Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice

Research output: Contribution to journalArticlepeer-review


  • Villo Muha
  • Ritchie Williamson
  • Rachel Hills
  • Alison D. McNeilly
  • Thomas G. McWilliams
  • Jana Alonso
  • Marianne Schimpl
  • Albert J.R. Heck
  • Calum Sutherland
  • Kevin D. Read
  • Rory J. McCrimmon
  • Simon P. Brooks
  • Daan M.F. Van Aalten

Colleges, School and Institutes

External organisations

  • University of Dundee
  • University of Bradford
  • Cardiff University
  • Utrecht University
  • Netherlands Proteomics Centre
  • University of Helsinki


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.


Original languageEnglish
Article number190192
Pages (from-to)1-15
Number of pages15
JournalOpen Biology
Issue number11
Publication statusPublished - 27 Nov 2019


  • cognitive function, CRMP2, crosstalk, O-GlcNAcylation