A Mouse Histone H1 Variant, H1b, Binds Preferentially to a Regulatory Sequence within a Mouse H3.2 Replication-dependent Histone Gene

H1 histones, found in all multicellular eukaryotes, associate with linker DNA between adjacent nucleosomes, presumably to keep the chromatin in a compact, helical state. The identification of multiple histone H1 subtypes in vertebrates suggests these proteins have specialized roles in chromatin orga...

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Veröffentlicht in:The Journal of biological chemistry 1997-06, Vol.272 (24), p.15120-15127
Hauptverfasser: Kaludov, Nikola K., Pabón-Peña, Lil, Seavy, Margaret, Robinson, Gail, Hurt, Myra M.
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Sprache:eng
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Zusammenfassung:H1 histones, found in all multicellular eukaryotes, associate with linker DNA between adjacent nucleosomes, presumably to keep the chromatin in a compact, helical state. The identification of multiple histone H1 subtypes in vertebrates suggests these proteins have specialized roles in chromatin organization and thus influence the regulation of gene expression in the multicellular organism. The mechanism by which the association of H1 with nucleosomal DNA is regulated is not completely understood, but affinity for different DNA sequences may play a role. Here we report that a specific H1 subtype in the mouse, namely H1b, selectively binds to a regulatory element within the protein-encoding sequence of a replication-dependent mouse H3.2 gene. We have previously shown that this coding region element, Ω, is the target of very specific interactions in vitro with another nuclear factor called the Ω factor. This element is required for normal gene expression in stably transfected rodent cells. The mouse H1b protein interacts poorly (100-fold lower affinity) with the comparable “Ω” sequence of a replication-independent mouse H3.3 gene. This H3.3 sequence differs at only 4 out of 22 nucleotide positions from the H3.2 sequence. Our findings raise the possibility that this H1b protein plays a specific role in regulation of expression of the replication-dependent histone gene family.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.272.24.15120