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Chromatin remodeling complexes serve as crucial regulators of chromatin structure in eukaryotes, governing the transcription, DNA repair, and genome stability. Compared with chromatin remodelers in yeast and animals, plant chromatin remodelers exhibit both conserved and lineage-specific features, which facilitate unique adaptive responses. Cutting-edge approaches in biochemistry, epigenomics, and proteomics are revealing unprecedented insights into plant chromatin remodeling mechanisms, and genetic studies continue to demonstrate their essential roles in maintaining chromatin state homeostasis during plant growth and stress adaptation. This review synthesizes current understanding of plant chromatin remodeling complexes, with particular focuses on their specialized subunit compositions, mechanistic diversity, and integrative roles in epigenetic regulation. Furthermore, we highlight how these complexes interact with histone modifications, DNA methylation pathways, and transcription factor networks to orchestrate plant development and stress responses.
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http://dx.doi.org/10.1016/j.molp.2025.08.004 | DOI Listing |
Cell Signal
September 2025
School of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan 453003, People's Republic of China.
Triple-negative breast cancer (TNBC) presents a formidable therapeutic challenge due to its aggressive behavior, molecular heterogeneity, and lack of actionable targets. This study identifies activation-induced cytidine deaminase (AID) as a pivotal epigenetic driver reprogramming the tumor microenvironment (TME) via non-canonical regulation of NOTCH signaling. Mechanistically, AID recruits histone acetyltransferase 1 (HAT1) to form a chromatin-remodeling complex that binds the JAG1 promoter region (-1.
View Article and Find Full Text PDFCancer Res
September 2025
University of Southern Denmark, Odense, Denmark.
Triple-negative breast cancer (TNBC) is a particularly aggressive subtype of breast cancer with high metastatic potential, limited treatment options, and low patient survival rates. By combining functional proteomics and genomics approaches, we identified an oncogenic transcriptional network in mesenchymal and invasive TNBC involving the glucocorticoid receptor (GR), GATA6, MYC, and AP-1 transcription factors. Although these transcription factors bound extensively to shared enhancers, they utilized different enhancer repertoires from this shared enhancer pool to drive distinct downstream oncogenic pathways.
View Article and Find Full Text PDFNanotoxicology
September 2025
Department of Biophysics of Environmental Pollution, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
The effect of non-functionalized polystyrene nanoparticles (PS-NPs) with diameters of 29, 44, and 72 nm on plasmid DNA integrity and the expression of genes involved in the architecture of chromatin was investigated in human peripheral blood mononuclear cells (PBMCs). The cells were incubated with PS-NPs at concentrations ranging from 0.001 to 100 µg/mL for 24 hours.
View Article and Find Full Text PDFFront Immunol
September 2025
Precision Pharmacy and Drug Development Center, Department of Pharmacy, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Gliomas are the most common primary malignant tumors of the central nervous system (CNS), and despite progress in molecular diagnostics and targeted therapies, their prognosis remains poor. In recent years, immunotherapy has emerged as a promising treatment modality in cancer therapy. However, the inevitable immune evasion by tumor cells is a key barrier affecting therapeutic efficacy.
View Article and Find Full Text PDFEMBO J
September 2025
Department of Biology, University of Crete, Vassilika Vouton, Heraklion, 70013, Greece.
In the presence of chromatin bridges in cytokinesis, human cells retain actin-rich structures (actin patches) at the base of the intercellular canal to prevent chromosome breakage. Here, we show that daughter nuclei connected by chromatin bridges are under mechanical tension that requires interaction of the nuclear membrane Sun1/2-Nesprin-2 Linker of Nucleoskeleton and Cytoskeleton (LINC) complex with the actin cytoskeleton, and an intact nuclear lamina. This nuclear tension promotes accumulation of Sun1/2-Nesprin-2 proteins at the base of chromatin bridges and local enrichment of the RhoA-activator PDZ RhoGEF through PDZ-binding to cytoplasmic Nesprin-2 spectrin repeats.
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