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Evolution of sexual reproduction

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Title: Evolution of sexual reproduction  
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Subject: Evolutionary biology, Sex, Paleontology, Timeline of the evolutionary history of life, Epistasis
Collection: Evolutionary Biology, Sex, Sexual Selection
Publisher: World Heritage Encyclopedia

Evolution of sexual reproduction

wolves mating
Ladybirds mating

The evolution of sexual reproduction describes how sexually reproducing animals, plants, fungi and protists evolved from a common ancestor that was a single celled eukaryotic species.[1][2][3] There are a few species which have secondarily lost the ability to reproduce sexually, such as Bdelloidea and some parthenocarpic plants. The evolution of sex contains two related, yet distinct, themes: its origin and its maintenance.

The maintenance of sexual reproduction in a highly competitive world has long been one of the major mysteries of biology given that asexual reproduction can reproduce much more quickly as 50% of offspring are not males, unable to produce offspring themselves. However, research published in 2015 indicates that sexual selection can explain the persistence of sexual reproduction.[4]

Since hypotheses for the origins of sex are difficult to test experimentally (outside of replication, where the offspring is identical to the parents. Recombination supplies two fault-tolerance mechanisms at the molecular level: recombinational DNA repair (promoted during meiosis because homologous chromosomes pair at that time) and complementation (also known as heterosis, hybrid vigor or masking of mutations).

Sexual reproduction has probably contributed to the evolution of parental investment. Males adopt strategies with lower investment in individual gametes and may present a higher mutation rate, while females may invest more resources and serve to conserve better-adapted solutions.


  • Historical perspective 1
  • Questions 2
  • Two-fold cost of sex 3
  • Sex decoupled from reproduction 4
  • Promotion of genetic variation 5
  • Advantages conferred by sex 6
    • Advantages due to genetic variation 6.1
    • Novel genotypes 6.2
    • Increased resistance to parasites 6.3
  • Deleterious mutation clearance 7
    • Evading harmful mutation build-up 7.1
    • Removal of deleterious genes 7.2
  • Other explanations 8
    • Speed of evolution 8.1
    • DNA repair and complementation 8.2
    • Libertine bubble theory 8.3
  • Origin of sexual reproduction 9
  • Mechanistic origin of sexual reproduction 10
    • Viral eukaryogenesis 10.1
    • Neomuran revolution 10.2
  • References 11
  • Further reading 12
  • External links 13

Historical perspective

Modern philosophical-scientific thinking on the problem can be traced back to Erasmus Darwin in the 18th century; it also features in Aristotle's writings. The thread was later picked up by August Weismann in 1889, who argued that the purpose of sex was to generate genetic variation, as is detailed in the majority of the explanations below. On the other hand, Charles Darwin concluded that the effects of hybrid vigor (complementation) "is amply sufficient to account for the ... genesis of the two sexes." This is consistent with the repair and complementation hypothesis, given below under "Other explanations."

Several explanations have been suggested by biologists including George C. Williams, Harris Bernstein, Carol Bernstein, Michael M. Cox, Frederic A. Hopf and Richard E. Michod to explain how sexual reproduction is maintained in a vast array of different living organisms.


Some questions biologists have attempted to answer include:

  • Why sexual reproduction exists, if in many organisms it has a 50% cost (fitness disadvantage) in relation to asexual reproduction?[5]
  • Did mating types (types of gametes, according to their compatibility) arise as a result of anisogamy (gamete dimorphism), or did mating types evolve before anisogamy?[6][7]
  • Why do most sexual organisms use a binary mating system?[8] Why do some organisms have gamete dimorphism?

Two-fold cost of sex

This diagram illustrates the twofold cost of sex. If each individual were to contribute to the same number of offspring (two), (a) the sexual population remains the same size each generation, where the (b) asexual population doubles in size each generation.

In most multicellular sexual species, the population consists of two sexes, only one of which is capable of bearing young (with the exception of simultaneous isogamous species which are sexual and do not have the problem of producing individuals which cannot directly replicate themselves.[10] The principal costs of sex is that males and females must search for each other in order to mate, and sexual selection often favours traits that reduce the survival of individuals.[9]

Flour beetle

Research published in 2015 indicates that sexual selection and the mate choices which "improves population health and protects against extinction, even in the face of genetic stress from high levels of inbreeding" and "ultimately dictates who gets to reproduce their genes into the next generation - so it's a widespread and very powerful evolutionary force."[4] The study involved the flour beetle over a ten-year period where the only changes were in the intensity of sexual selection.

