细胞外基质分子 Collagen XVIII/CLE-1 影响神经元树突棘。

microPublication biology Pub Date : 2024-11-05 eCollection Date: 2024-01-01 DOI:10.17912/micropub.biology.001331
Michele Lemons L, Hailey McKillop, Noelia Genao, Michael Francis M
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引用次数: 0

摘要

细胞外基质(ECM)是影响多种细胞功能的丰富的大分子集合;然而,人们对它在神经元突触中的作用还不完全了解。以秀丽隐杆线虫 GABA 能神经元的树突棘为模型,我们发现 ECM 成分胶原 XVIII/ CLE-1 定位于树突棘附近,对树突棘的正常发育和维持非常重要。在 GABA 能神经元中特异性表达 cle-1 可部分挽救 cle-1 ( cg120 ) 突变体中棘突数量的减少。总之,我们的研究结果表明,胶原 XVIII/ CLE-1 部分通过 GABA 能神经元的局部 CLE-1 沉积来调节树突棘。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The extracellular matrix molecule Collagen XVIII/CLE-1 affects neuronal dendritic spines.

The extracellular matrix (ECM) is a rich collection of macromolecules that influences numerous cellular functions; however, its roles at neuronal synapses are not fully understood. Using dendritic spines of Caenorhabditis elegans GABAergic neurons as a model, we found that the ECM component Collagen XVIII/ CLE-1 is localized in close proximity to dendritic spines and is important for their normal development and maintenance. Specific expression of cle-1 in GABAergic neurons partially rescued the reduction in spine number in cle-1 ( cg120 ) mutants . Together, our findings suggest that Collagen XVIII/ CLE-1 regulates dendritic spines, in part through local CLE-1 deposition from GABAergic neurons.

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