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Virulence regulates and boosts CRISPR-Cas9 immunity in Group B Streptococcus [CrispRseq]

ABSTRACT: Virulence regulates and boosts CRISPR-Cas9 immunity in Group B Streptococcus [CrispRseq]

PROVIDER: PRJNA1122103 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29341860.fastq.gz	Fastqsanger.gz
	SRR29341861.fastq.gz	Fastqsanger.gz
	SRR29341862.fastq.gz	Fastqsanger.gz
	SRR29341863.fastq.gz	Fastqsanger.gz
	SRR29341864.fastq.gz	Fastqsanger.gz

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Virulence regulates and boosts CRISPR-Cas9 immunity in Group B Streptococcus [CrispRseq]

Project description:Bacterial CRISPR-Cas9 immune systems protect against foreign DNA. However, immune efficiency is constrained by Cas9 off-target effects and toxicity. Here, we demonstrate that CRISPR-Cas9 immunity is regulated by CovR, the major regulator of virulence in Group B Streptococcus, a pathobiont responsible for neonatal invasive infections. We show that CovR binds to and represses a distal promoter of the cas operon, embedding immunity in the virulence regulatory network. Releasing CovR repression enhances immune efficiency against suboptimal spacers, originating from old immune memory or mutations, thereby transiently expanding the sequence space recognized and cleaved by Cas9. Furthermore, CovR inactivation promotes the acquisition of new spacers, enhancing immune memory. CovR-mediated immune regulation is conserved at the species level, with lineage-specific variability in the constitutive cas promoter and Cas9 variants, suggesting different evolutionary trajectories. Overall, we describe a coordinated regulatory mechanism between immunity and virulence that enhances the immune repertoire during acute infection phases.

2024-11-04 | GSE269471 | GEO

Virulence regulates and boosts CRISPR-Cas9 immunity in Group B Streptococcus.

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Virulence regulates and boosts CRISPR-Cas9 immunity in Group B Streptococcus [RNA-seq]

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Project description:Virulence regulates and boosts CRISPR-Cas9 immunity in Group B Streptococcus [RNA-seq]

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Virulence regulates and boosts CRISPR-Cas9 immunity in Group B Streptococcus.

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Project description:Epigenetic mechanism contributes to immune landscapes in cancer. Here we identify the SETDB1-TRIM28 complex as a critical suppressor of antitumor immunity. An epigenetic CRISPR-Cas9 screen of 1,218 chromatin regulators identified TRIM28 as a novel suppressor of PD-L1 expression. We revealed that expression of the SETDB1-TRIM28 complex negatively correlates with infiltration of effector CD8+ T cells. Inhibition of SETDB1-TRIM28 simultaneously upregulates PD-L1 and activates the cGAS-STING innate immune response to increase infiltration of CD8+ T cells. Mechanistically, SETDB1-TRIM28 inhibition leads to micronuclei formation in cytoplasm, a known activator of the cGAS-STING pathway. Thus, SETDB1-TRIM28 inhibition bridges the innate and adaptive immunity. Indeed, SETDB1 knockout enhances the antitumor effects of immune checkpoint blockade anti-PD-L1 in an ovarian cancer mouse model in a cGAS dependent manner. Our findings establish SETDB1-TRIM28 complex as a regulator of antitumor immunity and its loss activates cGAS-STING innate immunity to boost antitumor effects of immune checkpoint blockades.

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