Mice develop normally without the H10 linker histone

Allen M. Sirotkin, Winfried Edelmann, Genhong Cheng, Andres Klein-Szanto, Raju Kucherlapati, Arthur I. Skoultchi

Research output: Contribution to journalArticle

137 Scopus citations

Abstract

H1 histones bind to the linker DNA between nucleosome core particles and facilitate the folding of chromatin into a 30-nm fiber. Mice contain at least seven nonallelic subtypes of H1, including the somatic variants H1a through H1e, the testis-specific variant Hit, and the replacement linker histone H10. H10 accumulates in terminally differentiating cells from many lineages, at about the time when the cells cease dividing. To investigate the role of H10 in development, we have disrupted the single-copy H10 gene by homologous recombination in mouse embryonic stem cells. Mice homozygous for the mutation and completely lacking H10 mRNA and protein grew and reproduced normally and exhibited no anatomic or histologic abnormalities. Examination of tissues in which H10 is normally present at high levels also failed to reveal any abnormality in cell division patterns. Chromatin from H10-deficient animals showed no significant change in the relative proportions of the other H1 subtypes or in the stoichiometry between linker histones and nucleosomes, suggesting that the other H1 histones can compensate for the deficiency in H10 by occupying sites that normally contain H10. Our results indicate that despite the unique properties and expression pattern of H10, its function is dispensable for normal mouse development.

Original languageEnglish (US)
Pages (from-to)6434-6438
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume92
Issue number14
DOIs
StatePublished - Jul 3 1995

Keywords

  • Chromatin
  • Gene inactivation
  • Gene targeting

ASJC Scopus subject areas

  • General

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