# Regional Conservation and Transcriptional Regulation of Tumor-Associated Genes by macroH2A1 Deposition in Mammalian Cells

**Authors:** Yongzhuo Deng, Zeqian Xu, Le Zhang, Bishan Ye, Zhifeng Shao, Xinhui Li

PMC · DOI: 10.3390/biom15101386 · 2025-09-29

## TL;DR

This study shows that mH2A1, a histone variant, is dynamically deposited in human cells and may play a role in cancer.

## Contribution

The study is the first to demonstrate dynamic mH2A1 domains in human cells and their conservation across species.

## Key findings

- Dynamic mH2A1 domains are present in both normal and cancerous human cells.
- mH2A1 enrichment patterns are conserved across species.
- mH2A1 may influence malignant proliferation through epigenetic regulation.

## Abstract

Histone variant macroH2A1 (mH2A1) has been widely recognized as a suppressor of gene expression. Recently, a cell cycle-dependent deposition of mH2A1 was discovered in mouse cells, but whether this process exists in human chromatin is unclear, which might be crucial for related diseases, particularly cancer. In this study, with native chromatin immunoprecipitation (nChIP-seq), we firstly demonstrate that dynamic mH2A1 domains occur in both normal and cancerous human cells and have conserved enrichment patterns across species. Our findings further provide new epigenetic insights into the role of mH2A1 in malignant proliferation, offering a novel perspective for future cancer research.

## Linked entities

- **Proteins:** MACROH2A1 (macroH2A.1 histone), MACROH2A1 (macroH2A.1 histone)
- **Diseases:** cancer (MONDO:0004992)
- **Species:** Homo sapiens (taxon 9606), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** MACROH2A1 (macroH2A.1 histone) [NCBI Gene 9555] {aka H2A.y, H2A/y, H2AF12M, H2AFY, MACROH2A1.1, mH2A1}
- **Diseases:** Tumor (MESH:D009369)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12562687/full.md

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Source: https://tomesphere.com/paper/PMC12562687