= Solution
\b[<DNA repair> preserves usable inherited information, while <genetic recombination> can improve the combinations in which that information is transmitted.] Their <evolution> need not have the production or prevention of diversity as an ultimate goal. <natural selection> favors consequences for survival and reproduction in particular contexts; novelty is neither automatically beneficial nor something an <organism> must maximize.
<mutation> creates new sequence variants; <genetic recombination> usually rearranges variants already present. A <chromosomal crossover> can produce a new <haplotype> without changing the <allele frequency> at either of two <genetic loci>. Conversely, <DNA repair> can restore sequence integrity after damage without eliminating the inherited differences between individuals. In particular, a normal alternative <allele> is not an error merely because it differs from another individual's sequence. These operations address different features of inheritance.
Unrepaired damage can block <DNA replication> or <transcription>, break a <chromosome>, or generate a harmful <mutation>. <DNA repair> thus has immediate benefits to a <biological cell> and can reduce the future burden of deleterious changes in descendants. In multicellular <organisms>, <somatic mutation> can compromise tissue function, while <germline mutation> changes what offspring inherit. The relevant balance includes the biochemical costs of <DNA repair>, the probability and severity of damage, and the possibility of <DNA repair> errors. <natural selection> for increased fidelity can become weak relative to <genetic drift> when an additional improvement is extremely small; perfect fidelity need not evolve. Some error-prone damage responses can also improve immediate survival even if surviving descendants carry more <mutations>.
The biochemical relationship is complementary. <homologous recombination> repairs a <DNA double-strand break> by using a related intact sequence as a template. In <meiosis>, programmed breaks can be repaired using a <homologous chromosome>, sometimes producing <chromosomal crossovers> and sometimes noncrossover products. Biochemical identification of <Spo11> linked a component of the meiotic machinery to programmed break formation, demonstrating that meiotic diversification can begin with a controlled DNA-damage-and-repair process.<Meiosis-specific DNA double-strand breaks are catalyzed by Spo11, a member of a widely conserved protein family by Scott Keeney and others>[Cell 88, pp. 375–384; purification and identification of the protein covalently associated with meiotic breaks]{ref} Crossovers also help establish the physical connections needed for reliable segregation in many meiotic systems. This immediate transmission function can favor the machinery independently of any later benefit from a novel <haplotype>. <DNA repair> with <sister chromatids> in another context can preserve sequence without the same exchange between parental homologues.
There are also population-level benefits of reshuffling. Suppose two favorable <alleles>, $A$ and $B$, occur in different lineages as $Ab$ and $aB$. With no exchange, their lineages compete and either favorable <allele> can be lost when the other lineage prevails. <genetic recombination> can create $AB$, allowing selection to combine their benefits; it can also separate a favorable <allele> from linked harmful changes. This is the core of the <Fisher-Muller hypothesis> and relates to <Hill-Robertson interference>, the reduction in the efficacy of <natural selection> caused by associations among selected <genetic loci>. Recreating low-load <genotypes> can also slow <Muller's ratchet> in finite <biological populations>.
The bookkeeping illustrates why this is not simply increasing all diversity. Let $x_{AB},x_{Ab},x_{aB},x_{ab}$ be <haplotype frequencies> and $D=x_{AB}x_{ab}-x_{Ab}x_{aB}$ be <linkage disequilibrium>. Under the standard random-mating model with <recombination fraction> $r$ and no other evolutionary forces,
$$
x'_{AB}=x_{AB}-rD,\qquad D'=(1-r)D.
$$
For $x_{Ab}=x_{aB}=1/2$ and the other two zero, $D=-1/4$. At $r=0.1$, the next frequencies are $x'_{AB}=x'_{ab}=0.025$ and $x'_{Ab}=x'_{aB}=0.475$. Each favorable <allele> still has frequency $1/2$: the process creates both the favorable combination and its unfavorable counterpart. Subsequent <natural selection> determines their fates. If the original associations are already advantageous, breaking them can instead impose a <recombination load>.
In controlled yeast <experimental evolution>, sexual and asexual treatments differed in their rates and genomic routes of <adaptation>, with the sexual treatment more efficiently separating beneficial from deleterious changes.<Sex speeds adaptation by altering the dynamics of molecular evolution by Michael J. McDonald and others>[Nature 531, pp. 233–236; sexual versus asexual treatments, fitness changes and mutation trajectories]{ref} A mechanistic test should control the costs and bottlenecks of the sexual cycle, compare otherwise matched <genetic backgrounds>, and use reconstructed changes to distinguish <genetic linkage> from intrinsically different effects of a <mutation>. Such results establish a benefit under the tested population regime, not an unconditional advantage of sex in every environment. <genetic recombination> can disrupt favorable <epistasis>, and the costs of mating are distinct from those of crossover formation.
For an explanation of the <evolution> of the machinery itself, the association with its bearer matters. A <recombination modifier> must on average increase the representation of its own descendants, perhaps through improved segregation or through association with combinations that selection favors. Merely increasing long-run adaptability of the <species> is insufficient. Similarly, a <mutator allele> can spread in an asexual lineage by hitchhiking with a beneficial <mutation> it helped generate despite producing many harmful ones; exchange can weaken that association. The advantages of fidelity and of exchange consequently depend on <genetic linkage>, population size, environmental change and the current supply of beneficial variants.
<DNA repair> can regulate which exchanges are permitted as well. <DNA mismatch repair> corrects copying errors and can reject exchange between sufficiently diverged sequences. In bacteria, disabling mismatch-repair functions greatly relaxed a barrier to <genetic recombination> between divergent lineages.<The barrier to recombination between Escherichia coli and Salmonella typhimurium is disrupted in mismatch-repair mutants by Christiane Rayssiguier and others>[Nature 342, pp. 396–401; comparison of mismatch-repair-deficient mutants with the normal recombination barrier]{ref} An experiment separating these roles should compare <DNA repair> of copying errors with exchange between templates of controlled divergence, using a restored <DNA repair> <gene> as a rescue. \b[<DNA repair> and <genetic recombination> can therefore be parts of the same evolved solution: preserve functional sequence, transmit <chromosomes> reliably, and reshuffle existing <alleles> when doing so improves <reproductive success>.]
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