PubMed · 10478351
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I Nakano. 1999. [Polymicrogyria].. https://pubmed.ncbi.nlm.nih.gov/10478351/
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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.
Fifteen subjects participated in a matching task of visual stimuli. Two sequentially presented stimuli in a pair were the same shape (shape match), different shapes (shape mismatch), same human face (face match) or different faces (face mismatch). All four kinds of stimulus pairs were of equal probability. The shape mismatch pairs elicited a negative event-related potential component N270 (Peak latency: 262.1+/-16.5 ms, P4) after the second stimulus onset, while the face mismatch evoked N270 with longer peak latency (301.2+/-19.8 ms, P4) and N450. There exists a specific system for mismatch processing of a complex stimulus (face) in the human brain.