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開催概要

日時

2026年1月14日 (水) 14:00～15:00 (60分)

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ウェビナーにて開催 (ウェビナーとはWebを利用したオンラインによるセミナーです。)

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無料

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以下のホームページリンクより申し込みください
https://v2.nex-pro.com/campaign/88925/apply (セミナー配信会社のホームページへ移動します。)

スケジュール

14:00

開会・注意事項のご説明

14:05～14:30

1) SETDB1 regulates short interspersed nuclear elements and chromatin loop organization in mouse neural precursor cells
【演者：Yan Jiang 様　(Institutes of Brain Science Fudan University)】
《Abstract》
Transposable elements play a critical role in maintaining genome architecture during neurodevelopment. Short Interspersed Nuclear Elements (SINEs), a major subtype of transposable elements, are known to harbor binding sites for the CCCTC-binding factor (CTCF) and pivotal in orchestrating chromatin organization. However, the regulatory mechanisms controlling the activity of SINEs in the developing brain remains elusive.

In our study, we conduct a comprehensive genome-wide epigenetic analysis in mouse neural precursor cells using ATAC-seq, ChIP-seq, whole genome bisulfite sequencing, in situ Hi-C, and RNA-seq. Our findings reveal that the SET domain bifurcated histone lysine methyltransferase 1 (SETDB1)-mediated H3K9me3, in conjunction with DNA methylation, restricts chromatin accessibility on a selective subset of SINEs in neural precursor cells. Mechanistically, loss of Setdb1 increases CTCF access to these SINE elements and contributes to chromatin loop reorganization. Moreover, de novo loop formation contributes to differential gene expression, including the dysregulation of genes enriched in mitotic pathways. This leads to the disruptions of cell proliferation in the embryonic brain after genetic ablation of Setdb1 both in vitro and in vivo.

In summary, our study sheds light on the epigenetic regulation of SINEs in mouse neural precursor cells, suggesting their role in maintaining chromatin organization and cell proliferation during neurodevelopment.

14:30～15:00

2) 神経変性疾患モデルマウスと微小重力環境飼育マウスの脊髄および脊髄神経節の遺伝子発現解析／
Gene expression analysis of the spinal cord and dorsal root ganglion in neurodegenerative disease model mice and microgravity-exposed mice
【演者：吉川 雅朗 様 (大阪歯科大学)／Masaaki Yoshikawa (Osaka Dental University School of Dentistry) 】
《Abstract》
Motor neuron diseases like amyotrophic lateral sclerosis (ALS) and exposure to microgravity (MG) lead to motor deficits such as muscle wasting and reduced neuronal activity. However, the specific link between ALS and MG-related motor neuron degeneration is unclear. To clarify how each condition affects the motor system, we analyzed the impact of mutant SOD1 and MG on gene expression in various cell types of the mouse spinal cord. Using known cell-type markers identified in previous single-cell studies, we examined differentially expressed genes (DEGs) in the spinal cords of SOD1 and MG mice. Most cell types, including neurons, astrocytes, oligodendrocytes, oligodendrocyte precursor cells, meningeal cells, microglia, and vascular cells, exhibited extensive DEGs in the MG spinal cord. Overall, DEGs increased with ALS progression. At postnatal day 30 (P30), we observed distinct abnormalities in putative microglia, meningeal cells, and oligodendrocyte precursor cells in the SOD1 spinal cord. We also assessed neuronal populations in the spinal cord. Putative excitatory and inhibitory neurons were affected more than cholinergic neurons in MG and SOD1 mice. MG affected all putative neuron types, particularly visceral motor neurons, and axon initial segments. Neurons and neuronal components in the SOD1 spinal cord were less affected at P30 but showed an increase with age. These findings indicate ALS pathology and MG are non-cell autonomous and involve various cell types in motor neuron degeneration. We also studied the effects of mutant SOD1 and MG on gene expression in multiple cell types of the mouse dorsal root ganglion (DRG). Using known markers from previous studies, we identified the affected putative cell types in the DRGs of SOD1 and MG mice. DEGs were observed in most cell types, including large neurons, medium/small neurons, satellite glial cells, and Schwann cells, in both the SOD1 and MG DRGs. Abnormalities were observed in putative large/medium neurons and mechanoreceptors in the MG DRG.
The SOD1 DRG showed changes in putative medium neurons, mechanoreceptors, and nociceptors. These results suggest that ALS pathology and MG differentially affect various DRG neurons, potentially contributing to motor neuron degeneration.

15:00

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