PubMed · 9075014
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E S Roach. 1997. Tuberous sclerosis: function follows form.. https://doi.org/10.1177/088307389701200201
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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.
In neurophysiology, time delays between concurrently measured time series are usually estimated from the slope of a straight line fitted to the phase spectrum. We point out that this estimate is valid only in the case in which, one signal is a mere time-delayed copy of the other one. We present a procedure for delay estimation that applies to a much wider class of systems with nontrivial phase spectrum like for example lowpass filters. The procedure is based on the Hilbert transform relation between the phase of a linear system and its log gain. The Hilbert transform relation is nonlocal in frequency space, a fact that limits its applicability to experimental data. We explore these limits, and demonstrate that the method is applicable to neurophysiological time series. We present the successful application of the Hilbert transform behavior method to concurrently recorded epicortical brain activity and peripheral tremor. We point out and explain physiologically unreasonable delay estimates given by the traditional method. Finally, we discuss the assumptions underlying the applicability of the Hilbert transform method in the neuroscience context.
P300 event-related brain potential (ERP) amplitude is smaller in patients with schizophrenia compared to unaffected controls, but whether left temporal component amplitude is also smaller is debated. The present study employed meta-analytical methods to quantitatively assess previous P300 schizophrenia asymmetry findings. All P300 articles on schizophrenia using an auditory oddball paradigm published before January 2000 were obtained by comprehensive literature searches and cross-referencing for related articles. A total of 19 original articles reporting complete midline electrode data and 11 articles reporting lateral asymmetry electrode data were reviewed, which included different independent conditions that yielded 50 independent data sets. P300 amplitude differences between patients with schizophrenia and control subjects from the midline electrodes yielded effect sizes that differed among recording sites, such that Fz was significantly smaller than Pz, with Cz effect sizes smaller than Pz but larger than Fz. Comparison of P300 amplitude from the lateral data for the T3 and T4 electrodes found no reliable effect size difference when these electrodes were analyzed separately. However, comparison of P300 amplitude effect sizes from the TCP1 was significantly larger than that from the TCP2 when these electrodes were analyzed separately. P300 amplitude is smaller overall in patients with schizophrenia compared to control subjects and differs in its effect size topography across the midline and temporal electrode sites, with the strongest effect sizes obtained for the Pz midline and TCP1 lateral electrodes.