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63 results for “CRISPR-Cas”
The energy landscape for R-loop formation by the CRISPR-Cas Cascade complex - Minimal Dataset
<p>Minimal Dataset for "The energy landscape for R-loop formation by the CRISPR-Cas Cascade complex", published at <a href="https://www.nature.com/nsmb/">NSMB</a>.</p>
Type IV-A3 CRISPR-Cas systems drive inter-plasmid conflicts by acquiring spacers in trans
<p>Plasmid-encoded type IV-A CRISPR-Cas systems lack an acquisition module, feature a DinG helicase instead of a nuclease, and form ribonucleoprotein complexes. Type IV-A3 systems are carried by conjugative plasmids that often harbor antibiotic resistance genes. Their CRISPR array contents suggest a role in inter-plasmid conflicts, but this function remains unexplored. Here, we demonstrate that a plasmid-encoded type IV-A3 system co-opts the type I-E adaptation machinery from its host, Klebsiella pneumoniae, to update its CRISPR array. Furthermore, we reveal that robust interference of conjugative plasmids and phages is elicited through CRISPR RNA-dependent transcriptional repression. By silencing plasmid core functions, type IV-A3 impacts the horizontal transfer and stability of targeted plasmids, supporting its role in plasmid competition. Our findings shed light on the mechanisms and ecological function of type IV-A3 systems and demonstrate their practical efficacy for countering antibiotic resistance in clinically relevant strains.</p>
Type IV-A3 CRISPR-Cas systems drive inter-plasmid conflicts by acquiring spacers in trans
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Strains and constructs for: A chimeric nuclease substitutes a phage CRISPR-Cas system to provide sequence specific immunity against subviral parasites
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Dynamic interplay between target search and recognition for a Type I CRISPR-Cas system
<p>CRISPR-Cas effector complexes enable the defense against foreign nucleic acids and have recently been exploited as molecular tools for precise genome editing at a target locus. To bind and cleave their target, the CRISPR-Cas effectors have to interrogate the entire genome for the presence of a matching sequence. Here we dissect the target search and recognition process of the Type I CRISPR-Cas complex Cascade by simultaneously monitoring DNA binding and R-loop formation by the complex. We directly quantify the effect of DNA supercoiling on the target recognition probability and demonstrate that Cascade uses facilitated diffusion for its target search. We show that target search and target recognition are tightly linked and that DNA supercoiling and limited 1D diffusion need to be considered when understanding target recognition and target search by CRISPR-Cas enzymes and engineering more efficient and precise variants. </p>
Data from: The effect of bacterial mutation rate on the evolution of CRISPR-Cas adaptive immunity
CRISPR-Cas immune systems are present in around half of bacterial genomes. Given the specificity and adaptability of this immune mechanism, it is perhaps surprising that they are not more widespread. Recent insights into the requirement for specific host factors for the function of some CRISPR-Cas subtypes, as well as the negative epistasis between CRISPR-Cas and other host genes, have shed light on potential reasons for the partial distribution of this immune strategy in bacteria. In this study, we examined how mutations in the bacterial mismatch repair system, which are frequently observed in natural and clinical isolates and cause elevated host mutation rates, influence the evolution of CRISPR-Cas–mediated immunity. We found that hosts with a high mutation rate very rarely evolved CRISPR-based immunity to phage compared to wild-type hosts. We explored the reason for this effect and found that the higher frequency at which surface mutants pre-exist in the mutator host background causes them to rapidly become the dominant phenotype under phage infection. These findings suggest that natural variation in bacterial mutation rates may, therefore, influence the distribution of CRISPR-Cas adaptive immune systems.
Data from: Costs of CRISPR-Cas mediated resistance in Streptococcus thermophilus
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Data from: The effect of bacterial mutation rate on the evolution of CRISPR-Cas adaptive immunity
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CRISPR-Cas system of a prevalent human gut bacterium reveals hyper-targeting against phages in a human virome catalog
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Deep sequencing data from PAM screen of Pa83 type IV-A CRISPR-Cas system
GEO Series GSE211446. Escherichia coli. 6 samples. Type: Other.
Identification of collateral RNA cleavage mediated by Type VI CRISPR-Cas system from Leptotrichia shahiii
GEO Series GSE183061. Escherichia coli. 30 samples. Type: Other.
CRISPR-Cas screen in ILC2 identifies Mef2d as a regulator of GATA3 and type-2 immunity [ChIP-Seq]
GEO Series GSE242030. Mus musculus. 17 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
mRNA-Engineered CRISPR-Cas Epigenetic Editors Enable Durable and Efficient Gene Silencing in Vivo [RNA-seq]
GEO Series GSE299303. Mus musculus. 66 samples. Type: Expression profiling by high throughput sequencing.
Targeted transcriptional modulation with type I CRISPR-Cas systems in human cells (RNA-seq)
GEO Series GSE114857. Homo sapiens. 9 samples. Type: Expression profiling by high throughput sequencing.
DNA epigenome editing using CRISPR-Cas SunTag-directed DNMT3A
GEO Series GSE97816. Homo sapiens. 29 samples. Type: Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing.
DNA epigenome editing using CRISPR-Cas SunTag-directed DNMT3A [RNA-Seq]
GEO Series GSE97815. Homo sapiens. 5 samples. Type: Expression profiling by high throughput sequencing.
CRISPR-Cas screen in ILC2 identifies Mef2d as a regulator of GATA3 and type-2 immunity [CRISPR screen]
GEO Series GSE262028. Mus musculus. 8 samples. Type: Other.
DNA epigenome editing using CRISPR-Cas SunTag-directed DNMT3A [RRBS]
GEO Series GSE97813. Homo sapiens. 4 samples. Type: Methylation profiling by high throughput sequencing.
CRISPR-Cas protein Cas3 controls virulence in the oral pathogen Porphyromonas gingivalis.
GEO Series GSE154569. Galleria mellonella; Porphyromonas gingivalis. 46 samples. Type: Expression profiling by high throughput sequencing.
CRISPR-Cas screen in ILC2 identifies Mef2d as a regulator of GATA3 and type-2 immunity [ATAC-Seq]
GEO Series GSE242146. Mus musculus. 4 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
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