DSBR

DSBR stands for double-strand break repair, the set of cellular mechanisms that restore DNA when both strands of the double helix are broken. In genetics, DSBR is often discussed as the double-strand break repair model of homologous recombination, a framework for understanding how meiotic crossovers and genome maintenance are accomplished by using an intact homologous sequence as a template.

The DSBR model describes a canonical sequence of events after a DNA double-strand break is detected. Nuclease processing (resection) creates 3' single-stranded DNA tails. Recombinase proteins, such as Rad51 (and Dmc1 in meiosis), promote strand invasion to form a displacement loop (D-loop) using a homologous chromatid or chromosome as a template. DNA synthesis extends the invading end, followed by capture of the second end to establish a junction, typically a double Holliday junction. Resolution of these junctions by specialized resolvases can yield crossovers or non-crossovers, depending on the cleavage pattern. In meiosis, crossovers generated by DSBR underpin proper chromosome segregation and genetic diversity; in mitotic cells, DSBR helps maintain genome integrity.

DSBR is contrasted with other repair pathways, notably synthesis-dependent strand annealing (SDSA), which typically produces non-crossovers because second-end capture is not maintained as a junction. In many cells, double-strand breaks can also be repaired by non-homologous end joining (NHEJ), a resection-independent pathway.

Significance and clinical relevance stem from the role of homologous recombination in DSBR. Components such as BRCA1/2 and RAD51 are essential for high-fidelity repair, and defects in these pathways are linked to genome instability and cancer. Research uses model organisms like yeast to dissect the enzymatic steps and regulation of DSBR.