Increase in histone acetylation and transitions in histone variants during Friend cell differentiation.
Histone acetylation of Murine Erythroleukemia Cells (MELC) has been re-examined. It is demonstrated that sodium butyrate causes hyperacetylation of core histones in inducible as well as non-inducible MELC strains. This indicates that histone hyperacetylation per se is not sufficient to activate genes. However, [3H]acetate incorporation into core histones of the inducible MELC line F4N increases after induction of differentiation with dimethylsulfoxide (DMSO), in contrast to the non-inducible variant F4+. Thus histone acetylation may play a role as an auxiliary mechanism for gene activation (and inactivation). In addition, the appearance of a histone H3 variant during differentiation of MELC is reported.
D000107:Acetylation; D000818:Animals; D002087:Butyrates / Q000494:pharmacology; D020148:Butyric Acid; D002454:Cell Differentiation / Q000187:drug effects; D002478:Cells, Cultured; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D005622:Friend murine leukemia virus; D006657:Histones / Q000378:metabolism*; D004915:Leukemia, Erythroblastic, Acute / Q000378:metabolism* / Q000473:pathology; D051379:Mice
D002087:Butyrates; D006657:Histones; D020148:Butyric Acid; D004121:Dimethyl Sulfoxide