Intragenomic conflict

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Intragenomic conflict refers to the

selfish gene theory postulates that natural selection will increase the frequency of those genes whose phenotypic effects cause their transmission to new organisms, and most genes achieve this by cooperating with other genes in the same genome to build an organism capable of reproducing and/or helping kin to reproduce.[5] The assumption of the prevalence of intragenomic cooperation underlies the organism-centered concept of inclusive fitness. However, conflict among genes in the same genome may arise both in events related to reproduction (a selfish gene may "cheat" and increase its own presence in gametes or offspring above the expected according to fair Mendelian segregation and fair gametogenesis) and altruism (genes in the same genome may disagree on how to value other organisms in the context of helping kin because coefficients of relatedness diverge between genes in the same genome).[6][7][8]

Nuclear genes

Autosomic genes usually have the same mode of transmission in sexually reproducing species due to the fairness of Mendelian segregation, but conflicts among alleles of autosomic genes may arise when an allele cheats during gametogenesis (segregation distortion) or eliminates embryos that don't contain it (lethal maternal effects). An allele may also directly convert its rival allele into a copy of itself (homing endonucleases). Finally, mobile genetic elements completely bypass Mendelian segregation, being able to insert new copies of themselves into new positions in the genome (transposons).

Segregation distortion

In principle, the two parental

Mus musculus (mouse) and sk in Neurospora spp. (fungus). Possible examples have also been reported in humans.[10]
Segregation distorters that are present in sexual chromosomes (as is the case with the X chromosome in several Drosophila species[11][12]) are denominated sex-ratio distorters, as they induce a sex-ratio bias in the offspring of the carrier individual.

Killer and target

The simplest 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

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

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).[13] Maternal-effect selfish genes have been successfully synthesized in the lab.[14]

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. They are often called 'jumping genes' or parasitic DNA and were discovered by Barbara McClintock in 1944.

Homing endonuclease genes

Main article:
Homing endonucleases

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.[15]

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

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.[16]

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 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.[17] They are found in all major taxonomic groupings of both plants and animals
.

Cytoplasmic genes

Since nuclear and cytoplasmic genes usually have different modes of transmission, intragenomic conflicts between them may arise.[18] Mitochondria and chloroplasts are two examples of sets of cytoplasmic genes that commonly have exclusive maternal inheritance, similar to endosymbiont parasites in arthropods, like Wolbachia.[19]

Males as dead-ends to cytoplasmic genes

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.[20]

Feminization

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-killing

Male

insects
. In the case of male embryo death, a variety of bacteria have been implicated, including Wolbachia.

Male-sterility

In some cases

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

diploid
cells which therefore will be female. This produces an entirely female population. 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.[19]

Evolution of sex

Conflict between chromosomes has been proposed as an element in the

evolution of sex.[21]

See also

References

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  11. ^ ""Sex Ratio" Meiotic Drive in Drosophila testacea" (PDF).
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  13. PMID 1566060. Archived from the original
    (PDF) on 2012-03-13. Retrieved 2011-07-21.
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  20. doi:10.1146/annurev.ecolsys.110308.120206
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  21. ^ Julian D. O'Dea (2006). "Did conflict between chromosomes drive the evolution of sex?". Calodema. 8: 33–34. See also [1].

Further reading

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