Evidence that the cost is surmountable comes from asexual and sexual reproduction, such as certain lizards. These species time their sexual reproduction with periods of environmental uncertainty, and reproduce asexually when conditions are more favourable. The important point is that these species are observed to reproduce sexually when they could choose not to, implying that there is a selective advantage to sexual reproduction.[11]

It is widely believed that a disadvantage of sexual reproduction is that a sexually reproducing organism will only be able to pass on 50% of its genes to each offspring. This is a consequence of the fact that gametes from sexually reproducing species are haploid.[12] This, however, conflates sex and reproduction which are two separate events. The "two-fold cost of sex" may more accurately be described as the cost of

  • Why Sex is Good
  • An essay summarising the different theories, dating from around 2001

External links

  • Bernstein, Carol; Harris Bernstein (1991). Aging, sex, and DNA repair. Boston: Academic Press.  
  • Hurst, L.D.; J.R. Peck (1996). "Recent advances in the understanding of the evolution and maintenance of sex".  
  • Levin, Bruce R.; Richard E. Michod (1988). The Evolution of sex: an examination of current ideas. Sunderland, Mass: Sinauer Associates.  
  • Michod, Richard E. (1995). Eros and evolution: a natural philosophy of sex. Reading, Mass: Addison-Wesley Pub. Co.  
  • "Scientists put sex origin mystery to bed, Wild strawberry research provides evidence on when gender emerges".  
  • Taylor, Timothy (1996). The prehistory of sex: four million years of human sexual culture. New York: Bantam Books.  

