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Alpha-synuclein supports type 1 interferon signaling in neurons and brain tissue

ABSTRACT: To investigate broad difference in gene expression in mice wild-type for or knockout for alpha-synuclein during infeciton, we infected mice via footpad infection with West Nile Virus and measured full brain gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE205140 | GEO | 2022/06/02

REPOSITORIES: GEO

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Global gene expression in response to West Nile virus in mouse spleen and liver

Project description:Purpose of this experiment was to further understand how innate immune defenses impact host response and West Nile virus tissue tropism. This study examined host-transcriptional response to West Nile virus in permissive and nonpermissive tissues using wildtype mice and mice with genetically altered interferon signaling pathways. Age-matched six to twelve week old mice were inoculated subcutaneously in the left rear footpad with 100 PFU of West Nile virus isolate TX 2002-HC (WNV-TX) in a 10 microL inoculum diluted in Hanks balanced salt solution (HBSS) supplemented with 1% heat-inactivated FBS. Mice were monitored daily for morbidity and mortality. Expression oligonucleotide arrays were performed on RNA isolated from spleen and liver tissues from strain and time-matched mock infected mice (n=2) and WNV-TX infected wild type (WT; n=3; day 4 post-infection), Ips-1-/-(n=3; day 4 post-infection), Ifnar-/- (n=3; day 2 post-infection), and Ips-1-/-xIfnar-/- (DKO; n=3; day 4 post-infection) mice.

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Alpha-synuclein supports type 1 interferon signaling in neurons and brain tissue

Project description:Alpha-synuclein supports type 1 interferon signaling in neurons and brain tissue

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Global gene expression in response to West Nile virus in mouse spleen and liver

2012-12-19 | GSE39259 | GEO

Alpha-synuclein supports type 1 interferon signalling in neurons and brain tissue.

Project description:The protein alpha-synuclein is predominantly expressed in neurons and is associated with neurodegenerative diseases like Parkinson's disease and dementia with Lewy bodies. However, the normal function of alpha-synuclein in neurons is not clearly defined. We have previously shown that mice lacking alpha-synuclein expression exhibit markedly increased viral growth in the brain, increased mortality and increased neuronal cell death, implicating alpha-synuclein in the neuronal innate immune response. To investigate the mechanism of alpha-synuclein-induced immune responses to viral infections in the brain, we challenged alpha-synuclein knockout mice and human alpha-synuclein knockout dopaminergic neurons with RNA virus infection and discovered that alpha-synuclein is required for neuronal expression of interferon-stimulated genes. Furthermore, human alpha-synuclein knockout neurons treated with type 1 interferon failed to induce a broad range of interferon stimulated genes, implying that alpha-synuclein interacts with type 1 interferon signalling. We next found that alpha-synuclein accumulates in the nucleus of interferon-treated human neurons after interferon treatment and we demonstrated that interferon-mediated phosphorylation of STAT2 is dependent on alpha-synuclein expression in human neurons. Next, we found that activated STAT2 co-localizes with alpha-synuclein following type 1 interferon stimulation in neurons. Finally, we found that brain tissue from patients with viral encephalitis expresses increased levels of phospho-serine129 alpha-synuclein in neurons. Taken together, our results show that alpha-synuclein expression supports neuron-specific interferon responses by localizing to the nucleus, supporting STAT2 activation, co-localizing with phosphorylated STAT2 in neurons and supporting expression of interferon-stimulated genes. These data provide a novel mechanism that links interferon activation and alpha-synuclein function in neurons.

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