArticleScientificpeer-review

16 Citations (Scopus)

Abstract

The activated c-Ha-rasVal12 oncogene is often involved in the genesis of human malignancies. We show here that in c-Ha-rasVal12 oncogene-transformed mouse NIH 3T3 fibroblasts the copy number and expression level of the mutant ras oncogene correlates with the degree of chromatin decondensation, as assessed by micrococcal nuclease (MNase) and DNase I digestion. MNase and DNase I analyses further revealed that the nucleosomal repeat lengths were different in the normal and ras oncogene-transformed cells, 162.3 bp and 178.1 bp, respectively. These chromatin changes were accompanied by alterations in the content of histone H1 zero. Furthermore, using DNase I as a probe, we discovered that serum stimulation of normal and transformed cells, synchronized by serum starvation, induces rapid reversible changes in the structure of bulk chromatin that may be linked to transcriptional activation. Our data thus indicate that cell transformation by ras is associated with specific changes in chromatin structure that make it more vulnerable, and prone to additional mutations characteristic of cancer development in vivo.

Original languageEnglish
Pages (from-to)1-11
Number of pages11
JournalJournal of Cellular Biochemistry
Volume57
Issue number1
DOIs
Publication statusPublished - Jan 1995
MoE publication typeA1 Journal article-refereed

Keywords

  • 3T3 Cells
  • Animals
  • Cell Division
  • Cell Transformation, Neoplastic/genetics
  • Chromatin/chemistry
  • Culture Media, Serum-Free
  • DNA/chemistry
  • Fibroblasts/cytology
  • Gene Expression
  • Genes, ras
  • Histones/analysis
  • Mice
  • Nucleosomes/chemistry
  • Repetitive Sequences, Nucleic Acid

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