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Deciphering Motor Dysfunction and Microglial Activation in mThy1-α-Synuclein Mice: A Comprehensive Study of Behavioral, Gene Experssion, and Methylation Changes [Enzymatic Methyl-Seq]

ABSTRACT: Deciphering Motor Dysfunction and Microglial Activation in mThy1-α-Synuclein Mice: A Comprehensive Study of Behavioral, Gene Experssion, and Methylation Changes [Enzymatic Methyl-Seq]

PROVIDER: PRJNA1151599 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30352162_1.fastq.gz	Fastqsanger.gz
	SRR30352162_2.fastq.gz	Fastqsanger.gz
	SRR30352163.fastq.gz	Fastqsanger.gz
	SRR30352163_1.fastq.gz	Fastqsanger.gz
	SRR30352163_2.fastq.gz	Fastqsanger.gz

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Deciphering Motor Dysfunction and Microglial Activation in mThy1-α-Synuclein Mice: A Comprehensive Study of Behavioral, Gene Experssion, and Methylation Changes [Enzymatic Methyl-Seq]

Project description:BACKGROUND: Synucleinopathy disorders are characterized by aggregates of α-synuclein (α-syn), which engage microglia to elicit a neuroinflammatory response. However, the influence α-syn has on DNA methylation and gene expression patterns for other genes has not been thoroughly explored. Our objective is to determine gene expression and methylation changes in microglia induced by aggregate α-syn. METHODS: Transgenic mThy1-Asyn mice overexpressing human α-syn are a model of synucleinopathy. Microglia from 7 and 10-month-old mice were used to isolate nucleic acids for methylated DNA and RNA-sequencing. α-Syn-induced changes in gene expression and genomic methylation were determined and examined for pathway and functional enrichment. RESULTS: Microglial DNA isolated from our 7-month cohort had 6,712 differentially methylated regions (DMR), while RNA levels demonstrated a change in 1,141 differentially expressed genes (DEGs) between mThy1-Asyn mice and wild-type littermate controls. The 7-month DEGs and DMRs were highly associated with neuroinflammation likely via TLR pathways. We observed 8,531 DMRs and 1,686 DEGs in 10-month mThy1-Asyn mice. These genes were often predicted by Ingenuity Pathway Analysis to demonstrate inhibition of previously activated inflammatory pathways at 7 months. CONCLUSION: We observed significant α-syn-induced methylation and gene expression changes in microglia. Our data suggest that α-syn overexpression initiates microglial activation leading to neuroinflammation and cellular metabolic stresses, which is associated with disease progression.

2025-03-05 | GSE275511 | GEO

Deciphering Motor Dysfunction and Microglial Activation in mThy1-α-Synuclein Mice: A Comprehensive Study of Behavioral, Gene Experssion, and Methylation Changes

Project description:Deciphering Motor Dysfunction and Microglial Activation in mThy1-α-Synuclein Mice: A Comprehensive Study of Behavioral, Gene Experssion, and Methylation Changes

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Deciphering Motor Dysfunction and Microglial Activation in mThy1-α-Synuclein Mice: A Comprehensive Study of Behavioral, Gene Experssion, and Methylation Changes [RNA-Seq]

Project description:Deciphering Motor Dysfunction and Microglial Activation in mThy1-α-Synuclein Mice: A Comprehensive Study of Behavioral, Gene Experssion, and Methylation Changes [RNA-Seq]

| PRJNA1151598 | ENA

Quality evaluation of Enzymatic Methyl-seq library constructed using crude cell lysate

Project description:Enzymatic Methyl-seq (EM-seq) is an enzyme-based method giving us reliable methylome data from small amounts of purified DNA. However, it is unclear whether EM-seq library can be constructed from crude cell lysate containing genomic DNA. We evaluated the quality of EM-seq libraries directly prepared from crude cell lysate.

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Alpha-synuclein deficiency affects brain Foxp1 expression and ultrasonic vocalization

Project description:Alpha-synuclein is an abundant protein implicated in synaptic function and plasticity, but the molecular mechanism of its action is not understood. Missense mutations and gene duplication/triplication events result in Parkinson's disease, a neurodegenerative disorder of old age with impaired movement and emotion control. Here, we systematically investigated the striatal as well as the cerebellar transcriptome profile of alpha-synuclein-deficient mice via a genome-wide microarray survey in order to gain hypothesis-free molecular insights into the physiological function of alpha-synuclein. A genotype-dependent, specific and strong downregulation of forkhead box P1 (Foxp1) transcript levels was observed in all brain regions from postnatal age until old age and could be validated by qPCR. In view of the co-localization and heterodimer formation of FOXP1 with FOXP2, a transcription factor with a well established role for vocalization, and the reported regulation of both alpha-synuclein and FOXP2 expression during avian song learning, we performed a detailed assessment of mouse movements and vocalizations in the postnatal period. While there was no difference in isolation-induced behavioral activity in these animals, the alpha-synuclein-deficient mice exhibited an increased production of isolation-induced ultrasonic vocalizations (USVs). This phenotype might also reflect the reduced expression of the anxiety-related GABA-A receptor subunit gamma 2 (Gabrg2) we observed. Taken together, we identified an early behavioral consequence of alpha-synuclein deficiency and accompanying molecular changes, which supports the notion that the neural connectivity of sound or emotion control systems is affected. Factorial design comparing SNCA knock-out mice with wild type littermates in two different tissues (striatum, cerebellum) at two different timepoints (6 and 21 month)

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Alpha-synuclein deficiency affects brain Foxp1 expression and ultrasonic vocalization

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The responses of astrocytes stimulated by extracellular a-synuclein

Project description:Abnormal neuronal aggregation of a-synuclein is implicated in the development of Parkinson’s disease. Glial cells also show extensive a-synuclein pathology and are thought to contribute to disease progression. However, the mechanism that produces the glial a-synuclein pathology and the interaction between neurons and glia in the disease-inflicted microenvironment remain unknown. Here, we show that in neuronal cells misfolded a-synuclein proteins are selectively translocated into vesicles, leading to exocytosis of the aggregated forms. More importantly, our data demonstrate that astrocytes take up the neuron-derived a-synuclein aggregates and produce a-synuclein inclusions similar to the ones found in human brains. This uptake is paralleled by changes in the gene expression profile reflecting an inflammatory response. These results suggest that astroglial a-synuclein pathology is produced by cell-to-cell transmission of neuronal a-synuclein aggregates. This transmission step is thus an important mediator of pathogenic glial responses and could qualify as a new therapeutic target. To determine how astrocytes respond to extracellular a-synuclein, gene expression profiles were established and analyzed for nearly 22,000 rat genes using the Illumina RatRef-12 Expression BeadChip. Total RNA was isolated from astrocytes exposed for 6h or 24h to conditioned medium from cultures of a-synuclein or lacZ expressing cells.

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Impact of Hells loss-of-function on DNA methylation in B cells during humoral immune responses: kinetic comparison of Mb1-Hells knockout and control mice by enzymatic-methyl sequencing

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