Further reading

  1. ^ a b Letunic, I; Bork, P (2006). "Interactive Tree of Life". Retrieved 23 July 2011. 
  2. ^ Letunic, I; Bork, P (2007). "Interactive Tree of Life (iTOL): An online tool for phylogenetic tree display and annotation" (PDF).  
  3. ^ Letunic, I; Bork, P (2011). "Interactive Tree of Life v2: Online annotation and display of phylogenetic trees made easy" (PDF).  
  4. ^ a b Population benefits of sexual selection explain the existence of males May 18, 2015 Report on a study by the University of East Anglia
  5. ^ a b Ridley M (2004) Evolution, 3rd edition. Blackwell Publishing, p. 314.
  6. ^ T. Togashi, P. Cox (Eds.) The Evolution of Anisogamy. Cambridge University Press, Cambridge; 2011, p. 22-29.
  7. ^ Beukeboom, L. & Perrin, N. (2014). The Evolution of Sex Determination. Oxford University Press, p. 25 [6]. Online resources, [7].
  8. ^ Czárán, T.L.; Hoekstra, R.F. (2006). "Evolution of sexual asymmetry". BMC Evolutionary Biology 4: 34–46.  
  9. ^ a b John Maynard Smith The Evolution of Sex 1978.
  10. ^ a b Rolf Hoekstra 1987 The Evolution of Sex and its Consequences 1988 Birkhauser.
  11. ^ George C. Williams Sex and Evolution 1975, Princeton University Press, ISBN 0-691-08152-2
  12. ^ a b Matt Ridley 1995 The Red Queen: Sex and the Evolution of Human Nature 1995 Penguin.
  13. ^ Stelzer, Claus-Peter. "Does the avoidance of sexual costs increase fitness in asexual invaders?." Proceedings of the National Academy of Sciences 112.29 (2015): 8851-8858.
  14. ^ Beukeboom, L. & Perrin, N. (2014). The Evolution of Sex Determination. Oxford University Press, p. 5-6 [8]. Online resources, [9].
  15. ^ Weismann, A. 1889. Essays on heredity and kindred biological subjects. Oxford Univ. Press, Oxford, UK
  16. ^ Fisher, R. A. 1930. The genetical theory of natural selection. Clarendon Press, Oxford, UK
  17. ^ Muller, H. J. (1932). "Some genetic aspects of sex". Am. Nat. 66 (703): 118–138.  
  18. ^ Burt, A. (2000). "Perspective: sex, recombination, and the efficacy of selection—was Weismann right?". Evolution 54 (2): 337–351.  
  19. ^ Heng HH; Heng, Henry H.Q. (2007). "Elimination of altered karyotypes by sexual reproduction preserves species identity". Genome 50 (5): 517–524.  
  20. ^ Gorelick R, Heng HH; Heng (2011). "Sex reduces genetic variation: a multidisciplinary review". Evolution 65 (4): 1088–1098.  
  21. ^ Crow J.F. (1994). Advantages of Sexual Reproduction, Dev. Gen., vol.15, pp. 205-213.
  22. ^ Goldstein, R N (2010). 36 Arguments for the Existence of God: A Work of Fiction.  
  23. ^ Birdsell JA, Wills C (2003). The evolutionary origin and maintenance of sexual recombination: A review of contemporary models. Evolutionary Biology Series >> Evolutionary Biology, Vol. 33 pp. 27-137. MacIntyre, Ross J.; Clegg, Michael, T (Eds.), Springer. Hardcover ISBN 978-0306472619, ISBN 0306472619 Softcover ISBN 978-1-4419-3385-0.
  24. ^ Van Valen, L. (1973). "A New Evolutionary Law". Evolutionary Theory 1: 1–30. 
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  26. ^ a b Birdsell JA, Wills C (2003). The evolutionary origin and maintenance of sexual recombination: A review of contemporary models. Evolutionary Biology Series >> Evolutionary Biology, Vol. 33 pp. 27-137. MacIntyre, Ross J.; Clegg, Michael, T (Eds.), Springer. Hardcover ISBN 978-0306472619, ISBN 0306472619 Softcover ISBN 978-1-4419-3385-0.
  27. ^ Kuma, K.; Iwabe, N.; Miyata, T. (1995). "Functional constraints against variations on molecules from the tissue-level - slowly evolving brain-specific genes demonstrated by protein-kinase and immunoglobulin supergene families". Molecular Biology and Evolution 12 (1): 123–130.  
  28. ^ Wolfe KH, Sharp PM; Sharp (1993). "Mammalian gene evolution - nucleotide-sequence divergence between mouse and rat". Journal of molecular evolution 37 (4): 441–456.  
  29. ^ Jokela, Jukka; Dybdahl, Mark; Lively, Curtis (2009). "The Maintenance of Sex, Clonal Dynamics, and Host-Parasite Coevolution in a Mixed Population of Sexual and Asexual Snails". The American Naturalist 174 (s1): S43.  
  30. ^ "Parasites May Have Had Role In Evolution Of Sex". Science Daily. 31 July 2009. Retrieved 19 September 2011. 
  31. ^ Hanley KA, Fisher RN, Case TJ; Fisher; Case (1995). "Lower mite infestations in an asexual gecko compared with its sexual ancestors". Evolution 49 (3): 418–426.  
  32. ^ Morran, Levi T.; Schmidt, Olivia G.; Gelarden, Ian A.; Parrish Rc, Raymond C.; Lively, Curtis M. (2011). "Running with the Red Queen: Host-Parasite Coevolution Selects for Biparental Sex". Science 333 (6039): 216–218.  
  33. ^ "Sex -- As We Know It -- Works Thanks to Ever-Evolving Host-Parasite Relationships, Biologists Find". Science Daily. 9 July 2011. Retrieved 19 September 2011. 
  34. ^ Otto SP, Nuismer SL; Nuismer (2004). "Species interactions and the evolution of sex". Science 304 (5673): 1018–1020.  
  35. ^ Otto SP, Gerstein AC; Gerstein (August 2006). "Why have sex? The population genetics of sex and recombination". Biochemical Society Transactions 34 (Pt 4): 519–22.  
  36. ^ Parker MA (1994). "Pathogens and sex in plants". Evolutionary Ecology 8 (5): 560–584.  
  37. ^ Griffiths et al. 1999. Gene mutations, p197-234, in Modern Genetic Analysis, New York, W.H. Freeman and Company.
  38. ^ a b  
  39. ^ Muller, H.J. (1964). "The Relation of Recombination to Mutational Advance". Mutation Research 1: 2–9.  
  40. ^ Ridley M (2004) Evolution, 3rd edition. Blackwell Publishing.
  41. ^ Charlesworth B, Charlesworth D (2010) Elements of Evolutionary Genetics. Roberts and Company Publishers.
  42. ^ Whitlock, M. C.; Bourguet, D. (2000). "Factors affecting the genetic load in Drosophila: synergistic epistasis and correlations among fitness components". Evolution 54 (5): 1654–1660.  
  43. ^ Elena, S. F.; Lenski, R. E. (1997). "Test of synergistic interactions among deleterious mutations in bacteria". Nature 390 (6658): 395–398.  
  44. ^ Drake JW, Charlesworth B, Charlesworth D, Crow JF; Charlesworth; Charlesworth; Crow (April 1998). "Rates of spontaneous mutation". Genetics 148 (4): 1667–86.  
  45. ^ Eshel I, Feldman MW; Feldman (May 1970). "On the evolutionary effect of recombination". Theoretical population biology 1 (1): 88–100.  
  46. ^ Colegrave, N. (2002). "Sex releases the speed limit on evolution". Nature 420 (6916): 664–666.  
  47. ^ David MacKay (2003). Information Theory, Inference, and Learning Algorithms (PDF). Cambridge University Press, Cambridge. pp. 269–280. 
  48. ^ a b Bernstein H, Byerly HC, Hopf FA, Michod RE; Byerly; Hopf; Michod (1984). "Origin of sex". J. Theor. Biol. 110 (3): 323–51.  
  49. ^ Bernstein H, Byerly HC, Hopf FA, Michod RE; Byerly; Hopf; Michod (1985). "Genetic damage, mutation, and the evolution of sex". Science 229 (4719): 1277–81.  
  50. ^ Bernstein H, Hopf FA, Michod RE; Hopf; Michod (1987). "Advances in Genetics Volume 24". Adv. Genet. Advances in Genetics 24: 323–70.  
  51. ^ Cox MM (2001). "Historical overview: searching for replication help in all of the rec places". Proc. Natl. Acad. Sci. U.S.A. 98 (15): 8173–80.  
  52. ^ a b Bernstein H, Bernstein C, Michod RE (2011). “Meiosis as an evolutionary adaptation for DNA repair.” In “DNA Repair”, Intech Publ (Inna Kruman, editor), Chapter 19: 357-382 DOI: 10.5772/1751 ISBN 978-953-307-697-3 Available online from:
  53. ^ Darwin CR (1876). The effects of cross and self fertilisation in the vegetable kingdom. London: John Murray. [10] see page 462
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  56. ^ LODÉ T (2011). "The origin of sex was interaction, not reproduction (what's sex really all about), Big Idea". New Scientist 2837 (2837): 30–31.  
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  63. ^ a b c Olivia Judson (2002). Dr. Tatiana's sex advice to all creation. New York: Metropolitan Books. pp. 233–4.  
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  72. ^ Sterrer W (2002). "On the origin of sex as vaccination". Journal of Theoretical Biology 216 (4): 387–396.  
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An alternative theory, proposed by Thomas Cavalier-Smith, was labeled the Neomuran revolution. The designation "Neomuran revolution" refers to the appearances of the common ancestors of eukaryotes and archaea. Cavalier-Smith proposes that the first neomurans emerged 850 million years ago. Other molecular biologists assume that this group appeared much earlier, but Cavalier-Smith dismisses these claims because they are based on the "theoretically and empirically" unsound model of molecular clocks. Cavalier-Smith's theory of the Neomuran revolution has implications for the evolutionary history of the cellular machinery for recombination and sex. It suggests that this machinery evolved in two distinct bouts separated by a long period of stasis; first the appearance of recombination machinery in a bacterial ancestor which was maintained for 3 Gy, until the neomuran revolution when the mechanics were adapted to the presence of nucleosomes. The archaeal products of the revolution maintained recombination machinery that was essentially bacterial, whereas the eukaryotic products broke with this bacterial continuity. They introduced cell fusion and ploidy cycles into cell life histories. Cavalier-Smith argues that both bouts of mechanical evolution were motivated by similar selective forces: the need for accurate DNA replication without loss of viability.[75]

