Provided is a plant or plant part comprising a polynucleotide encoding a mutant TriA polypeptide, the expression of the polynucleotide confers to the plant or plant part tolerance to herbicides.

Provided is an oligonucleotide which may induce an editing activity of ADRC in cell and has excellent stability in a living body. The oligonucleotide includes a first oligonucleotide identifying a target RNA and a second oligonucleotide linked to the 5-side of the first oligonucleotide. The first oligonucleotide consists of a target-corresponding nucleotide residue, an oligonucleotide of 10 to 24 residues at the 3-side, and an oligonucleotide of 3 to 6 residues at the 5-side. The second oligonucleotide has no nucleotide residue corresponding to a nucleotide residue of the target RNA or has a nucleotide residue which does not form a complementary pair at the 3-end thereof and the number of residue is 3 to 6. The residue at the 3-side of the target-corresponding nucleotide residue is a 2-deoxynucleotide residue, and the third nucleotide residue counted in the 3-direction from the target-corresponding nucleotide in the oligonucleotide at the 3-side of the target-corresponding nucleotide residue is a 2-deoxy-2-fluoronucleotide residue.

Aspects of the disclosure relate to a gene therapy approach for diseases, disorders, or conditions caused by mutation in the stop codon utilizing modified tRNA. At least 10-15% of all genetic diseases, including muscular dystrophy (e.g. Duchene muscular dystrophy), some cancers, beta thalassemia, Hurler syndrome, and cystic fibrosis, fall into this category. Not to be bound by theory, it is believed that this approach is safer than CRISPR approaches due to minimal off-target effects and the lack of genome level changes.

A novel gRNA-ligand binding complex is provided. This complex may be used to bring Type V Cas proteins and additional effectors to DNA for base editing. The design of the systems allows for the production of efficient modular components that provide flexibility when editing DNA.

A novel gRNA-ligand binding complex is provided. This complex may be used to bring Type V Cas proteins and additional effectors to DNA for base editing. The design of the systems allows for the production of efficient modular components that provide flexibility when editing DNA.

The disclosure provides novel personalized therapies, kits, transmittable forms of information and methods for use in treating patients having cancer, wherein the cancer is amenable to therapeutic treatment with an inhibitor, e.g., an inhibitor of any of the targets disclosed herein. Kits, methods of screening for candidate inhibitors, and associated methods of treatment are also provided.

A method for producing 2-keto-3-deoxygluconate (KDG) from 2-(acetylamino)-2-deoxy-D-gluconic acid (GlcNAc1A) by two enzymes; GlcNAc1A is converted to KDG by incubating GlcNAc1A with a deacetylase OngB at 25? C. for 4-12 h and then with a deaminase OngC at 25? C. for another 10-15 h; it constructs two engineered E. coli/pET22b-ongB (carrying the ongB gene) and E. coli/pET22b-ongC (carrying the ongC gene) strains to prepare recombinant proteins OngB and OngC, respectively; at the action of these two enzymes, OngB and OngC, GlcNAc1A is converted to KDG, which solves the bottleneck of GlcNAc1A utilization during the bioconversion of chitin; the KDG is an important metabolic intermediate to synthesize furan derivatives, herbicides, food additives and other industrially important chemical compounds, having wide industrial applications.

Provided herein are systems, compositions, kits, and methods for the suppression of pain (e.g., chronic pain). Genes encoding ion channels (e.g., SCN9A) responsible for the propagation pain signals in neurons (e.g., DRG neurons) may be edited using a genome editing agent (e.g., a nucleobase editor). In some embodiments, loss-of-function ion channel mutants are generated, leading to pain suppression. In some embodiments, the genome editing agent is administered locally to the site of pain or to the nerves responsible for propagation of the pain signal.

Provided is a plant or plant part comprising a polynucleotide encoding a mutated TriA polypeptide. The expression of said polynucleotide confers to the plant or plant part tolerance to herbicides.

The invention relates to double stranded oligonucleotide complexes comprising an antisense oligonucleotide (AON) and a complementary sense oligonucleotide (SON), for use in the deamination of a target adenosine in a sense target RNA sequence in a cell by an ADAR enzyme, wherein at least the nucleotide in the AON that is directly opposite the target adenosine in the target RNA sequence does not have a 2-O-alkyl modification and the SON comprises nucleotides that are at least complementary to all nucleotides in the AON that do not have a 2-O-alkyl modification. The invention further relates to methods of RNA editing using the AON/SON complexes of the invention.