Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice
2019
Villo Muha | Ritchie Williamson | Rachel Hills | Alison D. McNeilly | Thomas G. McWilliams | Jana Alonso | Marianne Schimpl | Aneika C. Leney | Albert J. R. Heck | Calum Sutherland | Kevin D. Read | Rory J. McCrimmon | Simon P. Brooks | Daan M. F. van Aalten
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.
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