Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice
Research output: Contribution to journal › Article › peer-review
Authors
Colleges, School and Institutes
External organisations
- University of Dundee
- University of Bradford
- Cardiff University
- Utrecht University
- Netherlands Proteomics Centre
- University of Helsinki
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 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.
Details
Original language | English |
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Article number | 190192 |
Pages (from-to) | 1-15 |
Number of pages | 15 |
Journal | Open Biology |
Volume | 9 |
Issue number | 11 |
Publication status | Published - 27 Nov 2019 |
Keywords
- cognitive function, CRMP2, crosstalk, O-GlcNAcylation