The Cas9 from Neisseria meningitidis (Nme) is a particularly small and target-specific Cas9 orthologue
First-pass extracted concept
Neisseria meningitidis Cas9
Candidate: toolkit item3 source documents9 linked claims
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Aliases
Cas9 from Neisseria meningitidis, Nme Cas9, NmeCas9
Evidence Snippets
Supporting Sources
Linked Claims
Two AcrIIC3-LOV2 hybrids potently blocked NmeCas9 activity in the dark while permitting robust genome editing upon blue light irradiation.
Quoted textsource-backed
Two AcrIIC3-LOV2 hybrids from our collection potently blocked NmeCas9 activity in the dark, while permitting robust genome editing at various endogenous loci upon blue light irradiation.
The work demonstrates optogenetic regulation of a type II-C CRISPR effector and suggests a route for designing optogenetic anti-CRISPR proteins.
Quoted textsource-backed
Together, our work demonstrates optogenetic regulation of a type II-C CRISPR effector and might suggest a new route for the design of optogenetic Acrs.
This paper reports the first optogenetic tool to control NmeCas9 activity in mammalian cells via an engineered light-dependent anti-CRISPR protein.
Quoted textsource-backed
Here, we report the first optogenetic tool to control NmeCas9 activity in mammalian cells via an engineered, light-dependent anti-CRISPR (Acr) protein.
Structural analysis indicated that the LOV2 domain in the hybrids is located close to the Cas9 binding surface.
Quoted textsource-backed
Structural analysis revealed that, within these hybrids, the LOV2 domain is located in striking proximity to the Cas9 binding surface.
Two AcrIIC3-LOV2 hybrids blocked Nme Cas9 activity in the dark and permitted genome editing upon blue light irradiation.
Quoted textsource-backed
Two AcrIIC3-LOV2 hybrids from our collection potently blocked Nme Cas9 activity in the dark, while permitting robust genome editing at various endogenous loci upon blue light irradiation.
The work demonstrates optogenetic regulation of a type II-C CRISPR effector and suggests a route for designing optogenetic anti-CRISPR proteins.
Quoted textsource-backed
Together, our work demonstrates optogenetic regulation of a type II-C CRISPR effector and might suggest a new route for the design of optogenetic Acrs.
Structural analysis placed the LOV2 domain in close proximity to the Cas9 binding surface within the hybrids.
Quoted textsource-backed
Structural analysis revealed that, within these hybrids, the LOV2 domain is located in striking proximity to the Cas9 binding surface.
This work reports an optogenetic tool that controls Nme Cas9 activity in mammalian cells using an engineered light-dependent anti-CRISPR protein.
Quoted textsource-backed
Here, we report the first optogenetic tool to control Nme Cas9 activity in mammalian cells via an engineered, light-dependent anti-CRISPR (Acr) protein.
The Cas-ON system was adapted to Neisseria meningitidis Cas9 using its cognate inhibitors AcrIIC1 and AcrIIC3.
Quoted textsource-backed
Finally, to showcase its modularity, we adapted our Cas-ON system to the smaller and more target-specific Neisseria meningitidis (Nme) Cas9 orthologue and its cognate inhibitors AcrIIC1 and AcrIIC3.