Intragenomic conflict

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 a selfish genetic element, ultraselfish gene, or parasitic DNA).

These "gene-centric" mechanisms of natural selection explain a few features of genetics which are not explained by the traditional "organism-centric" view, which only takes into account the effect of the phenotype on the reproductive success of the organism as a whole.

Nuclear genes

This section deals with conflict between nuclear genes.

Segregation distortion

In principle, the two parental alleles have equal probabilities of being present in the mature gamete. However, there are several mechanisms that lead to an unequal transmission of parental alleles from parents to offspring. One example is a 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),[1] t haplotype in Mus musculus (mouse) and sk in Neurospora spp. (fungus). Possible examples have also been reported in humans.[2] Segregation distorters that are present in sexual chromosomes (as is the case with the X chromosome in several Drosophila species[3][4]) 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 oocyte 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 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).[5] Maternal-effect selfish genes have been successfully synthesized in the lab.[6]


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 genes

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.[7]

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.[8]


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.[9] 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 to increase the production of female descendants and eliminate offspring not containing them.[10]


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 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.


In some cases anther tissue (male gametophyte) is killed by mitochondria in monoecious angiosperms, increasing energy and material spent in developing female gametophytes. This leads to a shift from monoecy to gynodioecy, where part of the plants in the population are male-sterile.

Parthenogenesis induction

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 incomplete 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 to sexuality instantly, as the cytoplasmic bacteria forcing this behaviour upon them are 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 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 sex

Conflict between chromosomes has been proposed as an element in the evolution of sex.[11]

See also


  2. Yang, Liu; Liangliang Zhang; Shuhua Xu; Landian Hu; Laurence D. Hurst; Xiangyin Kong (July 2013). "Identification of Two Maternal Transmission Ratio Distortion Loci in Pedigrees of the Framingham Heart Study". Scientific Reports. 3. doi:10.1038/srep02147. Retrieved 10 July 2013.
  3. ""Sex Ratio" Meiotic Drive in Drosophila testacea" (PDF).
  4. "Geographical Distribution and Cytology of "Sex Ratio" in Drosophila Pseudoobscura and Related Species" (PDF). Genetics. 21: 473–90. Jul 1936. PMC 1208687Freely accessible. PMID 17246805.
  5. R. W. Beeman; K. S. Friesen; R. E. Denell (1992). "Maternal-effect selfish genes in flour beetles" (PDF). Science. 256 (5053): 89–92. doi:10.1126/science.1566060. PMID 1566060.
  6. Chun-Hong Chen; Haixia Huang; Catherine M. Ward; Jessica T. Su; Lorian V. Schaeffer; Ming Guo; Bruce A. Hay (2007). "A synthetic maternal-effect selfish genetic element drives population replacement in Drosophila". Science. 316 (5824): 597–600. doi:10.1126/science.1138595. PMID 17395794.
  7. Steven P. Sinkins; Fred Gould (2006). "Gene drive systems for insect disease vectors" (PDF). Nature Reviews Genetics. 7 (6): 427–435. doi:10.1038/nrg1870. PMID 16682981.
  8. Austin Burt; Vassiliki Koufopanou (2004). "Homing endonuclease genes: the rise and fall and rise again of a selfish element". Current Opinion in Genetics & Development. 14 (6): 609–615. doi:10.1016/j.gde.2004.09.010. PMID 15531154.
  9. Östergren, G. (1947). "Heterochromatic B-Chromosomes in Anthoxanthum". Hereditas. 33 (1–2): 261–296. doi:10.1111/j.1601-5223.1947.tb02804.x.
  10. Jan Engelstädter; Gregory D. D. Hurst (2009). "The ecology and evolution of microbes that manipulate host reproduction". Annual Review of Ecology, Evolution, and Systematics. 140: 127–149. doi:10.1146/annurev.ecolsys.110308.120206.
  11. Julian D. O'Dea (2006). "Did conflict between chromosomes drive the evolution of sex?". Calodema. Sydney: Trevor J. Hawkeswood. 8: 33–34. See also the author's blog post.

Further reading

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