Cellular differentiation requires extensive alterations in chromatin structure and function, which is elicited by the coordinated action of chromatin and transcription factors. By contrast with transcription factors, the roles of chromatin factors in differentiation have not been systematically characterized. Here, we combine bulk ex vivo and single-cell in vivo CRISPR screens to characterize the role of chromatin factor families in hematopoiesis. We uncover marked lineage specificities for 142 chromatin factors, revealing functional diversity among related chromatin factors (i.e. barrier-to-autointegration factor subcomplexes) as well as shared roles for unrelated repressive complexes that restrain excessive myeloid differentiation. Using epigenetic profiling, we identify functional interactions between lineage-determining transcription factors and several chromatin factors that explain their lineage dependencies. Studying chromatin factor functions in leukemia, we show that leukemia cells engage homeostatic chromatin factor functions to block differentiation, generating specific chromatin factor-transcription factor interactions that might be therapeutically targeted. Together, our work elucidates the lineage-determining properties of chromatin factors across normal and malignant hematopoiesis.
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http://dx.doi.org/10.1038/s41588-023-01471-2 | DOI Listing |
Methods Mol Biol
January 2025
Genes & Human Disease Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
ChIP-Seq is used to study DNA-protein interactions, unraveling chromatin states and gene regulatory properties of transcription factors. ChIP-Seq involves immunoprecipitation followed by sequencing using Next-Generation sequencing approaches. The ENCODE consortium provides extensive guidelines for ChIP-Seq analysis.
View Article and Find Full Text PDFMethods Mol Biol
January 2025
Department of Integrative Biology and Physiology, Medical School, Lillehei Heart Institute, University of Minnesota, Minneapolis, MN, USA.
Homeobox genes (HOX), the master regulators, deploy a unique set of target genes to coordinate and orchestrate the spatiotemporal development of an organism. HOX encoded transcriptional factors regulate the expression of target genes by binding to the specific sequences on the genome. Chromatin Immunoprecipitation (ChIP) and Chromatin Immunoprecipitation with Sequencing (ChIP-Seq) are widely used to map and understand specific gene locus and global regulatory regions on the genome.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
ATP-dependent chromatin remodeling protein ATRX is an essential regulator involved in maintenance of DNA structure and chromatin state and regulation of gene expression during development. ATRX was originally identified as the monogenic cause of X-linked α-thalassemia mental retardation (ATR-X) syndrome. Affected individuals display a variety of developmental abnormalities and skeletal deformities.
View Article and Find Full Text PDFCell
December 2024
Department of Genetics, University of Georgia, Athens, GA, USA. Electronic address:
Cis-regulatory elements (CREs) precisely control spatiotemporal gene expression in cells. Using a spatially resolved single-cell atlas of gene expression with chromatin accessibility across ten soybean tissues, we identified 103 distinct cell types and 303,199 accessible chromatin regions (ACRs). Nearly 40% of the ACRs showed cell-type-specific patterns and were enriched for transcription factor (TF) motifs defining diverse cell identities.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Medicine, Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Transmembrane integrin-associated protein functions as a potent innate immunity checkpoint and is upregulated by many types of malignant cells, including melanoma during tumor progression. Binding of to its target receptor, SIRPα, on myeloid cell lineages leads to the initiation of the downstream signaling cascades that inhibit innate immunity anti-tumor responses. Molecular mechanisms underlying upregulation of during melanoma progression remain largely unknown.
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