Neomuran revolution

The two viruses established in the cell would initiate replication in response to signals from the host cell. A mitosis-like cell cycle would proceed until the viral membranes dissolved, at which point linear chromosomes would be bound together with centromeres. The homologous nature of the two viral centromeres would incite the grouping of both sets into tetrads. It is speculated that this grouping may be the origin of crossing over, characteristic of the first division in modern meiosis. The partitioning apparatus of the mitotic-like cell cycle the cells used to replicate independently would then pull each set of chromosomes to one side of the cell, still bound by centromeres. These centromeres would prevent their replication in subsequent division, resulting in four daughter cells with one copy of one of the two original pox-like viruses. The process resulting from combination of two similar pox viruses within the same host closely mimics meiosis.[74]

Meiotic division in the VE hypothesis arose because of the evolutionary pressures placed on the lysogenic virus as a result of its inability to enter into the lytic cycle. This selective pressure resulted in the development of processes allowing the viruses to spread horizontally throughout the population. The outcome of this selection was cell-to-cell fusion. (This is distinct from the conjugation methods used by bacterial plasmids under evolutionary pressure, with important consequences.)[73] The possibility of this kind of fusion is supported by the presence of fusion proteins in the envelopes of the pox viruses that allow them to fuse with host membranes. These proteins could have been transferred to the cell membrane during viral reproduction, enabling cell-to-cell fusion between the virus host and an uninfected cell. The theory proposes meiosis originated from the fusion between two cells infected with related but different viruses which recognised each other as uninfected. After the fusion of the two cells, incompatibilities between the two viruses result in a meiotic-like cell division.[74]

For these transformations to lead to the eukaryotic cell cycle, the VE hypothesis specifies a pox-like virus as the lysogenic virus. A pox-like virus is a likely ancestor because of its fundamental similarities with eukaryotic nuclei. These include a double stranded DNA genome, a linear chromosome with short telomeric repeats, a complex membrane bound capsid, the ability to produce capped mRNA, and the ability to export the capped mRNA across the viral membrane into the cytoplasm. The presence of a lysogenic pox-like virus ancestor explains the development of meiotic division, an essential component of sexual reproduction.[74]

The viral eukaryogenesis (VE) theory proposes that eukaryotic cells arose from a combination of a lysogenic virus, an archaeon and a bacterium. This model suggests that the nucleus originated when the lysogenic virus incorporated genetic material from the archaeon and the bacterium and took over the role of information storage for the amalgam. The archaeal host transferred much of its functional genome to the virus during the evolution of cytoplasm but retained the function of gene translation and general metabolism. The bacterium transferred most of its functional genome to the virus as it transitioned into a mitochondrion.[73]

Viral eukaryogenesis

While theories positing fitness benefits that led to the origin of sex are often problematic, several theories addressing the emergence of the mechanisms of sexual reproduction have been proposed.

Mechanistic origin of sexual reproduction

Sex may also be derived from another prokaryotic process. A comprehensive 'origin of sex as vaccination' theory proposes that eukaryan sex-as-syngamy (fusion sex) arose from prokaryan unilateral sex-as-infection when infected hosts began swapping nuclearised genomes containing coevolved, vertically transmitted symbionts that provided protection against horizontal superinfection by more virulent symbionts. Sex-as-meiosis (fission sex) then evolved as a host strategy to uncouple (and thereby emasculate) the acquired symbiont genomes.[72]

[63] A third theory is that sex evolved as a form of

[71].plasmids, and swapping jumping genes through a combination of haloarchaea Similarly, it has been proposed that sexual reproduction evolved from ancient [63].F-plasmid. However, it does support the selfish genetic element theory, as it is propagated through such a "selfish gene", the horizontal gene transfer, a form of genetic exchange that some sources describe as sex, is not a form of reproduction, but rather an example of Bacterial conjugation [70] Another theory is that sexual reproduction originated from

