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

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Muha , V , Williamson , R , Hills , R , McNeilly , A D , McWilliams , T G , Alonso , J , Schimpl , M , Leney , A C , Heck , A J R , Sutherland , C , Read , K D , McCrimmon , R J , Brooks , S P & Van Aalten , D M F 2019 , ' Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice ' , Open biology , vol. 9 , no. 11 . https://doi.org/10.1098/rsob.190192

Title: Loss of CRMP2 O-GlcNAcylation leads to reduced novel object recognition performance in mice
Author: Muha, Villo; Williamson, Ritchie; Hills, Rachel; McNeilly, A.D.; McWilliams, T.G.; Alonso, Jana; Schimpl, Marianne; Leney, Aneika C.; Heck, Albert J.R.; Sutherland, Calum; Read, Kevin D.; McCrimmon, Rory J.; Brooks, S.P.; Van Aalten, Daan M.F.
Contributor organization: Department of Anatomy
STEMM - Stem Cells and Metabolism Research Program
Date: 2019
Language: eng
Number of pages: 15
Belongs to series: Open biology
ISSN: 2046-2441
DOI: https://doi.org/10.1098/rsob.190192
URI: http://hdl.handle.net/10138/326544
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. © 2019 The Authors. Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.
Subject: Cognitive function
CRMP2
Crosstalk
O-GlcNAcylation
collapsin response mediator protein-2
n acetylglucosamine
nerve protein
signal peptide
aging
amino acid sequence
animal
C57BL mouse
cell line
chemistry
cognition
exploratory behavior
female
gene knock-in
genetics
human
male
memory disorder
metabolism
mouse
point mutation
protein processing
short term memory
Acetylglucosamine
Aging
Amino Acid Sequence
Animals
Cell Line
Cognition
Exploratory Behavior
Female
Gene Knock-In Techniques
Humans
Intercellular Signaling Peptides and Proteins
Male
Memory Disorders
Memory, Short-Term
Mice
Mice, Inbred C57BL
Nerve Tissue Proteins
Point Mutation
Protein Processing, Post-Translational
1182 Biochemistry, cell and molecular biology
Peer reviewed: Yes
Rights: cc_by
Usage restriction: openAccess
Self-archived version: publishedVersion


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