Non-homologous end joining

Non-homologous end joining is a DNA repair pathway that reconnects broken DNA ends without using a homologous template. It can repair double-strand breaks quickly, sometimes introducing small insertions or deletions.

Ku protein: A DNA-end-binding protein complex that protects double-strand breaks and recruits repair factors. Ku70–Ku80 binds exposed ends first and organizes classical end joining.
DNA double-strand break: A DNA lesion in which both strands of the double helix are severed near the same position. This is the central lesion that non-homologous end joining reconnects.
CRISPR genome editing: A genome-editing approach that uses programmable nucleases to cut DNA at chosen sequences. Cells often repair CRISPR-induced breaks through end joining, creating edits at the cut site.
Alternative end joining: A set of DNA double-strand break repair routes that join ends without the classical Ku-dependent machinery. It provides backup end joining and often relies more heavily on end resection.
V(D)J recombination: A process that rearranges variable, diversity, and joining gene segments to generate diverse antigen receptors. It uses end-joining machinery to seal DNA ends created during receptor-gene rearrangement.
DNA-PKcs: A large protein kinase that partners with Ku in DNA repair and V(D)J recombination. Ku-bound DNA-PKcs helps hold broken ends together and coordinates their processing.
Homologous recombination: A DNA repair pathway that uses a homologous DNA sequence as a template to repair a break. It repairs the same class of breaks but depends on a matching template.
Gene knockout: The deliberate disruption of a gene to reduce or eliminate its function. Insertions and deletions from end joining can disrupt coding sequences.
Microhomology-mediated end joining: A mutagenic repair pathway that aligns short matching DNA sequences near broken ends before joining them. Its use of short sequence matches distinguishes it from template-free classical end joining.
Somatic hypermutation: A process that introduces mutations into immunoglobulin genes in activated B cells. End-joining factors influence how some antibody-gene breaks are repaired during immune diversification.

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