Dataset Information

Proteomics and phosphoproteomics of mouse bilateral striatum

ABSTRACT: Proteomics and phosphoproteomics of mouse bilateral striatum

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain

SUBMITTER: Yisheng Jiang

LAB HEAD: Zhiheng Xu

PROVIDER: PXD056740 | Pride | 2025-10-06

REPOSITORIES: Pride

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			Action	DRS
	LUMOS_20230417_XZH_JSY_TIO2_WT_L1.raw	Raw
	LUMOS_20230417_XZH_JSY_TIO2_WT_L2.raw	Raw
	LUMOS_20230417_XZH_JSY_TIO2_WT_L3.raw	Raw
	LUMOS_20230417_XZH_JSY_TIO2_WT_R1.raw	Raw
	LUMOS_20230417_XZH_JSY_TIO2_WT_R2.raw	Raw

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Publications

Autism-related proteins form a complex to maintain the striatal asymmetry in mice.

Jiang Yisheng Y Zhu Feipeng F Zhong Jie J Sun Xiaomei X Yuan Yuting Y Wang Shuo S Chen Haiyang H Xu Zhiheng Z

Cell research 20250902 10

The brain's hemispheres exhibit profound lateralization, yet the underlying mechanisms remain elusive. Using proteomic and phosphoproteomic analyses of the bilateral striatum - a hub for important brain functions and a common node of autism pathophysiology - we identified significant phosphorylation asymmetries. Particularly, the phosphorylation processes in the left striatum appear more prone to disturbance. Notably, SH3RF2, whose single-copy knockout leads to autism spectrum disorder (ASD)-lik ...[more]

PMID: 40890295

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Project description:Huntington’s disease is a fatal autosomal dominant neurodegenerative disorder, characterized by neuronal cell loss, primarily in the striatum, cortex, and hippocampus, causing motor, cognitive, and psychiatric impairments. Unfortunately, no treatments are yet available to modify the progression of the disease. Recent evidence from Huntington’s disease mouse models suggests that protein phosphorylation (catalysed by kinases and hydrolysed by phosphatases) might be dysregulated, making this major posttranslational modification a potential area of interest to find novel therapeutic targets. Furthermore, environmental enrichment (EE), used to model an active lifestyle in preclinical models, has been shown to alleviate Huntington’s disease-related motor and cognitive symptoms. However, the molecular mechanisms leading to these therapeutic effects are still largely unknown. In this study, we applied a phosphoproteomics approach combined with proteomic analyses on brain samples from pre-motor symptomatic R6/1 Huntington’s disease male mice (HD mice) and their wild-type (WT) littermates, after being housed either in EE conditions, or in standard housing (SH) conditions from 4 to 8 weeks of age (n=6 per group). We hypothesised that protein phosphorylation dysregulations occur prior to motor onset in this mouse model, in two highly affected brain regions, the striatum and hippocampus. Furthermore, we hypothesised that these phosphoproteome alterations are rescued by EE. When comparing 8-week-old HD mice and WT mice in SH conditions, our analysis revealed 229 differentially phosphorylated peptides in the striatum, compared to only 15 differentially phosphorylated peptides in the hippocampus (statistical thresholds FDR0.05, FC1.5). At the same disease stage, minor differences were found in protein expression, with 24 and 22 proteins dysregulated in the striatum and hippocampus, respectively. Notably, we found no differences in striatal protein phosphorylation and protein expression when comparing HD mice and their WT littermates in EE conditions. In the hippocampus, only four peptides were differentially phosphorylated between the two genotypes under EE conditions, and 22 proteins were differentially expressed. Together, our data indicates that protein phosphorylation dysregulations occur in the striatum of HD mice, prior to motor symptoms, and that the kinases and phosphatases leading to these changes in protein phosphorylation might be viable drug targets to consider for this disorder. Furthermore, we show that an early environmental intervention was able to rescue the changes observed in protein expression and phosphorylation in the striatum of HD mice and might underlie the beneficial effects of EE, thus identifying novel therapeutic targets.