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(Received for publication, January 10, 1997, and in revised form, February 5, 1997)
§
,
,
§
and
From the We have previously shown that mouse
phosphorylated histone H1b (pH1b) was localized near nuclear sites that
contained splicing factors. This observation suggested to us that pH1b
was associated with transcribing chromatin. Here we investigated the
relationship between phosphorylation of H1b and transcription. We
demonstrate that treatment of normal or ras-transformed
mouse fibroblasts with the transcription inhibitor actinomycin D for 70 min results in a dramatic decrease in the level of pH1b. Similar
results were observed when transcription was inhibited by
5,6-dichloro-1-
Manitoba Institute of Cell Biology,
University of Manitoba, Winnipeg, Manitoba R3E 0V9, Canada, the
§ Department of Biochemistry and Molecular Biology,
University of Manitoba, Winnipeg, Manitoba R3E OW3, Canada, and the
Department of Biology, University of Rochester,
Rochester, New York, 14627
-D-ribofuranosylbenzimidazole (DRB). When
DRB was removed, the level of pH1b was restored after 2 h.
Treatment of the cells with aphidicolin, a potent inhibitor of
replication, resulted in a marked decrease in the level of pH1b after
30 min. This is the first report showing a dependence of histone
modification upon ongoing transcription and replication. Inhibition of
transcription or replication may hinder accessibility of H1b to the H1
kinase, supporting the idea that pH1b is associated with transcribing
chromatin. Phosphorylation of H1b may be required to maintain a more
decondensed chromatin structure to facilitate transcription and
replication processes.
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