Canonical and non-canonical PRC1 differentially contribute to the regulation of neural stem cell fate
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ABSTRACT:
PROVIDER: PRJNA1147753 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30225773_1.fastq.gz | Fastqsanger.gz | |||
| SRR30225773_2.fastq.gz | Fastqsanger.gz | |||
| SRR30225774_1.fastq.gz | Fastqsanger.gz | |||
| SRR30225774_2.fastq.gz | Fastqsanger.gz | |||
| SRR30225775_1.fastq.gz | Fastqsanger.gz |
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Project description:Naturally occurring variations of Polycomb Repressive Complex 1 (PRC1) comprise a core assembly of Polycomb group proteins and additional factors that include, surprisingly, Autism Susceptibility Candidate 2 (AUTS2). While AUTS2 is often disrupted in patients with neuronal disorders, the underlying mechanism is unclear. We investigated the role of AUTS2 as part of a previously identified PRC1 complex (PRC1-AUTS2), and in the context of neurodevelopment. In contrast to the canonical role of PRC1 in gene repression, PRC1-AUTS2 activates transcription. Biochemical studies demonstrate that the CK2 component of PRC1-AUTS2 thwarts PRC1 repressive activity and AUTS2-mediated recruitment of P300 leads to gene activation. ChIP-seq of AUTS2 shows that it regulates neuronal gene expression through promoter association. Conditional CNS targeting of Auts2 in a mouse model leads to various developmental defects. These findings reveal a natural means of subverting PRC1 activity, linking key epigenetic modulators with neuronal functions and diseases. mRNA profiles of P1 brain from wild type mice were generated by deep sequencing
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