Sex may also have been present even earlier, in the RNA world that is considered to have preceded DNA cellular life forms.[66] A proposal for the origin of sex in the RNA world was based on the type of sexual interaction that is known to occur in extant single-stranded segmented RNA viruses such as influenza virus, and in extant double-stranded segmented RNA viruses such as reovirus.[67] Exposure to conditions that cause RNA damage could have led to blockage of replication and death of these early RNA life forms. Sex would have allowed re-assortment of segments between two individuals with damaged RNA, permitting undamaged combinations of RNA segments to come together, thus allowing survival. Such a regeneration phenomenon, known as multiplicity reactivation, occurs in influenza virus[68] and reovirus[69]

and adaptative adjustments would have followed a course in which bacterial transformation naturally gave rise to sexual reproduction in eukaryotes. [59] In extant organisms, proteins with central functions in meiosis are similar to key proteins in bacterial transformation. For example, recA recombinase, that catalyses the key functions of DNA homology search and strand exchange in the bacterial sexual process of transformation, has orthologs in eukaryotes that perform similar functions in meiotic recombination (see WorldHeritage articles [64][61] If, as evidence indicates, sexual reproduction arose very early in eukaryotic evolution, the essential features of meiosis may have already been present in the prokaryotic ancestors of eukaryotes.

[63] Organisms need to replicate their genetic material in an efficient and reliable manner. The necessity to repair genetic damage is one of the leading theories explaining the origin of sexual reproduction.

plants. parthenocarpic and some Bdelloidea There are a few species which have secondarily lost this feature, such as [62][61][52][1] Many

Origin of sexual reproduction

The "libertine bubble theory" proposes that meiotic sex evolved in proto-eukaryotes to solve a problem that bacteria did not have,[58] namely a large amount of DNA material, occurring in an archaic step of proto-cell formation and genetic exchanges. So that, rather than providing selective advantages through reproduction, sex could be thought of as a series of separate events which combines step-by-step some very weak benefits of recombination, meiosis, gametogenesis and syngamy.[59] Therefore, current sexual species could be descendants of primitive organisms that practiced more stable exchanges in the long term, while asexual species have emerged, much more recently in evolutionary history, from the conflict of interest resulting from anisogamy.

[57] According to the [54] The evolution of sex can alternatively be described as a kind of gene exchange that is independent from reproduction.

Libertine bubble theory

In the view of the repair and complementation hypothesis, the removal of DNA damage by recombinational repair produces a new, less deleterious form of informational noise, allelic recombination, as a by-product. This lesser informational noise generates genetic variation, viewed by some as the major effect of sex, as discussed in the earlier parts of this article.

However, outcrossing may be abandoned in favor of parthogenesis or selfing (which retain the advantage of meiotic recombinational repair) under conditions in which the costs of mating are very high. For instance, costs of mating are high when individuals are rare in a geographic area, such as when there has been a forest fire and the individuals entering the burned area are the initial ones to arrive. At such times mates are hard to find, and this favors parthenogenic species.

In some lines of descent from the earliest organisms, the diploid stage of the sexual cycle, which was at first transient, became the predominant stage, because it allowed complementation — the masking of deleterious recessive mutations (i.e. hybrid vigor or heterosis). Outcrossing, the second fundamental aspect of sex, is maintained by the advantage of masking mutations and the disadvantage of inbreeding (mating with a close relative) which allows expression of recessive mutations (commonly observed as inbreeding depression). This is in accord with Charles Darwin,[53] who concluded that the adaptive advantage of sex is hybrid vigor; or as he put it, "the offspring of two individuals, especially if their progenitors have been subjected to very different conditions, have a great advantage in height, weight, constitutional vigor and fertility over the self fertilised offspring from either one of the same parents."

The repair and complementation hypothesis assumes that genetic recombination is fundamentally a DNA repair process, and that when it occurs during meiosis it is an adaptation for repairing the genomic DNA which is passed on to progeny. Recombinational repair is the only repair process known which can accurately remove double-strand damages in DNA, and such damages are both common in nature and ordinarily lethal if not repaired. For instance, double-strand breaks in DNA occur about 50 times per cell cycle in human cells [see DNA damage (naturally occurring)]. Recombinational repair is prevalent from the simplest viruses to the most complex multicellular eukaryotes. It is effective against many different types of genomic damage, and in particular is highly efficient at overcoming double-strand damages. Studies of the mechanism of meiotic recombination indicate that meiosis is an adaptation for repairing DNA.[51][52] These considerations form the basis for the first part of the repair and complementation hypothesis.

An alternative "informational" approach to this problem has led to the view that the two fundamental aspects of sex, genetic recombination and outcrossing, are adaptive responses to the two major sources of "noise" in transmitting genetic information. Genetic noise can occur as either physical damage to the genome (e.g. chemically altered bases of DNA or breaks in the chromosome) or replication errors (mutations)[48][49][50] This alternative view is referred to as the repair and complementation hypothesis, to distinguish it from the traditional variation hypothesis.

