Homologous Recombination and Double-Strand Break Repair
A break across both strands is repaired by invading a matching sequence and copying from it, which is also how crossovers form in meiosis. The same mechanism is what makes targeted gene replacement possible.
What a learner can do afterwards
- Traces a double-strand break through strand invasion to a repaired duplex.
- Explains why this route needs a homologous partner and the alternative route does not.
- Links the mechanism to the crossovers counted in a linkage map.
1 · Read
A double-strand break is the most dangerous lesion because both backbones are severed with no intact template in the same duplex. Homologous recombination repairs it accurately by trimming the ends to single-stranded tails, invading the sister chromatid or homolog, and copying the missing sequence from that partner. Resolving the joint molecule restores two intact duplexes, sometimes with a crossover between them.
Accuracy has a price: dependence on a partner, which is why this route dominates in S and G2 when sisters are present. The alternative, end joining, simply trims and ligates the broken ends with no template at all. It works all cycle long and needs no partner, but small insertions or deletions often remain at the join.
Meiosis puts the same machinery to a second use. Homologs pair, exchange segments, and lock together with structures that help them segregate correctly. The same strand invasion that fixes breaks now deliberately shuffles parental alleles onto recombinant chromatids.
Every crossover scored in a linkage map is one of these exchange events caught in the act. One percent recombinants means one crossover per hundred meioses in that interval, on average. Linked genes travel together precisely because crossovers between them are rare.
Copy from a partner for fidelity, ligate directly for speed, and count crossovers on the map.
More to read
14.6 DNA Repair
A double strand break is the most dangerous DNA lesion because both backbones are severed with no intact template in the same duplex. Homologous recombination repairs it accurately by resecting the ends to single stranded tails, invading the sister chromatid or homolog, and copying the missing sequence from that partner. Resolution of the joint molecule restores two intact duplexes, sometimes with a crossover between them. The price of accuracy is dependence on a homologous partner, which is why this route dominates in S and G2 when sisters are present.
The alternative, nonhomologous end joining, simply trims and ligates the broken ends with no template at all. It works all cycle long and needs no partner, but small insertions or deletions often remain at the join. Cells therefore choose by context: high fidelity repair with a partner when one is available, quick direct ligation when none is.
7.3 Variations in Meiosis
Meiotic crossing over is homologous recombination put to a second use. Homologs pair, exchange segments, and lock together with chiasmata that help them segregate correctly. The same strand invasion machinery that fixes breaks now deliberately shuffles parental alleles onto recombinant chromatids. Every crossover scored in a linkage map is one of these repair like events caught in the act.
That identity explains why map distance is measured by recombination frequency. One percent recombinants means one crossover per hundred meioses in that interval, on average. Variation in crossover placement between sexes, regions, and individuals then shows up directly as variation in mapped distances.
13.1 Chromosomal Theory and Genetic Linkage
Linked genes travel together precisely because crossovers between them are rare, and each crossover is a homologous recombination event. When exchanges do fall between two markers, the chromatids emerge recombinant and the offspring reveal it. Morgan's linkage work and modern maps both rest on this exchange process. Without recombination machinery there would be no recombinants to count and no maps to draw.
Recombination frequency therefore doubles as a readout of repair pathway activity during meiosis. Mutants defective in strand exchange proteins show both break sensitivity and collapsed map distances, tying the two phenotypes to one mechanism. Following a single break from resection through invasion to resolution shows the full path that a mapped crossover also took.
Explore more
2 · Watch
Take it off screen
Where it sits
Optional connections
8 questions wait behind this lesson, each with its answer explained. Every answer feeds the sky: stars light as they are learned, and dim when it is time to come back.