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Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [ATAC-seq]

ABSTRACT: Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [ATAC-seq]

PROVIDER: PRJNA731879 | ENA |

REPOSITORIES: ENA

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Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model

Project description:Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model

| PRJNA731874 | ENA

Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [PolII_Ser5_Chip-seq]

Project description:Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [PolII_Ser5_Chip-seq]

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Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [Total_PolII_Chip-seq]

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Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [TotalStranded-RNA-seq]

Project description:Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [TotalStranded-RNA-seq]

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Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [polyA-RNA-seq]

Project description:Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [polyA-RNA-seq]

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Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [ATAC-seq]

Project description:Purkinje cells are large (>40um) and highly euchromatic, although detailed structural aspects of chromatin in these cells is lacking. To understand if the susceptibility of Purkinje neurons to DNA damage involves chromatin structure, we used ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to examine chromatin accessibility.

2021-12-14 | GSE174838 | GEO

Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [polyA-RNA-seq]

Project description:DNA damage can promote altered RNA splicing and decreased gene expression (Gregersen and Svejstrup, 2018; Milek et al., 2017; Munoz et al., 2009; Shkreta and Chabot, 2015), and aberrant splicing is implicated in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Fragile X syndrome and spinal muscular atrophy (SMA) (Conlon et al., 2016; Jia et al., 2012; Loomis et al., 2014; Qiu et al., 2014; Scotti and Swanson, 2016). Therefore, we used RNA-seq data to assess RNA-splicing in double-mutant brain tissue using multivariate analysis of transcriptional splicing (rMATS) (Shen et al., 2014) and a splicing deficiency score algorithm (Bai et al., 2013) to assess intron retention.

2021-12-14 | GSE174841 | GEO

Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-14 | GSE174842 | GEO

Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [Total_PolII_Chip-seq]

Project description:Alterations in RNA Polymerase II kinetics can affect key co-transcriptional processes such as normal splicing and transcript elongation and can influence nonsense mediated decay (Fong et al., 2014; Jonkers and Lis, 2015). Specific types of DNA damage can variably influence RNA Pol II activity. We performed Total RNA Pol ll ChIP-seq to investigate how the chronic DNA damage can affect RNA Pol ll activity in the cerebellum tissues.

2021-12-14 | GSE176511 | GEO

Examining Pathogenesis in Genome Instability Associated Neurodegenerative Mouse Model [PolII_Ser5_Chip-seq]

Project description:Alterations in RNA Polymerase II kinetics can affect key co-transcriptional processes such as normal splicing and transcript elongation and can influence nonsense mediated decay (Fong et al., 2014; Jonkers and Lis, 2015). Specific types of DNA damage can variably influence RNA Pol II activity. Thus, we performed RNA Pol ll pSer5 ChIP-seq to investigate how the chronic DNA damage can affect to RNA Pol ll activity in the cerebellum tissues.

2021-12-14 | GSE174839 | GEO

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