As discussed in the earlier part of this article, sexual reproduction is conventionally explained as an adaptation for producing genetic variation through allelic recombination. As acknowledged above, however, serious problems with this explanation have led many biologists to conclude that the benefit of sex is a major unsolved problem in evolutionary biology.

DNA repair and complementation

An information theoretic analysis using a simplified but useful model shows that in asexual reproduction, the information gain per generation of a species is limited to 1 bit per generation, while in sexual reproduction, the information gain is bounded by \surd G, where G is the size of the genome in bits.[47]

It has recently been shown in experiments with Chlamydomonas algae that sex can remove the speed limit on evolution.[46]

Ilan Eshel suggested that sex prevents rapid evolution. He suggests that recombination breaks up favourable gene combinations more often than it creates them, and sex is maintained because it ensures selection is longer-term than in asexual populations - so the population is less affected by short-term changes.[26]:85–86[45] This explanation is not widely accepted, as its assumptions are very restrictive.

Speed of evolution

Other explanations

There has been much criticism of Kondrashov's theory, since it relies on two key restrictive conditions. The first requires that the rate of deleterious mutation should exceed one per genome per generation in order to provide a substantial advantage for sex. While there is some empirical evidence for it (for example in Drosophila[42] and E. coli[43]), there is also strong evidence against it. Thus, for instance, for the sexual species Saccharomyces cerevisiae (yeast) and Neurospora crassa (fungus), the mutation rate per genome per replication are 0.0027 and 0.0030 respectively. For the nematode worm Caenorhabditis elegans, the mutation rate per effective genome per sexual generation is 0.036.[44] Secondly, there should be strong interactions among loci (synergistic epistasis), a mutation-fitness relation for which there is only limited evidence. Conversely, there is also the same amount of evidence that mutations show no epistasis (purely additive model) or antagonistic interactions (each additional mutation has a disproportionally small effect).

Kondrashov argues that the slightly deleterious nature of mutations means that the population will tend to be composed of individuals with a small number of mutations. Sex will act to recombine these genotypes, creating some individuals with fewer deleterious mutations, and some with more. Because there is a major selective disadvantage to individuals with more mutations, these individuals die out. In essence, sex compartmentalises the deleterious mutations.

Similarly, an organism may be able to cope with a few defects, but the presence of many mutations could overwhelm its backup mechanisms.

By way of analogy, think of a car with several minor faults. Each is not sufficient alone to prevent the car from running, but in combination, the faults combine to prevent the car from functioning.

This hypothesis was proposed by synergistic epistasis.

Diagram illustrating different relationships between numbers of mutations and fitness. Kondrashov's model requires synergistic epistasis, which is represented by the red line[40][41] - each mutation has a disproproportionately large effect on the organism's fitness.

Removal of deleterious genes

For sexually reproducing populations, mutations in the DNA are more likely to be removed due to recombination in the process of meiosis. The offspring are also not direct genetic clones of a single parent. The alleles from both parents contribute to the offspring. This creates the ability to mask a mutation in the form of heterozygotes. Selection can also work in removing mutations from a sexual population. The lessened amounts of harmful mutations within an organism can lead to increased reproductive success. Natural selection will select for the reduced number of deleterious mutations. Many believe that this ability to evade the accumulation of harmful and possibly lethal mutations produces a substantial advantage for sexually reproducing populations.

While DNA is able to recombine to modify alleles, DNA is also susceptible to mutations within the sequence that can affect an organism in a negative manner. Asexual organisms do not have the ability to recombine their genetic information to form new and differing alleles. Once a mutation occurs in the DNA or other genetic carrying sequence, there is no way for the mutation to be removed from the population until another mutation occurs that ultimately deletes the primary mutation. This is rare among organisms. Hermann Joseph Muller introduced the idea that mutations build up in asexual reproducing organisms. Muller described this occurrence by comparing the mutations that accumulate as a ratchet. Each mutation that arises in asexually reproducing organisms turns the ratchet once. The ratchet is unable to be rotated backwards, only forwards. The next mutation that occurs turns the ratchet once more. Additional mutations in a population continually turn the ratchet and the mutations, mostly deleterious, continually accumulate without recombination.[39] These mutations are passed onto the next generation because the offspring are exact genetic clones of their parent. The genetic load of organisms and their populations will increase due to the addition of multiple deleterious mutations and decrease the overall reproductive success and fitness.

Evading harmful mutation build-up

There are two main hypotheses which explain how sex may act to remove deleterious genes from the genome.

[38]. Sexual reproduction is believed to be more efficient than asexual reproduction in removing those mutations from the genome.natural selection If a mutation has a deleterious effect, it will then usually be removed from the population by the process of [37]

Deleterious mutation clearance

Critics of the Red Queen hypothesis question whether the constantly changing environment of hosts and parasites is sufficiently common to explain the evolution of sex. In particular, Otto and Nuismer [34] presented results showing that species interactions (e.g. host vs parasite interactions) typically select against sex. They concluded that, although the Red Queen hypothesis favors sex under certain circumstances, it alone does not account for the ubiquity of sex. Otto and Gerstein [35] further stated that “it seems doubtful to us that strong selection per gene is sufficiently commonplace for the Red Queen hypothesis to explain the ubiquity of sex.” Parker [36] reviewed numerous genetic studies on plant disease resistance and failed to uncover a single example consistent with the assumptions of the Red Queen hypothesis.

