PubMed · 6080655
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A Katzenstein. 1967. [EEG studies under hypnosis].. https://pubmed.ncbi.nlm.nih.gov/6080655/
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DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.
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Schizophrenia remains an enigmatic condition. It would appear that both genetic and environmental influences are relevant to the aetiopathogenesis of the disorder. Although a great amount of research has been carried out concerning the condition, the results have often lead to further questions and attempts to more closely delineate the object of study have lead to the originally observed findings becoming tenuous. One way to objectively view some aspects of this large body of work is to consider the condition as a cerebral situs inversus, as data from various lines of reasoning have suggested an inversion of the situation seen in normal controls. The hypothesis presented here draws on existing biological evidence to argue the likely role of light as a relevant, stimulatory variable which may interact with asymmetrical cerebral maturation in the establishment of functional laterality.