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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 it 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 in detriment to the rest of the genome (this last kind of gene is usually called selfish genetic element, or ultraselfish gene).
Nuclear genes
This section deals with conflict between nuclear genes.
Meiotic drive
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 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.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 itself is 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. Other systems do not involve gamete detruction, but rather use the assymetry of meiosis in females : the driving allele ends up in the ovocyte instead of in the polar bodies with a probability superior to 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 several chromosomal rearrangements in mammals. The general molecular evolution of centromeres is likely to involve such mechanims.
Lethal Maternal-effects
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).Transposons
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.Homing endonuclease genes
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.B-chromosome
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 in higher-than-expected frequencies, leading to their accumulation in progenies. In some cases, there is strong evidence to support the contention that they are simply selfish and that they exist as parasitic chromosomes. They are found in all major taxonomic groupings of both plants and animals.Cytoplasmic genes
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 genes
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 that increase the production of female descendants and/or eliminates offspring not containing them.Feminization
Organisms are converted into females by cytoplasmic inherited protists (Microsporidia) or bacteria (Wolbachia), regardless of nuclear sex-determining factors. It occurs in amphipod and isopod Crustacea and Lepidoptera.Male-killing
Male embryos (in the case of cytoplasmic inherited bacteria) or male larvae (in the case of Microsporidia) are killed, increasing the investment in females who can transmit these cytoplasmic elements. It occurs in many insects.Male-sterility
Anther tissue (male gametophyte) is killed by mitochondria in monoicous angiosperms, increasing energy and material spent in developing female gametophytes.Parthenogenesis induction
In certain haplodiploid Hymenoptera, where males are produced asexually, Wolbachia can induce duplication of the chromosomes and thus converts them into females. The cytoplasmic bacterium forces haploid cells to go through mitosis to produce diploid cells which hence 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 incompatibility
In many arthropods zygotes produced by sperm of infected males and ova of non-infected females can be killed by Wolbachia or Cardinium.Plasmids
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.References
- Burt, A. & Trivers, R.L. (2006) Genes in Conflict : The Biology of Selfish Genetic Elements. Belknap Press, Harvard. ISBN 0674017137
- 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 0192177737
- 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.
- Jones, R.N. (1991) B-chromosome drive. The American Naturalist, 137(3), 430-442.
"Intragenomic conflict"