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Chromatin is dynamically modified throughout the plant life cycle to regulate gene expression in response to environmental and developmental cues. Although such epigenetic information can be inherited across generations in plants, chromatin features that regulate gene expression are typically reprogrammed during plant gametogenesis and directly after fertilization. Nevertheless, environmentally induced epigenetic marks on genes can be transmitted across generations. Moreover, epigenetic information installed on early embryonic chromatin can be stably inherited during subsequent growth and influence how plants respond to environmental conditions much later in development. Here, we review recent breakthroughs towards deciphering mechanisms underlying epigenetic reprogramming and transcriptional priming during early plant embryogenesis.
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http://dx.doi.org/10.1016/j.pbi.2024.102612 | DOI Listing |
Cell Immunol
September 2025
Shaanxi Key Laboratory of Agricultural and Environmental Microbiology, College of Life Sciences, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address:
Both trained immunity (TRIM) and endotoxin tolerance (ET) initiate similar metabolic reprogramming characterized by enhanced glycolysis following an initial stimulus. However, TRIM exhibited heightened immune activation upon restimulation, whereas ET showed suppressed innate immune response. This divergence is attributed to distinct metabolic intermediates accumulated after the initial stimulation.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Department of Biosciences, JIS University, 81, Nilgunj Road, Agarpara, Kolkata, West Bengal 700109, India. Electronic address:
The malignant manifestation of breast cancer is driven by complex molecular alterations that extend beyond genetic mutations to include epigenetic dysregulation. Among these, DNA methylation is a critical and reversible epigenetic modification that significantly influences breast cancer initiation, progression, and therapeutic resistance. This process, mediated by DNA methyltransferases (DNMTs), involves the addition of methyl groups to cytosine residues within CpG dinucleotides, resulting in transcriptional repression of genes.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
School of Life Sciences, Anhui Medical University, Hefei, 230032, China; Translational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metaboli
Melanoma is the most aggressive and lethal form of skin cancer, posing significant challenges for prognosis assessment and treatment. Recently, metabolic reprogramming and epigenetic regulation have gained attention for their roles in cancer progression. The role of the key metabolic enzyme dihydrolipoic acid succinyltransferase (DLST) in cancer is currently unclear.
View Article and Find Full Text PDFBiomaterials
September 2025
Key Laboratory of Biopharmaceutical Preparation and Delivery, Institute of Process Engineering, Chinese Academy of Sciences, Beijing, 100190, PR China; University of Chinese Academy of Sciences, Beijing, 100049, PR China. Electronic address:
The stimulator of interferon genes (STING) pathway represents a promising target in cancer immunotherapy. However, the clinical translation of cyclic dinucleotide (CDN)-based STING agonists remains hindered by insufficient formation of functional CDN-STING complexes. This critical bottleneck arises from two interdependent barriers: inefficient cytosolic CDN delivery and tumor-specific STING silencing via DNA methyltransferase-mediated promoter hypermethylation.
View Article and Find Full Text PDFMol Biomed
September 2025
National Key Laboratory of Immunity and Inflammation & Institute of Immunology, College of Basic Medical Sciences, Naval Medical University, Shanghai, 200433, China.
Dendritic cells (DCs) play a central role in coordinating immune responses by linking innate and adaptive immunity through their exceptional antigen-presenting capabilities. Recent studies reveal that metabolic reprogramming-especially pathways involving acetyl-coenzyme A (acetyl-CoA)-critically influences DC function in both physiological and pathological contexts. This review consolidates current knowledge on how environmental factors, tumor-derived signals, and intrinsic metabolic pathways collectively regulate DC development, subset differentiation, and functional adaptability.
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