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BCL7A 包含的 SWI/SNF/BAF 复合物在神经祖细胞分化过程中调节线粒体生物能量学。

BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

机构信息

German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

Institute of Reconstructive Neurobiology, University of Bonn Medical Faculty and University Hospital Bonn, Bonn, Germany.

出版信息

EMBO J. 2022 Dec 1;41(23):e110595. doi: 10.15252/embj.2022110595. Epub 2022 Oct 28.

DOI:10.15252/embj.2022110595
PMID:36305367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9713712/
Abstract

Mammalian SWI/SNF/BAF chromatin remodeling complexes influence cell lineage determination. While the contribution of these complexes to neural progenitor cell (NPC) proliferation and differentiation has been reported, little is known about the transcriptional profiles that determine neurogenesis or gliogenesis. Here, we report that BCL7A is a modulator of the SWI/SNF/BAF complex that stimulates the genome-wide occupancy of the ATPase subunit BRG1. We demonstrate that BCL7A is dispensable for SWI/SNF/BAF complex integrity, whereas it is essential to regulate Notch/Wnt pathway signaling and mitochondrial bioenergetics in differentiating NPCs. Pharmacological stimulation of Wnt signaling restores mitochondrial respiration and attenuates the defective neurogenic patterns observed in NPCs lacking BCL7A. Consistently, treatment with an enhancer of mitochondrial biogenesis, pioglitazone, partially restores mitochondrial respiration and stimulates neuronal differentiation of BCL7A-deficient NPCs. Using conditional BCL7A knockout mice, we reveal that BCL7A expression in NPCs and postmitotic neurons is required for neuronal plasticity and supports behavioral and cognitive performance. Together, our findings define the specific contribution of BCL7A-containing SWI/SNF/BAF complexes to mitochondria-driven NPC commitment, thereby providing a better understanding of the cell-intrinsic transcriptional processes that connect metabolism, neuronal morphogenesis, and cognitive flexibility.

摘要

哺乳动物 SWI/SNF/BAF 染色质重塑复合物影响细胞谱系决定。虽然这些复合物对神经祖细胞 (NPC) 增殖和分化的贡献已有报道，但对于决定神经发生或神经胶质发生的转录谱知之甚少。在这里，我们报告 BCL7A 是 SWI/SNF/BAF 复合物的调节剂，可刺激 ATP 酶亚基 BRG1 的全基因组占据。我们证明 BCL7A 对于 SWI/SNF/BAF 复合物的完整性不是必需的，而对于调节分化 NPC 中的 Notch/Wnt 信号通路和线粒体生物发生是必需的。Wnt 信号通路的药理学刺激恢复了线粒体呼吸，并减弱了缺乏 BCL7A 的 NPC 中观察到的神经发生模式缺陷。一致地，使用线粒体生物发生的增强剂吡格列酮处理可部分恢复线粒体呼吸并刺激 BCL7A 缺陷 NPC 的神经元分化。使用条件性 BCL7A 敲除小鼠，我们揭示了 NPC 和有丝分裂后神经元中 BCL7A 的表达对于神经元可塑性是必需的，并支持行为和认知表现。总之，我们的研究结果定义了含有 BCL7A 的 SWI/SNF/BAF 复合物对线粒体驱动的 NPC 分化的特定贡献，从而更好地理解了连接代谢、神经元形态发生和认知灵活性的细胞内在转录过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c87/9713712/27d15c7d2b9c/EMBJ-41-e110595-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c87/9713712/9f6adf73824f/EMBJ-41-e110595-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c87/9713712/2dea36b91dd3/EMBJ-41-e110595-g005.jpg
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