ArticleProceedings of the National Academy of Sciences of the United States of America1995
Mice develop normally without the H1(0) linker histone.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 183 citations in OpenAlex.
- Linker Histones: The Multiple Binding Modes of the Enigmatic 5th Histone.Biomolecules · 2026Review
- A Rahman Syndrome mutation in histone H1.4 disrupts chromatin compaction and phase separation.Nature communications · 2026Article
- Linker histone H1.5 contributes to centromere integrity.Nucleic acids research · 2026Article
- Linker histone regulates the myeloid versus lymphoid bifurcation of multipotent hematopoietic stem and progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Article
- Histone H1.0 couples cellular mechanical behaviors to chromatin structure.Nature cardiovascular research · 2024Article
- Post-Translation Modifications and Mutations of Human Linker Histone Subtypes: Their Manifestation in Disease.International journal of molecular sciences · 2023Review
- Chromatin transitions triggered by LH density as epigenetic regulators of the genome.Nucleic acids research · 2022Article
- Histone variants in skeletal myogenesis.Epigenetics · 2021Review
- Article
- The missing linkGenes & development · 2021Review
- Alternative linker histone permits fast paced nuclear divisions in early Drosophila embryo.Nucleic acids research · 2020Article
- Aberrant Function of the C-Terminal Tail of HIST1H1E Accelerates Cellular Senescence and Causes Premature Aging.American journal of human genetics · 2019Article
- A Robust Method for the Purification and Characterization of Recombinant Human Histone H1 Variants.Biochemistry · 2019Article
- Spermatid-specific linker histone HILS1 is a poor condenser of DNA and chromatin and preferentially associates with LINE-1 elements.Epigenetics & chromatin · 2018Article
- H1.0 Linker Histone as an Epigenetic Regulator of Cell Proliferation and Differentiation.Genes · 2018Review
- Temporally and Spatially Regulated Expression of the Linker Histone H1fx During Mouse Development.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2017Article
- Linker histone H1 prevents R-loop accumulation and genome instability in heterochromatin.Nature communications · 2017Article
- Micronucleus-specific histone H1 is required for micronuclear chromosome integrity in Tetrahymena thermophila.PloS one · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
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 H1t, and the replacement linker histone H1(0). H1(0) accumulates in terminally differentiating cells from many lineages, at about the time when the cells cease dividing. To investigate the role of H1(0) in development, we have disrupted the single-copy H1(0) gene by homologous recombination in mouse embryonic stem cells. Mice homozygous for the mutation and completely lacking H1(0) mRNA and protein grew and reproduced normally and exhibited no anatomic or histologic abnormalities. Examination of tissues in which H1(0) is normally present at high levels also failed to reveal any abnormality in cell division patterns. Chromatin from H1(0)-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 H1(0) by occupying sites that normally contain H1(0). Our results indicate that despite the unique properties and expression pattern of H1(0), its function is dispensable for normal mouse development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.