Chromatin state transitions in the Drosophila intestinal lineage reveal principles of cell type specification [DamID]
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE224965 | GEO | 2023/10/26
REPOSITORIES: GEO
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Project description:To investigate the chromatin state into an adult stem cell lineage, we generate cell-type specific chromatin state maps in the adult Drosophila intestine and identify principal chromatin state transitions during lineage determination. we profiled the binding sites of five chromatin-associated proteins from which the previously described five major types of chromatin.
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Project description:DNA methylation, in concert with other epigenetic regulators, controls the accessibility of transcription factors to DNA. While comprehensively described in the development of neuronal progenitors, the role of DNA methylation/demethylation in neuronal lineage/subtype specification is not known. By profiling two distinct neuronal lineages, and five neuron subtypes in the hippocampus and striatum, we uncovered a set of five principles that govern DNA methylation dynamics in neurodevelopment. By dividing neurodevelopment to three alternating methylation and demethylation periods and applying the principles to each of these stages, we created a matrix that comprehensively describes the targets, genomic contexts, functional consequences and putative mechanisms of methylation/demethylation events. The overarching theme is that the developmental methylation program is remarkably similar in the hippocampal and striatal lineages, with significant divergence only occurring during subtype specification. Our matrix can be cross-referenced with disease-associated epigenetic changes to specify the possible events and underlying principles compromised in disease. Compared tissue from C57BL6 male animals at differenent developmental timepoints and regions for differences in DNA methylation and RNA expression. Additionally Dnmt3a conditional knockdown mice were used to determine role of Dnmt3a during development.
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Project description:ZNF462 haploinsufficiency is linked to Weiss-Kruszka Syndrome, a genetic disorder characterized by neurodevelopmental defects including Autism. Though conserved in vertebrates and essential for embryonic development the molecular functions of ZNF462 remain unclear. We identified its murine homolog ZFP462 in a screen for mediators of epigenetic gene silencing. Here, we show that ZFP462 safeguards neural lineage specification of mouse embryonic stem cells (ESCs) by targeting the H3K9-specific histone methyltransferase complex G9A/GLP to silence mesoendodermal genes. ZFP462 binds to transposable elements (TEs) that are potential enhancers harboring ESC-specific transcription factor (TF) binding sites. Recruiting G9A/GLP, ZFP462 seeds heterochromatin, restricting TF binding. Loss of ZFP462 in ESCs results in increased chromatin accessibility at target sites and ectopic expression of mesoendodermal genes. Taken together, ZFP462 confers lineage- and locus-specificity to the broadly expressed epigenetic regulator G9A/GLP. Our results suggest that aberrant activation of lineage non-specific genes in the neuronal lineage underlies ZNF462-associated neurodevelopmental pathology.
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Project description:UNLABELLED:Although comprehensively described during early neuronal development, the role of DNA methylation/demethylation in neuronal lineage and subtype specification is not well understood. By studying two distinct neuronal progenitors as they differentiate to principal neurons in mouse hippocampus and striatum, we uncovered several principles governing neuronal DNA methylation during brain development. (1) The program consists of three stages: an initial genome-wide methylation during progenitor proliferation is followed by loss of methylation during the transition of regional progenitors to "young" hippocampal/striatal neurons, which is then reversed by gain in methylation during maturation to subtype-specific neurons. (2) At the first two stages, gain and loss of methylation are limited to CpGs, whereas during the third maturation stage, methylation also occurs at non-CpG sites in both lineages. (3) Methylation/demethylation, similar to transcription, are initially highly similar in the two lineages, whereas diversification in methylation and transcription during maturation creates subtype-specific methylation differences. (4) Initially, methylation targets all genomic locations, whereas later, during early and late differentiation, the preferred targets are intronic/intergenic sequences with enhancer-like activity. (5) Differentially methylated genes are enriched in sequential neurodevelopmental functions (such as progenitor proliferation, migration, neuritogenesis, and synaptic transmission); upregulated genes represent current and consecutive stage-specific functions, and downregulated genes represent preceding functions that are no longer required. The main conclusion of our work is that the neuronal methylation/demethylation program is predominantly developmental with minimal lineage specificity, except in the final stage of development when neuron subtype-specific differences also emerge. SIGNIFICANCE STATEMENT:Our work is the first to describe a set of relatively simple rules that govern DNA methylation and demethylation in neuronal development in vivo. By dividing neurodevelopment to three major stages and applying rules to each of them, we created a matrix that comprehensively describes DNA methylation/demethylation events in two neuronal lineages, with a total of 10 cell types spanning the entire neurodevelopment. Beyond increasing our understanding of the epigenetic regulation of normal development, our work will be useful in deciphering how environmental perturbations, such as gestational toxins, drugs, stress, infection, and offspring neglect/maltreatment, interfere with the developmental methylation program.
| S-EPMC4737779 | biostudies-literature