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Cell cycle-related accumulation of H1(0) mRNA: induction in murine erythroleukemia cells.

Abstract
H1(0), a member of histone H1 family, is associated with cell differentiation in vivo and in vitro. Unlike other histones its synthesis is known to be constitutive during the cell cycle. The present paper provides evidence showing that, in murine erythroleukemia (MEL) cells, H1(0) mRNA accumulation is coupled to DNA replication, but this mRNA is stable enough to remain present all over the cell cycle. Moreover the experiments suggest that H1(0) mRNA accumulates in mid or late S phase rather than when cells initiate DNA replication as does H3 mRNA. H1(0) gene transcription is drastically induced by chemical inducers of differentiation in this cell line. In an attempt to better understand the mechanism of this process, we have studied the inducibility of this gene with respect to the position of the cells in the cell cycle. The experiments show that the most efficient accumulation of H1(0) is observed when cells are treated by the inducer during the S phase of the cell cycle. In the same conditions, H3 mRNA accumulation remains unaffected. These results show that H1(0) mRNA, like H3 mRNA, accumulates during DNA replication, although at a different stage in this phase. The two genes differ, however, in their response to the inducer, suggesting that different regulatory elements might be involved in such a response.
AuthorsD Grunwald, S Khochbin, J J Lawrence
JournalExperimental cell research (Exp Cell Res) Vol. 194 Issue 2 Pg. 174-9 (Jun 1991) ISSN: 0014-4827 [Print] United States
PMID2026174 (Publication Type: Journal Article)
Chemical References
  • Acetamides
  • DNA Probes
  • Hematinics
  • Histones
  • RNA, Messenger
  • hexamethylene bisacetamide
Topics
  • Acetamides (pharmacology)
  • Animals
  • Cell Cycle (drug effects)
  • Cell Line
  • Clone Cells
  • DNA Probes
  • Hematinics (pharmacology)
  • Histones (genetics)
  • Kinetics
  • Leukemia, Erythroblastic, Acute
  • Leukemia, Experimental
  • Mice
  • RNA, Messenger (drug effects, genetics, metabolism)

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