In 2011, researchers used the microscopic roundworm Caenorhabditis elegans as a host and the pathogenic bacteria Serratia marcescens to generate a host-parasite coevolutionary system in a controlled environment, allowing them to conduct more than 70 evolution experiments testing the Red Queen Hypothesis. They genetically manipulated the mating system of C. elegans, causing populations to mate either sexually, by self-fertilization, or a mixture of both within the same population. Then they exposed those populations to the S. marcescens parasite. It was found that the self-fertilizing populations of C. elegans were rapidly driven extinct by the coevolving parasites while sex allowed populations to keep pace with their parasites, a result consistent with the Red Queen Hypothesis.[32][33]

However, Hanley et al.[31] studied mite infestations of a parthenogenetic gecko species and its two related sexual ancestral species. Contrary to expectation based on the Red Queen hypothesis, they found that the prevalence, abundance and mean intensity of mites in sexual geckos was significantly higher than in asexuals sharing the same habitat.

Further evidence for the Red Queen hypothesis was provided by observing long‐term dynamics and parasite coevolution in a "mixed" (sexual and asexual) population of snails (Potamopyrgus antipodarum). The number of sexuals, the number asexuals, and the rates of parasite infection for both were monitored. It was found that clones that were plentiful at the beginning of the study became more susceptible to parasites over time. As parasite infections increased, the once plentiful clones dwindled dramatically in number. Some clonal types disappeared entirely. Meanwhile, sexual snail populations remained much more stable over time.[29][30]

Evidence for this explanation for the evolution of sex is provided by comparison of the rate of molecular evolution of genes for kinases and immunoglobulins in the immune system with genes coding other proteins. The genes coding for immune system proteins evolve considerably faster.[27][28]

In other words, like Lewis Carroll's Red Queen, sexual hosts are continually adapting in order to stay ahead of their parasites.

In reality, there will be several genes involved in the relationship between hosts and parasites. In an asexual population of hosts, offspring will only have the different parasitic resistance if a mutation arises. In a sexual population of hosts, however, offspring will have a new combination of parasitic resistance alleles.

Imagine, for example that there is one gene in parasites with two alleles p and P conferring two types of parasitic ability, and one gene in hosts with two alleles h and H, conferring two types of parasite resistance, such that parasites with allele p can attach themselves to hosts with the allele h, and P to H. Such a situation will lead to cyclic changes in allele frequency - as p increases in frequency, h will be disfavoured.

When an environment changes, previously neutral or deleterious alleles can become favourable. If the environment changed sufficiently rapidly (i.e. between generations), these changes in the environment can make sex advantageous for the individual. Such rapid changes in environment are caused by the co-evolution between hosts and parasites.

One of the most widely discussed theories to explain the persistence of sex is that it is maintained to assist sexual individuals in resisting parasites, also known as the Red Queen's Hypothesis.[12][24][25][26]:113–117

Increased resistance to parasites

Supporters of these theories respond to the balance argument that the individuals produced by sexual and asexual reproduction may differ in other respects too – which may influence the persistence of sexuality. For example, in the heterogamous water fleas of the genus Cladocera, sexual offspring form eggs which are better able to survive the winter versus those the fleas produce asexually.

Ronald Fisher also suggested that sex might facilitate the spread of advantageous genes by allowing them to better escape their genetic surroundings, if they should arise on a chromosome with deleterious genes.

Sex could be a method by which novel genotypes are created. Because sex combines genes from two individuals, sexually reproducing populations can more easily combine advantageous genes than can asexual populations. If, in a sexual population, two different advantageous alleles arise at different loci on a chromosome in different members of the population, a chromosome containing the two advantageous alleles can be produced within a few generations by recombination. However, should the same two alleles arise in different members of an asexual population, the only way that one chromosome can develop the other allele is to independently gain the same mutation, which would take much longer. Several studies have addressed counterarguments, and the question of whether this model is sufficiently robust to explain the predominance of sexual versus asexual reproduction.[23]:73–86

This diagram illustrates how sex might create novel genotypes more rapidly. Two advantageous alleles A and B occur at random. The two alleles are recombined rapidly in a sexual population (top), but in an asexual population (bottom) the two alleles must independently arise because of clonal interference.

Novel genotypes

On the other hand, the maintenance of sex based on DNA repair and complementation applies widely to all sexual species.

The classes of hypotheses based on the creation of variation are further broken down below. It is important to realise that any number of these hypotheses may be true in any given species (they are not mutually exclusive), and that different hypotheses may apply in different species. However, a research framework based on creation of variation has yet to be found that allows one to determine whether the reason for sex is universal for all sexual species, and, if not, which mechanisms are acting in each species.

