CRISPR & editing
Can Cas13a fight RNA viruses in plants?
Open access · cc by · source: Europe PMC
CRISPR/Cas13a interferes with TuMV in plants, cutting viral RNA and reducing reporter/virus accumulation.
Study at a glance
- Design
- Animal / in-vitro — Programmed Cas13a targeting TuMV genomic regions in plants
- N
- Plant molecular interference assays — no single primary analytic N in stored text
- Population
- Plants infected with Turnip mosaic virus (TuMV)
- Outcome
- Cas13a-mediated reduction of viral GFP and accumulation
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
Cas13a mediates interference against a plant RNA virus; targeting different regions reduced GFP and viral accumulation.
Methodology
Programmed Cas13a against TuMV genomic regions in plants and measured molecular interference.
Limitations
Not a full field deployment across all RNA viruses; guide design still matters.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Not every tagged paper is a western-first study. APEX2 maps (22 OMM, 72 ERM proteins) are mass-spectrometry inventories; Wnt5a work uses purified ligand and receptor context to turn β-catenin–TCF signalling on or off; Cas13a plant antiviral work measures GFP and viral accumulation after targeting TuMV regions. Blots may appear as supporting assays, not as the experimental core.
Evidence for the claim as stated.
APEX2, Wnt5a, and Cas13a illustrate false-positive or peripheral lexicon hits: proximity proteomics, ligand/receptor signalling, and CRISPR interference on an RNA virus. Citing them as if they were western-blot method papers overstates how the method was used.
Evidence for the claim as stated.
Cas13a can be programmed as an antiviral in plants. Targeting different TuMV genomic regions reduced GFP and viral accumulation, showing sequence-specific RNA-virus interference rather than a DNA double-strand break. Guide choice still mattered, and the paper is not a field deployment against all RNA viruses.
Evidence for the claim as stated.
The strongest tension is naming. The 2007 array paper and the Listeria pan-genome treat CRISPR as a genomic feature of bacteria; the Cas13a and dCas9 papers treat CRISPR–Cas as a laboratory tool. Both usages are historically connected, but a finding about repeat RNA folding does not license a claim about editing a human promoter, and a CasIP result does not catalogue environmental CRISPR diversity.
Evidence for the claim as stated.
Even among tool papers, the enzyme is not always Cas9 cutting DNA. Cas13a targets RNA viruses; dCas9 in CasIP binds without requiring a cut. Calling every experiment a 'CRISPR knockout' is false for this set.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
APEX2, Wnt5a, and Cas13a illustrate false-positive or peripheral lexicon hits: proximity proteomics, ligand/receptor signalling, and CRISPR interference on an RNA virus. Citing them as if they were western-blot method papers overstates how the method was used.
The strongest tension is naming. The 2007 array paper and the Listeria pan-genome treat CRISPR as a genomic feature of bacteria; the Cas13a and dCas9 papers treat CRISPR–Cas as a laboratory tool. Both usages are historically connected, but a finding about repeat RNA folding does not license a claim about editing a human promoter, and a CasIP result does not catalogue environmental CRISPR diversity.
- Supports · CRISPR repeats conserve RNA-like structure
- Supports · FLI1 circRNA FECR1 drives metastasis
- Supports · How open is the Listeria pan-genome?
Even among tool papers, the enzyme is not always Cas9 cutting DNA. Cas13a targets RNA viruses; dCas9 in CasIP binds without requiring a cut. Calling every experiment a 'CRISPR knockout' is false for this set.
- Supports · FLI1 circRNA FECR1 drives metastasis
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