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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Escherichia coli Streptococcus agalactiae

PROVIDER: GSE269473 | GEO | 2024/11/04

REPOSITORIES: GEO

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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 [RNA-seq]

2024-11-04 | GSE269472 | GEO

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

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

| PRJNA1122100 | ENA

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

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

| PRJNA1122103 | ENA

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

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

| PRJNA1122105 | ENA

The CovR regulatory network drives the evolution of Group B Streptococcus virulence

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-23 | GSE158049 | GEO

Genome-wide CRISPR-Cas9 screen identifies functionally relevant microRNAs in AML

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-01 | E-GEOD-71544 | biostudies-arrayexpress

CD300ld regulates tumor immunity - In vivo Crispr-Cas9 screening

Project description:To identify surface proteins on myeloid cells involved in the establishment of the tumor immune microenvironment, we selected transmembrane protein encoding genes with a high myeloid/lymphoid expression ratio to construct a sgRNA library. The sgRNA pool was transduced into hematopoietic stem/progenitor cells of Cas9 mice to transplant the lethal irradiated mice for immune system reconstitution, then followed by B16-F10 tumor inoculation. Once the tumor was established, the tumor and bone marrow (BM) were collected for sgRNA deep sequencing and comparison.

2023-06-26 | GSE199603 | GEO

CRISPR/Cas9 knock down line

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-01-08 | GSE126351 | GEO

Bacteriophage Cooperation Suppresses CRISPR-Cas3 and Cas9 Immunity.

Project description:Bacteria utilize CRISPR-Cas adaptive immune systems for protection from bacteriophages (phages), and some phages produce anti-CRISPR (Acr) proteins that inhibit immune function. Despite thorough mechanistic and structural information for some Acr proteins, how they are deployed and utilized by a phage during infection is unknown. Here, we show that Acr production does not guarantee phage replication when faced with CRISPR-Cas immunity, but instead, infections fail when phage population numbers fall below a critical threshold. Infections succeed only if a sufficient Acr dose is contributed to a single cell by multiple phage genomes. The production of Acr proteins by phage genomes that fail to replicate leave the cell immunosuppressed, which predisposes the cell for successful infection by other phages in the population. This altruistic mechanism for CRISPR-Cas inhibition demonstrates inter-virus cooperation that may also manifest in other host-parasite interactions.

| S-EPMC6086726 | biostudies-literature

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