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Genome-wide maps of histone H3K9/K14 acetylation state in HeLa cells control (Mock) or silenced for Gb3 globoside synthase (Gb3S_KD) or silenced for the epigenetic modulator AUTS2 (AUTS2_KD)

ABSTRACT: Genome-wide maps of histone H3K9/K14 acetylation state in HeLa cells control (Mock) or silenced for Gb3 globoside synthase (Gb3S_KD) or silenced for the epigenetic modulator AUTS2 (AUTS2_KD)

PROVIDER: PRJNA418910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6301943.fastq.gz	Fastqsanger.gz
	SRR6301944.fastq.gz	Fastqsanger.gz
	SRR6301945.fastq.gz	Fastqsanger.gz
	SRR6301946.fastq.gz	Fastqsanger.gz
	SRR6301947.fastq.gz	Fastqsanger.gz

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Genome-wide maps of histone H3K9/K14 acetylation state in HeLa cells control (Mock) or silenced for Gb3 globoside synthase (Gb3S_KD) or silenced for the epigenetic modulator AUTS2 (AUTS2_KD)

Project description:Glycosphingolipid metabolism is reprogrammed during neural development with a switch from globo to ganglio-series glycosphingolipids production. We discovered that globo-series glycosphingolipids repress the epigenetic regulator of neuronal genes expression AUTS2. AUTS2 in turn, binds and activates the promoter of the first and rate limiting ganglioside producing enzyme GM3 synthase, thus fostering the synthesis of gangliosides. By this mechanism the globo-AUTS2 axis controls glycosphingolipid reprogramming and neural genes expression during neural differentiation, which involves this circuit in neurodevelopment and its defects in neuropathology. We report Gb3 globoside suppresses the expression of the epigenetic modulator AUTS2. The silencing of Gb3 synthase in HeLa cells induces the thepletion of Gb3 globoside, consequentially promoting AUTS2 expression. AUTS2 in turn, binds and activates the promoter of the target genes promoting local histone hyperacetylation and gene expression. Thus, the globo-series glycosphingolipids, by counteracting the expression of AUTS2, decrease histone acetylation at neuronal gene promoters repressing their transcription in HeLa cells.

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AUTS2 project

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The lipid Gb3 promotes germinal center B cell responses and anti-viral immunity

Project description:Influenza viruses escape immunity due to rapid antigenic evolution, which requires vaccination strategies that allow for broadly protective antibody responses. Here, we demonstrate that the lipid globotriaosylceramide (Gb3) expressed on germinal center (GC) B cells is essential for the production of high-affinity antibodies. Mechanistically, Gb3 binds and disengages CD19 from its chaperone CD81 for subsequent translocation to the B cell receptor (BCR) complex to trigger signaling. Moreover, this lipid regulates MHC-II expression to increase diversity of T follicular helper (Tfh) and GC B cells reactive with subdominant epitopes. In influenza infection, Gb3 promotes broadly reactive antibody responses and cross-protection. Thus, we show that Gb3 determines affinity as well as breadth in B cell immunity and propose this lipid as potential vaccine adjuvant against viral infection.

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RNA-seq analysis dataset: Hippocampal tissues from Emx1-Cre;Auts2-flox/flox and Auts2-flox/flox mice at P14

Project description:Previous studies have revealed that AUTS2 regulates cytoskeletal organization as well as gene expression during prenatal brain development. Its involvement in controlling synapses, however, remains unclear. Here, we report the increased dendritic spine formation in Auts2 mutant mice as well as the primary cultured neurons from Auts2 mutant mice. To investigate the involvement of AUTS2 function in the regulation of gene expression, we performed transcriptome analysis. RNA-seq on total RNA from the hippocampal tissues of Emx1Cre/+;Auts2flox/flox homozygous conditional KO mice at P14 reveals changes in gene associated with brain development including synapse formation. These results suggest that AUTS2 regulates the expression of genes that are related to synapse formation/function, and some of which may be involved in spine number restriction. Aberrant expression of such synaptic genes may cause synaptic dysfunction in patients with AUTS2 mutations.

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An Auts2-Containing RNA-Binding Complex Regulates Transcript Expression in Developing Cerebral Cortex

Project description:Molecular functions of the intellectual disability syndrome gene AUTS2 remain uncertain. Two mechanisms of Auts2 function have been proposed. One study found that Auts2 modifies Polycomb repressive complex 1 (PRC1) to activate transcription of target neurodevelopmental genes by recruiting EP300, a histone acetyltransferase. A second study found that cytoplasmic AUTS2 regulates cytoskeletal assembly through PREX1 to promote neurite outgrowth and migration. To further investigate Auts2 functions, we screened for AUTS2 interactors in cerebral cortex, and profiled changes of transcript expression in the developing cortex of Auts2 conditional mutant mice. AUTS2 immunoprecipitation experiments identified interactions with proteins involved in pre-mRNA processing, and mRNAs, including those encoding EP300 and PREX1, both bound by AUTS2-containing complexes and dysregulated in Auts2 mutant cortex. We propose that AUTS2 interacts with an RNA-binding complex that directly targets transcripts encoding Auts2 effectors. This mechanism provides a unifying model that accounts for previously disparate hypotheses of AUTS2 functions.

2021-05-21 | GSE112792 | GEO

AUTS2 confers transcriptional activation to PRC1 in the CNS (RNA-Seq)

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.

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AUTS2 confers transcriptional activation to PRC1 in the CNS (ChIP-Seq)

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NRF1 Association with AUTS2-Polycomb Mediates Specific Gene Activation in the Brain

Project description:Polycomb group (PcG) proteins are evolutionarily conserved chromatin-modifying factors that regulate gene expression to control tissue development. We previously discovered an AUTS2?Polycomb complex activates gene expression by recruiting Casein kinase 2 (CK2) and P300. But the mechanisms underlying the recruitment of AUTS2-PRC1 to chromatin and the physiological relevance of AUTS2-P300 interaction during neurodevelopment remain unknown. Here, we report that the transcription factor Nuclear Respiratory Factor 1 (NRF1) physically interacts with AUTS2 and overlaps with AUTS2 on chromatin binding. In a functional study combined with the single cell RNA-seq approach, we demonstrate that NRF1 is required for AUTS2 recruitment to chromatin, ncPRC1 associated active transcription in motor neuron and thereby modulates multipotent progenitors to motor neuron differentiation. Moreover, we discover that mutations within AUTS2 HX repeat region, which associate with RSTS phenotype disrupt AUTS2-P300 interaction and AUTS2 mediated transcriptional activation. Together, these findings reveal the underlying mechanism by which the AUTS2-containing ncPRC1 complex is recruited and activates transcription and mutations in the AUTS2 HX repeat region exert a dominant negative effect on AUTS2-P300 mediated transcriptional activation in RSTS.

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