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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE174839 | GEO | 2021/12/14

REPOSITORIES: GEO

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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 [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.

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Project description:DNA damage response (DDR) involves dramatic transcriptional alterations, the mechanisms of which remain obscure. Here we show that following DNA damage, the RNA-binding motif protein 7 (RBM7) stimulates RNA polymerase II (Pol II) elongation and increases cell viability by activating the positive transcription elongation factor b (P-TEFb). This is mediated by DNA damage-enhanced binding of RBM7 to 7SK, the scaffold of the 7SK small nuclear ribonucleoprotein (snRNP) that inhibits P-TEFb. As a result, P-TEFb relocates from 7SK snRNP to chromatin to activate transcription of key DDR genes and multiple classes of non-coding RNAs. By alleviating the inhibition of P-TEFb, RBM7 thus promotes Pol II elongation to activate a transcriptional response that is crucial for cell fate upon genotoxic insult. Our work highlights a novel paradigm in stress-dependent control of Pol II pause release, and offers the promise of combating cancer by RBM7 and P-TEFb antagonists in combination with established DNA damage-inducing chemotherapeutics.

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