AMONG EUKARYOTES, sexual reproduction is more common than asexual reproduction, and often organisms that reproduce asexually also have a supplementary means of sexual reproduction. While sexual reproduction does have some drawbacks, it appears that in general the benefits outweigh these.

The first benefit of sexual reproduction is allele shuffling due to crossing over, a form of genetic recombination. Crossing over is a phenomenon that occurs during meiosis, the type of cell division that leads to gametes. At this time the two copies of each chromosome, one copy from each parent, match up together. Portions of the chromosomes will then cross over each other, and the chromosomes are cut at the crossing points and the intermediate segments swapped from one chromosome to the other. This means that the swapped alleles now share a chromosome with new alleles for other genes, and this prevents some traits from always appearing with the same other trait.

For instance, imagine a chromosome containing two genes, one for hunting ability and one for gardening ability. The hunting gene can have an incompletely dominant allele H that produces mighty hunters and a recessive allele h that produces people who can’t step into the woods without getting lost. The gardening gene can have an incompletely dominant allele G for someone with a green thumb, or a recessive allele g for someone with a black thumb! Imagine that every chromosome has either the allele combination Hg or hG. This leads to the following combinations:

HHgg: Great hunter, lousy gardener.
hhGG: Lousy hunter, great gardener.
HhGg: Not really great at either, but competent.

If we then allow crossing over, these alleles can be shuffled. Suddenly we find chromosomes with the alleles HG and hg! The new possibilities:

HHGG: Superb hunter and gardener!
HHGg: Great hunter, competent gardener.
HhGG: Competent hunter, great gardener.
hhGg: Lousy hunter, competent gardener.
Hhgg: Competent hunter, lousy gardener.
hhgg: All-around failure.

Obviously the offspring inheriting HG is going to be extremely flexible and highly successful, especially if it’s lucky enough to get dual homozygous dominant (HHGG). An organism unlucky enough to get hhgg will probably not do so well. The result is to increase the prevalence of alleles H and G in the population while h and g decrease (probably due to their dual homozygous recessive carriers starving!) There will still be people carrying Hg and hG in various combinations, but since HHGG carriers do so well and hhgg carriers tend to die out, the end result will be the reduction of h and g to low levels, and perhaps in the end their loss through genetic drift. This simply cannot happen in asexual reproduction, meaning asexual populations are much more slow to eliminate detrimental mutations and amplify positive ones. Asexual populations more often have to settle for mediocrity.

After examining this example, the second benefit is easy to see. Suppose there is a strain of asexually reproducing organisms with the genotype Hhgg. It will take one mutation for that organism to pick up a good gardening allele. Then the clonal line will have to incur two more mutations before producing HHGG offspring. It could take quite a while before these three useful mutations occur consecutively. But if this organism were sexually reproducing, it could breed with another organism carrying G and instantly introduce that allele into its offspring population. Once again, asexually reproducing populations usually have to settle more often for mediocrity.

The inability of asexually reproducing organisms to gradually eliminate negative mutations by crossing over (un-)fortuitously sorting a heavy mutational load into an unlucky offspring means that mutations tend to gradually build up in an asexually reproducing population as the least-mutated genotypes are stochastically lost through genetic drift. This process is known as Muller’s ratchet, after the scientist who first proposed this difficulty. Since each mutation in a clonal line of asexually reproducing organisms is irrepairable through recombination, each mutation is like another click on a ratchet that is slowly tightening. These mutations can be simple things like breaking a H allele by turning it into an h, but can also include processes such as the actual loss of DNA by accidental deletions. Muller’s ratchet is responsible for the very short genomes in some asexually reproducing organisms.

Muller’s ratchet doesn’t just apply to organisms that do not undergo sexual reproduction, but also to chromosomes that fail to recombine with their pairing partners. This is seen in the Y chromosome. The autosomal chromosome pairs recombine extensively, but because the sex chromosomes need to store separately genes beneficial to females on the X chromosome and genes beneficial to males on the Y chromosome, recombination between the X and Y chromosome is limited to a short pseudoautosomal region. The X chromosomes are present in pairs in females, so they recombine fully (which can result in the fortuitous shifting of a negative mutation load to one X chromosome, which then is eliminated in the offspring by selection, while the repaired partner X chromosome ends up in a different egg cell and produces a healthy offspring). The Y chromosome does have palindromic (reversed) sequences that can bend back upon their complements and undergo a sort of self-recombination, but this is just a temporary fix. The Y chromosome is slowly shortening by the accumulation of small deletions, and unless a translocation splices a segment of an autologous chromosome onto it and lengthens it, it will eventually disappear. This will require one of two preceding events–either the sex-determining genes present on the Y chromosome will have to be transferred to one of the autologous chromosomes, or a gene on a different chromosome will have to mutate to take over this role.

This actually has happened in the mole vole. The males of this species have no Y chromosome and no apparent SRY gene (sex-determining region Y gene, responsible for male differentiation). It appears a gene on some other chromosome picked up SRY’s function, and with the Y chromosome’s necessity gone, the removal of selection for its preservation resulted in its eventual loss. The next step in mole vole evolution will be the construction of a new Y chromosome, as selective forces favor the segregation of male- and female-favoring genes to different chromosomes.

So if sex is so great, why doesn’t everyone do it? The answer is it is incredibly inefficient. Each sexually-reproducing organism passes on only half of its genome to each descendant, while from a selfish-gene viewpoint producing an identical offspring would be preferable. Sexually reproducing organisms have to invest resources into competing for a mate. And since typically only half of the population is female (why this is so is a question I may address in a future entry!), that means only half of the population can produce offspring. If the population reproduced asexually, every single individual would be able to produce offspring. An asexually reproducing population can ramp up its numbers at a much greater rate than a sexually reproducing population with a similar life cycle. This is why many organisms alternate between asexual and sexual reproduction. In static conditions, an organism may undergo asexual reproduction to produce a massive population. When conditions suddenly change it’s likely this genotype is not useful any more, so the population quickly converts to sexual reproduction to take advantage of the introduction of new alleles from other clonal lines and the testing of various allele combinations. After a period of sexual reproduction, it’s back to asexual reproduction until the next emergency!

Sex is so critical for the elimination of detrimental mutations and introduction of new genetic material that even organisms that reproduce solely asexually have found proxies for sex, such as lateral gene transfer by conjugation between bacteria and recombination between viruses.

  • Muller, H. J. “Some Genetic Aspects of Sex.” The American Naturalist 1932, 66, 118-138.
  • Muller, H.J. “The Relation of Recombination to Mutational Advance”. Mutational Research 1964, 106, 2-9.
  • Vogel, W.; Jainta, S.; Rau, W.; Geerkens, C.; Baumstark, A. Correa-Cerro, L.-S.; Ebenhoch, W. “Sex determination in Ellobius lutescens: The story of an enigma.” Cytogenetics and Cell Genetics 1998, 80, 214-221.