non-homologous end joining
/ NHEJ /
Non-homologous end joining is the cell's quick-and-dirty way of repairing a double-strand break: it grabs the two broken ends and glues them straight back together, with no template and no concern for whether a few letters are lost in the process. Imagine a snapped rope being tied back into a knot — strong enough to hold, but a little frayed and slightly shorter at the join.
Mechanically, proteins recognise and bind the exposed broken ends and hold them close together so they cannot drift apart and get lost. The rough ends are then trimmed and tidied — which often nibbles away or adds a handful of nucleotides — and finally a ligase welds the backbone closed. Because the joining does not consult an undamaged copy of the sequence, the seam frequently carries a small insertion or deletion. Often this scar is harmless; in a coding region it can cause a frameshift.
Despite its sloppiness, non-homologous end joining is indispensable. It is the dominant break-repair route in human cells, and crucially it works at any time — including before DNA has been copied, when there is no sister chromatid to serve as a template, so accurate repair is impossible anyway. Better a slightly scarred but intact chromosome than a lost one. The immune system even exploits this controlled imprecision: the deliberate cutting and rejoining of antibody and T-cell-receptor gene segments uses non-homologous end joining, and its small added or deleted bases help generate the huge diversity of immune receptors.
Two broken ends ...ACGT| |TGCA... are held together, trimmed, and ligated into ...ACGTGCA... — a few bases shorter, but the chromosome is whole again.
Fast and template-free — at the cost of a small scar at the join.
Calling NHEJ simply 'error-prone' undersells it. Its imprecision is often the lesser evil, and the immune system deliberately harnesses that imprecision to diversify antibodies.