ArticleJournal of cell science2022
The histone variant macroH2A1.1 regulates RNA polymerase II-paused genes within defined chromatin interaction landscapes.
Article in Journal of cell science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 0 citations in OpenAlex.
- Loss of histone macroH2A1.1 causes kidney abnormalities secondary to a change in nutrient metabolization.Science advances · 2025Article
- Epigenetic control of topoisomerase 1 activity presents a cancer vulnerability.Nature communications · 2025Article
- Dynamic deployment of H2A.Z positive nucleosome mediated transcriptomic plasticity within vascular smooth muscle cell.BMC genomics · 2025Article
- Regulation of Genome Architecture in Huntington's Disease.Biochemistry · 2025Article
- Multifunctional histone variants in genome function.Nature reviews. Genetics · 2025Review
- The Function of H2A Histone Variants and Their Roles in Diseases.Biomolecules · 2024Review
- Deficiency of histone variant macroH2A1.1 is associated with sexually dimorphic obesity in mice.Scientific reports · 2023Article
- Article
- MacroH2A histone variants modulate enhancer activity to repress oncogenic programs and cellular reprogramming.Communications biology · 2023Article
- Histone H2A variants: Diversifying chromatin to ensure genome integrity.Seminars in cell & developmental biology · 2023Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The histone variant macroH2A1.1 plays a role in cancer development and metastasis. To determine the underlying molecular mechanisms, we mapped the genome-wide localization of endogenous macroH2A1.1 in the human breast cancer cell line MDA-MB-231. We demonstrate that macroH2A1.1 specifically binds to active promoters and enhancers in addition to facultative heterochromatin. Selective knock down of macroH2A1.1 deregulates the expression of hundreds of highly active genes. Depending on the chromatin landscape, macroH2A1.1 acts through two distinct molecular mechanisms. The first mitigates excessive transcription by binding over domains including the promoter and the gene body. The second stimulates expression of RNA polymerase II (Pol II)-paused genes, including genes regulating mammary tumor cell migration. In contrast to the first mechanism, macroH2A1.1 specifically associates with the transcription start site of Pol II-paused genes. These processes occur in a predefined local 3D genome landscape, but do not require rewiring of enhancer-promoter contacts. We thus propose that macroH2A1.1 serves as a transcriptional modulator with a potential role in assisting the conversion of promoter-locked Pol II into a productive, elongating Pol II.
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