Nucleic Acids Research, Vol 24, Issue 14 2718-2722, Copyright © 1996 by Oxford University Press
Y Liu, L Sun and JP Jost
Upon the onset of mouse myoblast differentiation there is a rapid drop in
DNA methyltransferase activity followed by a genome wide demethylation
[Jost and Jost (1994) J. Biol. Chem. 269, 10040-10043]. Here we show by
using specific antibodies directed against DNA methyltransferase that upon
differentiation there was a rapid drop in nuclear DNA methyltransferase
whilst the internal control histone H1 remained constant. The loss of
nuclear methyltransferase was not due to a translocation of the enzyme from
the nucleus to the cytoplasm where there was an increase in creatine
phosphokinase protein. In vitro run on experiments carried out with growing
and differentiating myoblast nuclei showed no difference in the rate of DNA
methyltransferase mRNA synthesis. As measured by Northern blot
hybridization the relative half life of DNA methyltransferase mRNA in
growing and differentiating cells in the presence of Actinomycin D was 5 h
and 1 h 30 min respectively, whereas in the same cells the half life of
histone H4 mRNA was in both cases 80 min. As measured by a combination of
pulse chase experiments with labeled leucine and immunoprecipitation, the
relative half-life of DNA methyltransferase in growing and differentiating
cells was approximately 18 h and 4 h 30 min respectively.
ARTICLES
In differentiating mouse myoblasts DNA methyltransferase is posttranscriptionally and posttranslationally regulated
Friedrich Miescher Institut, Basel, Switzerland.
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