title: Histone H1b phosphorylation is dependent upon ongoing transcription and replication in normal and ras-transformed mouse fibroblasts.
abstract: 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-beta-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.
authors.affiliation: Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Manitoba R3E 0V9, Canada.
authors.forename: D N
authors.initials: DN
authors.lastname: Chadee
authors.forename: C D
authors.initials: CD
authors.lastname: Allis
authors.forename: J A
authors.initials: JA
authors.lastname: Wright
authors.forename: J R
authors.initials: JR
authors.lastname: Davie
mesh_terms: D000818:Animals; D016590:Aphidicolin / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002472:Cell Transformation, Viral; D002843:Chromatin / Q000378:metabolism; D003609:Dactinomycin / Q000494:pharmacology; D004004:Dichlororibofuranosylbenzimidazole / Q000494:pharmacology; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D019084:Fluorescent Antibody Technique, Indirect; D011905:Genes, ras; D006657:Histones / Q000378:metabolism*; D051379:Mice; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D010766:Phosphorylation; D012313:RNA / Q000096:biosynthesis; D012318:RNA Polymerase I / Q000037:antagonists & inhibitors; D012319:RNA Polymerase II / Q000037:antagonists & inhibitors; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D002843:Chromatin; D006657:Histones; D019384:Nucleic Acid Synthesis Inhibitors; D003609:Dactinomycin; D016590:Aphidicolin; D004004:Dichlororibofuranosylbenzimidazole; D012313:RNA; D012319:RNA Polymerase II; D012318:RNA Polymerase I