During development, neural progenitor cells (NPCs) that are capable of self-renewing maintain a proliferative cellular pool while generating all differentiated neural cell components. Although the genetic network of transcription factors (TFs) required for neural specification has been well characterized, the unique set of histone modifications that accompanies this process has only recently started to be investigated. In vitro neural differentiation of pluripotent stem cells is emerging as a powerful system to examine epigenetic programs. Deciphering the histone code and how it shapes the chromatin environment will reveal the intimate link between epigenetic changes and mechanisms for neural fate determination in the developing nervous system. Furthermore, it will offer a molecular framework for a stringent comparison between native and induced neural stem cells (iNSCs) generated by direct neural cell conversion.
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http://dx.doi.org/10.1016/j.gde.2015.08.003 | DOI Listing |
Indian J Endocrinol Metab
December 2024
Rajiv Gandhi Centre for Diabetes and Endocrinology, J N Medical College and Hospital, Aligarh Muslim University, Aligarh, Uttar Pradesh, India.
Type 2 diabetes (T2D) is a long-term metabolic condition that presents considerable health challenges globally. As the disease progresses, the interplay between genetic, environmental, and lifestyle factors becomes increasingly evident, leading to complications. Epigenetics has emerged as a critical area of research, providing insights into how these factors can modify the expression and cellular behavior without altering the underlying DNA sequence.
View Article and Find Full Text PDFCommun Biol
January 2025
Department of Physiology and Pharmacology, College of Veterinary Medicine, University of Georgia, Athens, GA, 30602, USA.
In mammalian oocytes, large-scale chromatin organization regulates transcription, nuclear architecture, and maintenance of chromosome stability in preparation for meiosis onset. Pre-ovulatory oocytes with distinct chromatin configurations exhibit profound differences in metabolic and transcriptional profiles that ultimately determine meiotic competence and developmental potential. Here, we developed a deep learning pipeline for the non-invasive prediction of chromatin structure and developmental potential in live mouse oocytes.
View Article and Find Full Text PDFGenes Dev
January 2025
Laboratory of Developmental Neurobiology, The Rockefeller University, New York, New York 10065, USA;
Neuronal maturation is guided by changes in the chromatin landscape that control developmental gene expression programs. Histone bivalency, the co-occurrence of activating and repressive histone modifications, has emerged as an epigenetic feature of developmentally regulated genes during neuronal maturation. Although initially associated with early embryonic development, recent studies have shown that histone bivalency also exists in differentiated and mature neurons.
View Article and Find Full Text PDFBioinformatics
January 2025
Department of Medical Bioinformatics, University Medical Center Göttingen, Göttingen, 37099, Germany.
Motivation: Histone modifications play an important role in transcription regulation. Although the general importance of some histone modifications for transcription regulation has been previously established, the relevance of others and their interaction is subject to ongoing research. By training Machine Learning models to predict a gene's expression and explaining their decision making process, we can get hints on how histone modifications affect transcription.
View Article and Find Full Text PDFAging Cell
January 2025
Molecular Biology and Genetics Unit, Transcription and Disease Laboratory, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru, India.
SYNGAP1 is a Ras GTPase-activating protein that plays a crucial role during brain development and in synaptic plasticity. Sporadic heterozygous mutations in SYNGAP1 affect social and emotional behaviour observed in intellectual disability (ID) and autism spectrum disorder (ASD). Although neurophysiological deficits have been extensively studied, the epigenetic landscape of SYNGAP1 mutation-mediated intellectual disability is unexplored.
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