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Intragenomic conflict

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The selfish gene theory postulates that natural selection will increase the frequency of those genes whose phenotypic effects ensure their successful replication. Generally, a gene achieves this goal by building, in cooperation with other genes, an organism capable of transmitting the gene to descendants. Intragenomic conflict arises when genes inside a genome are not transmitted by the same rules, or when a gene causes its own transmission to the detriment of the rest of the genome (this last kind of gene is usually called selfish genetic element, or ultraselfish gene or parasitic DNA).

Nuclear genesEdit

This section deals with conflict between nuclear genes.

Meiotic driveEdit

All nuclear genes in a given diploid genome cooperate because each allele has an equal probability of being present in a gamete. This fairness is guaranteed by meiosis. However, there is one type of gene, called a segregation distorter, that "cheats" during meiosis or gametogenesis and thus is present in more than half of the functional gametes. The most studied examples are sd in Drosophila melanogaster (fruit fly), t haplotype in Mus musculus (mouse) and sk in Neurospora sp. (fungus). Segregation distorters that are present in sexual chromosomes (as the X chromosome in several Drosophila species) are denominated sex-ratio distorters, as they induce a sex-ratio bias in the offspring of the carrier individual.

Killer and targetEdit

The most simple model of meiotic drive involves two tightly linked loci: a Killer locus and a Target locus. The segregation distorter set is composed by the allele Killer (in the Killer locus) and the allele Resistant (in the Target locus), while its rival set is composed by the alleles Non-killer and Non-resistant. So, the segregation distorter set produces a toxin to which it is itself resistant, while its rival is not. Thus, it kills those gametes containing the rival set and increases in frequency. The tight linkage between these loci is crucial, so these genes usually lie on low recombination regions of the genome.

True meiotic drive Edit

Other systems do not involve gamete destruction, but rather use the asymmetry of meiosis in females : the driving allele ends up in the ovocyte instead of in the polar bodies with a probability greater than one half. This is termed true meiotic drive, as it does not rely on a post-meiotic mechanism. The best-studied examples include the neocentromeres (knobs) of maize, as well as several chromosomal rearrangements in mammals. The general molecular evolution of centromeres is likely to involve such mechanisms.

Lethal Maternal-effectsEdit

Main article: Maternal effect dominant embryonic arrest

The Medea gene causes the death of progeny from a heterozygous mother that do not inherit it. It occurs in the flour beetle (Tribolium castaneum).[1] Maternal-effect selfish genes have been successfully synthesized in the lab.[2]

TransposonsEdit

Transposons are autonomous replicating genes that encode the ability to move to new positions in the genome and therefore accumulate in the genomes. They replicate themselves in spite of being detrimental to the rest of the genome. They are often called 'jumping genes' or parasitic DNA and were discovered by Barbara McClintock in 1944.

Homing endonuclease genesEdit

Main article: Homing endonucleases

Homing endonuclease genes (HEG) convert their rival allele into a copy of themselves, and are thus inherited by nearly all meiotic daughter cells of a heterozygote cell. They achieve this by encoding an endonuclease which breaks the rival allele. This break is repaired by using the sequence of the HEG as template.[3]

HEGs encode sequence-specific endonucleases. The recognition sequence (RS) is 15-30 bp long and usually occurs once in the genome. HEGs are located in the middle of their own recognition sequences. Most HEGs are encoded by self-splicing introns (group I & II) and inteins. Inteins are internal protein fragments produced from protein splicing and usually contain endonuclease and splicing activities. The allele without the HEGs are cleaved by the homing endonuclease and the double-strand break are repaired by homologous recombination (gene conversion) using the allele containing HEGs as template. Both chromosomes will contain the HEGs after repair.[4]

B-chromosomeEdit

B-chromosomes are nonessential chromosomes; not homologous with any member of the normal (A) chromosome set; morphologically and structurally different from the A's; and they are transmitted at higher-than-expected frequencies, leading to their accumulation in progeny. In some cases, there is strong evidence to support the contention that they are simply selfish and that they exist as parasitic chromosomes[How to reference and link to summary or text]. They are found in all major taxonomic groupings of both plants and animals.

Cytoplasmic genesEdit

This section deals with conflict between nuclear and cytoplasmic genes. Mitochondria represent one such example of a set of cytoplasmic genes, as do plasmids and bacteria which have integrated themselves into another species' cytoplasm.

Males as dead-ends to cytoplasmic genesEdit

Anisogamy generally produces zygotes that inherit cytoplasmic elements exclusively from the female gamete. Thus, males represent dead-ends to these genes. Because of this fact, cytoplasmic genes have evolved a number of mechanisms to increase the production of female descendants and/or eliminate offspring not containing them.