For the advantage due to DNA repair, there is an immediate large benefit of removing DNA damage by recombinational DNA repair during meiosis, since this removal allows greater survival of progeny with undamaged DNA. The advantage of complementation to each sexual partner is avoidance of the bad effects of their deleterious recessive genes in progeny by the masking effect of normal dominant genes contributed by the other partner.

For the advantage due to genetic variation, there are three possible reasons this might happen. First, sexual reproduction can combine the effects of two beneficial mutations in the same individual (i.e. sex aids in the spread of advantageous traits). Also, the necessary mutations do not have to have occurred one after another in a single line of descendants.[22] Second, sex acts to bring together currently deleterious mutations to create severely unfit individuals that are then eliminated from the population (i.e. sex aids in the removal of deleterious genes). However, in organisms containing only one set of chromosomes, deleterious mutations would be eliminated immediately, and therefore removal of harmful mutations is an unlikely benefit for sexual reproduction. Lastly, sex creates new gene combinations that may be more fit than previously existing ones, or may simply lead to reduced competition among relatives.

Advantages due to genetic variation

Reproductive advantages of the asexual forms are in quantity of the progeny and the advantages of the hermaphrodite forms – in maximum diversity. Transition from the hermaphrodite to dioecious state leads to a loss of at least half of the diversity. So, the main question is to explain the advantages given by sexual differentiation, i.e. the benefits of two separate sexes compare to hermaphrodites rather than to explain benefits of sexual forms (hermaphrodite + dioecious) over asexual ones. It has already been understood that since sexual reproduction is not associated with any clear reproductive advantages, as compared with asexual, there should be some important advantages in evolution.[21]

It is important to mention that the concept of sex includes two fundamental phenomena: the sexual process (fusion of genetic information of two individuals) and sexual differentiation (separation of this information into two parts). Depending on the presence or absence of these phenomena, the existing ways of reproduction can be divided into asexual, hermaphrodite and dioecious forms. The sexual process and sexual differentiation are different phenomena, and, in essence, are diametrically opposed. The first creates (increases) diversity of genotypes, and the second decreases it in half.

Advantages conferred by sex

In contrast to the view that sex promotes genetic variation, Heng[19] and Gorelick and Heng[20] reviewed evidence that sex actually acts as a constraint on genetic variation. They consider that sex acts as a coarse filter, weeding out major genetic changes, such as chromosomal rearrangements, but permitting minor variation, such as changes at the nucleotide or gene level (that are often neutral) to pass through the sexual sieve.

"Although once popular, the tangled bank hypothesis now seems to face many problems, and former adherents are falling away. The theory would predict a greater interest in sex among animals that produce lots of small offspring that compete with each other. In fact, sex is invariably associated with organisms that produce a few large offspring, whereas organisms producing small offspring frequently engage in parthenogenesis [asexual reproduction]. In addition, the evidence from fossils suggests that species go for vast periods of [geologic] time without changing much."

The hypothesis, proposed by Michael Ghiselin in his 1974 book, The Economy of Nature and the Evolution of Sex, suggests that a diverse set of siblings may be able to extract more food from its environment than a clone, because each sibling uses a slightly different niche. One of the main proponents of this hypothesis is Graham Bell of McGill University. The hypothesis has been criticised for failing to explain how asexual species developed sexes. In his book, Evolution and Human Behavior (MIT Press, 2000), John Cartwright comments:

"It is interesting to contemplate an entangled bank, clothed with many plants of many kinds, with birds singing on the bushes, with various insects flitting about, and with worms crawling through the damp earth, and to reflect that these elaborately constructed forms, so different from each other, and dependent on each other in so complex a manner, have all been produced by laws acting around us."

A similar hypothesis is named the tangled bank hypothesis after a passage in Charles Darwin's The Origin of Species:

elm tree. In the forest of this example, empty patches between trees can support one individual each. When a patch becomes available because of the death of a tree, other trees' seeds will compete to fill the patch. Since the chance of a seed's success in occupying the patch depends upon its genotype, and a parent cannot anticipate which genotype is most successful, each parent will send many seeds, creating competition between siblings. Natural selection therefore favours parents which can produce a variety of offspring (see lottery principle).

August Weismann proposed in 1889[15] an explanation for the evolution of sex, where the advantage of sex is the creation of variation among siblings. It was then subsequently explained in genetics terms by Fisher[16] and Muller[17] and has been recently summarised by Burt in 2000.[18]

Promotion of genetic variation

Some species avoid the cost of 50% of sexual reproduction, although they have "sex" (in the sense of genetic recombination). In these species (e.g., bacteria, ciliates, dinoflagellates and diatoms), "sex" and reproduction occurs separately.[5][14]

Sex decoupled from reproduction

Studies on the costs of sex suggest that sexual reproduction is often stabilized by highly lineage-specific mechanisms (e.g. beneficial traits that evolved within a species and became tightly associated with sex or lineage-specific factors might prevent asexuals from reaching their full potential) - suggesting that the costs of sex are highly variable and often lower than theoretical considerations implied, which has consequences for the magnitude of universal benefits required to resolve the paradox of sex.[13]

The two-fold cost of sex may be compensated for in some species in many ways. Females may eat males after mating, males may be much smaller or rarer, or males may help raise offspring.


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