PubMed · 14892870
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B KLOTZ. 1951-10-26. [Psychosomatic perspectives].. https://pubmed.ncbi.nlm.nih.gov/14892870/
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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.
OBJECTIVE: The aim of this study was to examine the relationship between cortical development and cerebral electrical activity at early gestational ages. METHODS: We obtained EEGs (7.2+/-3.8 days) and MR brain images (3.2+/-2.9 days) after birth in 17<30 week gestation infants without evidence of focal brain injury The EEGs were assessed for discontinuity and characteristic maturational features (delta brush, occipital and temporal sawtooth); cortical development was quantified from MR scans using a specially designed computer programme to measure cortical folding. RESULTS: The inter-burst interval shortened and cortical folding increased with increasing post-menstrual age (PMA). In contrast, the minimum duration of bursts was independent of PMA and cortical folding. Delta brush (8-20 Hz activities) was seen at all PMAs; temporal and occipital sawtooth activities were always more prominent than delta brush but were seen less frequently with increasing PMA and complexity of cortical folding. CONCLUSION: There was a positive correlation between some but not all maturational features of the preterm neonatal EEG and the complexity of whole brain cortical folding and PMA. These relationships were strong for the inter-burst interval, a global measure of maturation, but not strongly seen for regional features such as occipital and temporal sawtooth within this gestational age range. SIGNIFICANCE: Combining neurophysiological examination with detailed neuroimaging gives insights into developmental changes occurring in the very preterm brains and suggests further comparative studies focusing on measures of focal brain development at different gestational ages.
INTRODUCTION: We report three cases of brain malformation presenting with a midline mass of dysplastic cortex that we have termed "brain in brain" malformation. RESULTS: The three cases have holoprosencephalic features, including bilateral hemispheric continuity across the midline, single ventricle, midline facial defect and missing olfactory bulbs. All three cases have a midline conglomerate mass of deeply infolded, cortex-lined fissures with major arterial branches, heterotopia and large amount of white matter. The dysplastic mass of cortex and white matter extended into the third ventricle. The cortex and white matter of the dysplastic lesion was continuous with the cortex and white matter, respectively, of the cerebral hemispheres. CONCLUSION: The midline "brain in brain" malformations have some similarities to subcortical heterotopia and extracerebral glioneuronal heterotopia. However, the continuity with the cerebral hemispheres and extension into the ventricle were not reported in subcortical or glioneuronal heterotopia. The common involvement of the midline cortex and extension into the third ventricle implied an anterior segmental prosencephalic abnormality (prosomeres 5/6). However, its pathogenesis remains to be explained.