O-GlcNAcylation is an abundant post-translational modification in the nervous system, linked to both neurodevelopmental and neurodegenerative disease. However, the mechanistic links between these phenotypes and site-specific O-GlcNAcylation remain largely unexplored. Here, we show that Ser517 O-GlcNAcylation of the microtubule-binding protein Collapsin Response Mediator Protein-2 (CRMP2) increases with age. By generating and characterizing a Crmp2S517A knock-in mouse model, we demonstrate that loss of O-GlcNAcylation leads to a small decrease in body weight and mild memory impairment, suggesting that Ser517 O-GlcNAcylation has a small but detectable impact on mouse physiology and cognitive function.

中文翻译：

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CRMP2 O-GlcNAcylation的丢失导致小鼠中新对象识别性能的降低。

O-GlcNAcylation是神经系统中大量的翻译后修饰，与神经发育和神经退行性疾病相关。但是，这些表型和特定于位点的O-GlcNAcylation之间的机制联系仍未开发。在这里，我们显示微管结合蛋白Collapsin Response Mediator Protein-2（CRMP2）的Ser517 O-GlcNAcylation随着年龄的增长而增加。通过生成和表征Crmp2S517A敲入小鼠模型，我们证明了O-GlcNAcylation的缺失导致体重的轻度降低和轻度的记忆障碍，这表明Ser517 O-GlcNAcylation对小鼠的生理和认知能力有很小但可检测的影响功能。