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The cell fate decision leading to gametogenesis requires the convergence of multiple signals on the promoter of a master regulator. In fission yeast, starvation-induced signaling leads to the transcriptional induction of the ste11 gene, which encodes the central inducer of mating and gametogenesis, known as sporulation. We find that the long intergenic non-coding (linc) RNA rse1 is transcribed divergently upstream of the ste11 gene. During vegetative growth, rse1 directly recruits a Mug187-Lid2-Set1 complex that mediates cis repression at the ste11 promoter through SET3C-dependent histone deacetylation. The absence of rse1 bypasses the starvation-induced signaling and induces gametogenesis in the presence of nutrients. Our data reveal that the remodeling of chromatin through ncRNA scaffolding of repressive complexes that is observed in higher eukaryotes is a conserved, likely very ancient mechanism for tight control of cell differentiation.
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http://dx.doi.org/10.1016/j.cub.2017.12.048 | DOI Listing |
Tissue Eng Regen Med
September 2025
Department of Biomedical Science, Catholic Kwandong University, 24 Beomil-ro 579beon-gil, Gangneung-si, Gangwon-do, South Korea.
Background: Neurotraumatic conditions, such as spinal cord injury, brain injury, and neurodegenerative conditions, such as amyotrophic lateral sclerosis, pose a challenge to the field of rehabilitation for its complexity and nuances in management. For decades, the use of cell therapy in treatment of neurorehabilitation conditions have been explored to complement the current, mainstay treatment options; however, a consensus for standardization of the cell therapy and its efficacy has not been reached in the medical community. This study aims to provide a comparative review on the very topic of cell therapy use in neurorehabilitation conditions in an attempt to bridge the gap in knowledge.
View Article and Find Full Text PDFACS Nano
September 2025
Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, Key Laboratory of Innovation and Transformation of Advanced Medical Devices of Ministry of Industry and Information Technology, National Medical Innovation Platform for Industry-Education Integration in Advanced Medical Dev
Hyperglycemia-induced oxidative stress and inflammation critically impair diabetic bone defect repair. Here, a radially oriented microchannel scaffold (D-GSH@QZ) was developed via a directional freezing technique integrated with photo-cross-linking strategies. The scaffold was fabricated from gelatin methacryloyl, silk fibroin methacryloyl, and nanohydroxyapatite (HAp) to mimic the natural bone matrix, while incorporating quercetin-loaded ZIF-8 nanoparticles (Qu@ZIF-8) for pathological microenvironment modulation.
View Article and Find Full Text PDFAdv Mater
September 2025
State Key Laboratory of Crystal Materials, Shandong University, Jinan, 250100, P. R. China.
Regulating the differentiation of implanted stem cells into neurons is crucial for stem cell therapy of traumatic brain injury (TBI). However, due to the migratory nature of implanted stem cells, precise and targeted regulation of their fate remains challenging. Here, neural stem cells (NSCs) are bio-orthogonally engineered with hyaluronic acid methacryloyl (HAMA) microsatellites capable of sustained release of differentiation modulators for targeted regulation of their neuronal differentiation and advanced TBI repair.
View Article and Find Full Text PDFBrain
September 2025
Okinawa Institute of Science and Technology Graduate University, Okinawa, 904-0495, Japan.
Animal models of the pathology of Parkinson's disease (PD) have provided most of the treatments to date, but the disease is restricted to human patients. In vitro models using human pluripotent stem cells (hPSCs)-derived neural organoids have provided improved access to study PD etiology. This study established a method to generate human striatal-midbrain assembloids (hSMAs) from hPSCs for modeling alpha-synuclein (α-syn) propagation and recapitulating basal ganglia circuits, including nigrostriatal and striatonigral pathways.
View Article and Find Full Text PDFFront Mol Neurosci
August 2025
Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Lemole Center for Integrated Lymphatics and Vascular Research, Temple University, Philadelphia, PA, United States.
Introduction: Endothelial-to-mesenchymal transition (EndoMT), cell death, and fibrosis are increasingly recognized as contributing factors to Alzheimer's disease (AD) pathology, but the underlying transcriptomic mechanisms remain poorly defined. This study aims to elucidate transcriptomic changes associated with EndoMT, diverse cell death pathways, and fibrosis in AD using the 3xTg-AD mouse model.
Methods: Using RNA-seq data and knowledge-based transcriptomic analysis on brain tissues from the 3xTg-AD mouse model of AD.