FeminizationEdit

Male organisms are converted into females by cytoplasmic inherited protists (Microsporidia) or bacteria (Wolbachia), regardless of nuclear sex-determining factors. This occurs in amphipod and isopod Crustacea and Lepidoptera.

Male-killingEdit

Male embryos (in the case of cytoplasmic inherited bacteria) or male larvae (in the case of Microsporidia) are killed. In the case of embryo death, this diverts investment from males to females who can transmit these cytoplasmic elements (for instance, in ladybird beetles, infected female hosts eat their dead male brothers, which is positive from the viewpoint of the bacterium). In the case of microsporidia-induced larval death, the agent is transmitted out of the male lineage (through which it cannot be transmitted) into the environment, where it may be taken up again infectiously by other individuals. Male-killing occurs in many insects. In the case of male embryo death, a variety of bacteria have been implicated, including Wolbachia.

Male-sterilityEdit

Anther tissue (male gametophyte) is killed by mitochondria in monoicous angiosperms, increasing energy and material spent in developing female gametophytes.

Parthenogenesis inductionEdit

In certain haplodiploid Hymenoptera and mites, in which males are produced asexually, Wolbachia and Cardinium can induce duplication of the chromosomes and thus convert the organisms into females. The cytoplasmic bacterium forces haploid cells to go through mitosis to produce diploid cells which therefore will be female. This produces an entirely female population. Interestingly, if antibiotics are administered to populations which have become asexual in this way, they revert back to sexuality instantly, as the cytoplasmic bacteria forcing this behaviour upon them is removed.

Cytoplasmic incompatibilityEdit

In many arthropods, zygotes produced by sperm of infected males and ova of non-infected females can be killed by Wolbachia or Cardinium.

PlasmidsEdit

Plasmids are additional circular chromosomes present in many bacteria. Most plasmids promote conjugation between their host and other bacteria, infecting new cytoplasms while retaining a copy inside the original host. Chromosomal genes are usually not transmitted. Therefore, they bear the costs of replicating the donated plasmid and the costs of increased exposure to viruses, but gain little in return (but the genes on plasmids may direct production of proteins that are beneficial to bacteria such as those that confer antibiotic resistance properties).

Evolution of sexEdit

Conflict between chromosomes has been proposed as an element in the evolution of sex. [5]

ReferencesEdit

  1. Beeman R, Friesen K & Denell R (1992) Maternal-effect selfish genes in flour beetles. Science: 256(5053):89-92. DOI: 10.1126/science.1566060
  2. Chen C, Huang H, Ward C, Su J, Schaeffer L, Guo M & Hay B (2007) A Synthetic Maternal-Effect Selfish Genetic Element Drives Population Replacement In Drosophila. Science: 316(5824):597-600. DOI: 10.1126/science.1566060
  3. Sinkins, S. & Gould F. (2006) Gene drive systems for insect disease vectors. Nature Reviews, 7, 427-435.
  4. Burt A and Koufopanou V (2004) Current Opinion in Genetics & Development 14:609-615.
  5. O'Dea, JD (2006) Did Conflict Between Chromosomes Drive the Evolution of Sex? Calodema, 8: 33-34. [1]

Further readingEdit

  • Burt, A. & Trivers, R.L. (2006) Genes in Conflict : The Biology of Selfish Genetic Elements. Belknap Press, Harvard. ISBN 0-674-01713-7
  • Sinkins, S. & Gould F. (2006) Gene drive systems for insect disease vectors. Nature Reviews, 7, 427–435.
  • Cosmides, L.M. & Tooby, J. (1981) Cytoplasmic inheritance and intragenomic conflict. Journal of Theoretical Biology, 89, 83–129.
  • Dawkins, R. (1976) The Selfish Gene. Oxford University Press, Oxford. ISBN 0-19-217773-7
  • Eberhard, W.G. (1980) Evolutionary consequences of intracellular organelle competition. Quarterly Review of Biology, 55, 231–249.
  • Haig, D. (1997) The social gene. In Krebs, J. R. & Davies, N. B. (editors) Behavioural Ecology: an Evolutionary Approach, pp. 284–304. Blackwell Publishers, London.
  • Hurst, L.D., Atlan A. & Bengtsson, B. O. (1996) Genetic conflicts. Quarterly Review of Biology, 71(3), 317–364.
  • Hurst, G.D.D. & Werren, J.H. (2001) The role of selfish genetic elements in eukaryotic evolution. Nature Review Genetics, 2, 597–606. [2]
  • Jones, R.N. (1991) B-chromosome drive. The American Naturalist, 137(3), 430–442.
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