Intragenomic conflict
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2008-07-13T07:08:28Z
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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 [[DNA replication|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 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 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]]'' ([[Drosophilidae|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 target===
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 ===
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 several chromosomal rearrangements in mammals. The general molecular evolution of centromeres is likely to involve such mechanisms.
===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'').<ref name=beeman>Beeman R, Friesen K & Denell R (1992) Maternal-effect selfish genes in flour beetles. ''Science'': 256(5053):89-92. [http://www.sciencemag.org/cgi/content/abstract/256/5053/89 DOI: 10.1126/science.1566060]</ref> Maternal-effect selfish genes have been successfully synthesized in the lab.<ref name=chen>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. [http://www.sciencemag.org/cgi/content/abstract/sci;316/5824/597 DOI: 10.1126/science.1566060]</ref>
===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-chromosome]]s are nonessential [[chromosome]]s; not [[homology (biology)|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{{Fact|date=October 2007}}. They are found in all major taxonomic groupings of both [[plant]]s and [[animal]]s.
==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 [[plasmid]]s 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 to increase the production of female descendants and/or eliminate offspring not containing them.
===Feminization===
Male 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. 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-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]] and [[mites]], in which males are produced asexually, ''[[Wolbachia]]'' and ''[[Cardinium]]'' can induce duplication of the [[chromosome]]s 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 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===
[[Plasmid]]s are additional circular chromosomes present in many [[bacteria]]. Most plasmids promote [[Bacterial conjugation|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 [[virus]]es, 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 sex===
Conflict between chromosomes has been proposed as an element in the evolution of sex. <ref name=O'Dea>O'Dea, JD (2006) Did Conflict Between Chromosomes Drive the Evolution of Sex? Calodema, 8: 33-34. [http://julianodea.blogspot.com/2005_12_01_julianodea_archive.html]</ref>
==References==
{{reflist}}
==Further Reading==
* '''Burt, A. & [[Robert Trivers|Trivers, R.L.]]''' (2006) ''Genes in Conflict : The Biology of Selfish Genetic Elements.'' Belknap Press, Harvard. ISBN 0-674-01713-7
* '''[[Leda Cosmides|Cosmides, L.M.]]''' & '''[[John Tooby|Tooby, J.]]''' (1981) ''Cytoplasmic inheritance and intragenomic conflict.'' Journal of Theoretical Biology, 89, 83-129.
* '''[[Richard Dawkins|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.
* '''[[David Haig (biologist)|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. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11483984&query_hl=1&itool=pubmed_docsum]
* '''Jones, R.N.''' (1991) ''B-chromosome drive.'' The American Naturalist, 137(3), 430-442.
[[Category:Evolution]]
[[Category:Evolutionary biology]]
[[Category:Selection]]