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Virus-induced apoptosis in human cerebral organoids occurs primarily in committed neurons and is associated with a limited interferon stimulated gene response

ABSTRACT: Virus-induced apoptosis in human cerebral organoids occurs primarily in committed neurons and is associated with a limited interferon stimulated gene response

PROVIDER: PRJNA543536 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9087166.fastq.gz	Fastqsanger.gz
	SRR9087167.fastq.gz	Fastqsanger.gz
	SRR9087168.fastq.gz	Fastqsanger.gz
	SRR9087169.fastq.gz	Fastqsanger.gz

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Virus-induced apoptosis in human cerebral organoids occurs primarily in committed neurons and is associated with a limited interferon stimulated gene response

Project description:La Crosse virus (LACV) is the leading cause of pediatric arboviral encephalitis in the USA. Although the hallmarks of disease are infection and apoptosis of neurons, there is limited knowledge of neuronal responses to virus infection at differing neurodevelopmental stages. Here, we infected induced pluripotent stem-cell (iPSC)-derived human cerebral organoids (COs) containing actively maturing populations of neuronal-lineage cells to examine this process. LACV readily infected COs and caused reduced cell viability. Although neural progenitors and committed neurons were similarly infected, significantly more committed neurons underwent apoptosis. Committed neurons expressed fewer interferon (IFN)-inducible transcripts in response to infection compared to neural progenitors, suggesting a poor anti-viral response. Treatment of infected COs with recombinant IFNs enhanced cell viability, demonstrating a therapeutic potential. This study demonstrates that LACV differentially induces apoptosis in neuronal-lineage cells depending on their stage of maturation and provides analysis for why these cells differ in their responses.

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Promoter-enhancer communication occurs primarily within Gene Unit Sub-TADs (GUSTs)

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Project description:Metazoan chromosomes are sequentially partitioned into topologically associating domains (TADs) and then into smaller sub-domains. One class of sub-domains, insulated neighborhoods, are proposed to spatially sequester and insulate the enclosed genes through self-association and chromatin looping. However, it has not been determined functionally whether promoter-enhancer interactions and gene regulation are broadly restricted to within these loops. Here, we employed published datasets from murine embryonic stem cells (mESCs) to identify insulated neighborhoods that confine promoter-enhancer interactions and demarcate gene regulatory regions. To directly address the functionality of these regions, we depleted estrogen-related receptor β (Esrrb), which binds the Mediator co-activator complex, to impair enhancers of genes within 222 insulated neighborhoods without causing mESC differentiation. Esrrb depletion reduces Mediator binding, promoter-enhancer looping, and expression of both nascent RNA and mRNA within the insulated neighborhoods without significantly affecting the flanking genes. Our data indicate that insulated neighborhoods represent functional regulons in mammalian genomes.

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Project description:Hematopoietic conditional knockout (cKO) of Phf6 in a mouse retroviral-HoxA9 AML model led to increased transplantability. We performed bulk RNA-Seq on the 'committed' population (c-Kit+, Ly6C+) sort purified from primary recipients of HoxA9-transduced Ctrl (Vav-Cre/+, Phf6 +/Y marrow transduced with HoxA9) and cKO cells (Vav-Cre/+, Phf6 flox/Y marrow transduced with HoxA9) 8 weeks after transplantation. Our results reveal that Phf6 deletion has minimal effects on the transcriptome of the committed population (see separately deposited series for effects on the transcriptome of leukemia initiating [LIC-e] cells).

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Promoter-enhancer communication occurs primarily within Gene Unit Sub-TADs (GUSTs)

Project description:The mammalian genome is sequentially partitioned from chromosomes into looped chromatin regions termed Topologically Associating Domains (TADs), and then into numerous smaller sub-TAD loops, each bounded and insulated by CTCF and Cohesin. The sub-TADs encompass enhancers, promoters and often multiple genes but whether promoter-enhancer interactions and gene regulation are broadly restricted to within the sub-TAD loops has not been functionally determined. Here we identify “Gene Unit Sub-TADs” or GUSTs as a class of sub-TADs that confine promoter-enhancer interactions and demarcate functional gene regulatory regions. We depleted Estrogen-related receptor β (Esrrb), which binds to the Mediator co-activator complex, to impair the activity of enhancers controlling 245 mouse embryonic stem cell genes. We find that most Esrrb-responsive enhancers lack significant Cohesin binding but instead correlate with Mediator binding. Esrrb depletion causes reduced Mediator binding, decreased nascent RNA expression and diminished promoter-enhancer looping. In 88% of the cases examined, the effects of Esrrb depletion are restricted to enhancers and target genes within GUSTs. In some GUSTs, active genes lay alongside inactive ones but are distinguished by their proximal promoter chromatin accessibility, explaining further the specificity of enhancer-promoter interactions within GUSTs. Our data indicate that GUSTs represent functional gene regulons in mammalian genomes.

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