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A novel 14-3-3θ phosphomimetic mouse model demonstrates social dominance defects
Mary A Gannon1, Thanushri Srikantha1, Rudradip Pattanayak1
1University of Alabama at Birmingham, Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, Birmingham, AL 35294, USA.
Biology Open
|May 21, 2025
Summary
This study introduces a new mouse model to investigate the role of 14-3-3θ phosphorylation in neurodegenerative diseases like Parkinson's disease (PD). The model shows mild motor deficits but no signs of key disease pathologies.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- 14-3-3 proteins, especially 14-3-3θ, show neuroprotective effects in Parkinson's disease (PD) models.
- Increased 14-3-3θ phosphorylation in neurodegenerative diseases suggests a potential pathogenic role.
Purpose of the Study:
- To create and evaluate a novel mouse model expressing a phosphomimetic mutation (S232D) in 14-3-3θ.
- To investigate the behavioral and pathological consequences of 14-3-3θ phosphorylation at S232 in vivo.
Main Methods:
- Generated a conditional knock-in mouse expressing the 14-3-3θ S232D mutation.
- Crossed with Emx1-Cre mice for cortical and hippocampal expression.
- Assessed behavioral phenotypes, cognitive function, anxiety, and neuropathology.
Main Results:
- Mice with S232D mutation exhibited mild motor deficits and reduced social dominance.
- Cognition and anxiety levels remained normal compared to controls.
- No α-synuclein or phospho-tau pathology was observed; dendritic arborization was normal.
Conclusions:
- The novel S232D phosphomimetic mouse model is a valuable tool for studying 14-3-3θ phosphorylation in neurodegenerative contexts.
- This model can elucidate the specific effects of S232 phosphorylation on neuronal function and disease pathology.
