Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice. Issue 11 (27th November 2019)

• Record Type: Journal Article
• Authors: Muha, Villo; Williamson, Ritchie; Hills, Rachel; McNeilly, Alison D.; McWilliams, Thomas G.; Alonso, Jana; Schimpl, Marianne; Leney, Aneika C.; Heck, Albert J. R.; Sutherland, Calum; Read, Kevin D.; McCrimmon, Rory J.; Brooks, Simon P.; van Aalten, Daan M. F.
• Is Part Of: Open biology. Volume 9:Issue 11(2019)
• Publication Date: 2019-11-27
• Subjects: O-GlcNAcylation -- CRMP2 -- crosstalk -- cognitive function; Biology -- Periodicals; 570
• DOI: 10.1098/rsob.190192
• Languages: English
• ISSNs: 2046-2441

Abstract

Abstract : Abstract : 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 Crmp2 S517A 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.